Nolvadex Question - Cycle Ancillary - Doctors Please

[BBC3]

OK Conciliator, let me have it. As some of you know I have determined that I have a problem that may result in an account at Victoria Secret if not addressed. My recent lab work indicates that I have an Estradiol level of 114. Yes, that is on a scale that maxes out around 60. I am attempting to mitigate with Nolvadex for the first time. I have never concerned myself with testing that number before as I did not have any evidence for cause. I have absolutely no indication of gyno, etc. But lately, I have been suspicious that I am not getting all that I can out of my testosterone supplementation for this reason, and now bloodwork has confirmed this high number. It seems easy enough to talk about these drugs in theory, but like anything else, once you become personally involved the waters become clouded. My question would be, how do you know what results you are getting from a SERM. Nolvadex is only going to prevent the effect of the estrogen on my body (chest, etc) by means of preventing the estrogen from affecting the area by blocking those receptors. Correct or not? If so, then how do you measure. What would blood work look like with Nolva in the mix. If Novla is just blocking the estrogens from "biting" on the desired areas (protection from gyno, etc), Does the level of E2 not still remain high in the blood stream? Probably so if you still render the good effects on cholesterol levels, etc. So how do you measure the effectiveness other than physical response? Even so, are we sure that the body does not signal back through a means such as the nervous system and tell the Hypothalmus that Estrogen is now not reaching those area, and thus signal for even more? I humbly request the help of all those who can shed some light here. I am reaching a crossroad that mandates some estrogen control and I am not sure the best way to proceed. I have a feeling I will wind up with a combination of a SERM and an AI. I only have Nolva and Clomid for now, so while on cycle I am choosing to go with the Nolva. What is the relationship between the nervous system and hormones. I can not help but think there must be a direct feedback involved via the nervous system as well. This aspect of hormone modulation does not seem to be very well addressed. Everyone always seems to focus on the direct impact of homones in the bloodstream ingnoring how the central nervouse system may relate. Also please do not forget the other question, as to while dosed on Nolva, how should my estrogens in my bloodwork read?

 

[brang]

For the record i am not a doctor nor an expert.. so take my answers accordingly (with as much cred as you would give to reading anything on the 'net.)

My recent lab work indicates that I have an Estradiol level of 114. Yes, that is on a scale that maxes out around 60. I am attempting to mitigate with Nolvadex for the first time.

Wasting your time and money. Nolva will not help here.

I have never concerned myself with testing that number before as I did not have any evidence for cause. I have absolutely no indication of gyno, etc. But lately, I have been suspicious that I am not getting all that I can out of my testosterone supplementation for this reason, and now bloodwork has confirmed this high number.

Take an AI to prevent aromatisation.

My question would be, how do you know what results you are getting from a SERM.

Your negative side effects go away.

Nolvadex is only going to prevent the effect of the estrogen on my body (chest, etc) by means of preventing the estrogen from affecting the area by blocking those receptors. Correct or not?

Correct.

What would blood work look like with Nolva in the mix.

The same.

If Novla is just blocking the estrogens from "biting" on the desired areas (protection from gyno, etc), Does the level of E2 not still remain high in the blood stream?

Yes.

Even so, are we sure that the body does not signal back through a means such as the nervous system and tell the Hypothalmus that Estrogen is now not reaching those area, and thus signal for even more?

Yes. That's why its called a negative feedback loop.

I humbly request the help of all those who can shed some light here.

Go back and read the previous thread(s) where you argued like a child. All the information is there in plain English.


HTH.
- b

 

[Conciliator]

Are you on a cycle of test right now? If so, what dose? I'm assuming you are on cycle when you say that you're suspicious you're "not getting all that you can out of your testosterone supplementation." What are you trying to get out of it? Realize that estrogen has beneficial effects.

If you are on test right now, there's nothing to worry about. The elevated numbers are to be expected as much more testosterone is availabile to aromatize. If you're not suffering from side effects like gyno or bloating, then what's the problem?

 

[bigbench]

Are you on a cycle of test right now? If so, what dose? I'm assuming you are on cycle when you say that you're suspicious you're "not getting all that you can out of your testosterone supplementation." What are you trying to get out of it? Realize that estrogen has beneficial effects.

If you are on test right now, there's nothing to worry about. The elevated numbers are to be expected as much more testosterone is availabile to aromatize. If you're not suffering from side effects like gyno or bloating, then what's the problem?

Agreed, its not always about how MUCH estro is in the system, but about the ratio of test:estro. When that ratio gap begins to close, then you know you need to do something. But if no signs are present, then its not enough to effect the body in a negative manor

 

[BBC3]

As soon as I get the results for the testosterone portion of the labs i'll post them. I was only supplementing about 150-200mgs test cyp/week. I had been doing so for about 10 weeks straight at the time of the labwork. I have briefly increased the dose for specialized training. I did this post bloodwork and prior to any test results. I understand the proportions go up. I do have the complaint of water retention. I am borderline gyno. Same as past probably. I have been able to supp a gram a week of test before and only wind up with sensative nips. Cold sweaty t-shirts, etc. Try a racquetball blasted off one of those titties will get your attention!!

The reason for my concern with E2 is that I come from a line of prostate cancer. I am not near that age in my genetic curve. I am guessing that level of E2 was way too high for 150-200 mgs /week. I AM CONVIINCED that Estrogen is the cause of prostate cancer. This is my reason for concern.

A good question would be. HOW well does Nolva affect the ability of E2 to bind to prostate cells.? I was assuming that Nolva would be good for this. I may have jumped the gun. Perhaps Adex is the better option here? Anyone know if Nolva prevents Estrogen from affecting prostate? It obviously works on pecks, but then again, I guess that is why it is a breast cancer drug??

 

[BBC3]

Hi Brang, thanks for your response. I would like to clarify one point of confusion. My biggest curiosity with this post is the relationship of the CENTRAL NERVOUS SYSTEM and the HTPA. This seems omitted. What signals are nerves sending the brain. How does this apply ? Most people speak of negative fedback in this world as how one level of hormones "scrapes" another, or maker of.???

Hello Conciliator, I agree with you here with the exception of my personal quest to prevent prostate issues. I would like to point out the relationship between the E2 and DHT, etc. Some much more can be achieved from testosterone with a low, controlled level of E2. This seems to be the big thing everyone misses over here. I am telling you that the same goals can be achieved with as little as 1/4 the supplemented testosterone, if the others are balanced right. Obviously from one point as if it is not turning into E2, then probably turning into DHT, maybee, right.

One other thought I have is that if I do elect to use Arimidex, how do I know it is not hendering the rate at which DHT is produced. Or worse, How do I not know it is not hendering the anabolic effects i am looking for.?? anyone here?? I would like to see a curve of effectiveness that Adex may have on preventing this aromatization. As you state and we all know, we need estrogen. A good dose of Adex can wind you up with none in a hurry. Is this determined with bloodwork and time.?

 

[Conciliator]

As soon as I get the results for the testosterone portion of the labs i'll post them. I was only supplementing about 150-200mgs test cyp/week. I had been doing so for about 10 weeks straight at the time of the labwork.

So you were more than doubling your natural testosterone levels. it's not surprising to me that your estrogen levels were also double the upper normal range.

The reason for my concern with E2 is that I come from a line of prostate cancer. I am not near that age in my genetic curve. I am guessing that level of E2 was way too high for 150-200 mgs /week. I AM CONVIINCED that Estrogen is the cause of prostate cancer. This is my reason for concern.

Why are you convinced of that? Prostate cancer is a classic example of an androgen-dependent tumor. Hormone therapy in later stages of prostate cancer involve lowering the levels of ANDROGENS in the body. If prostate cancer is a significant risk for you, you should go off anabolic/androgenic steroids and never take them again. Seriously.

A good question would be. HOW well does Nolva affect the ability of E2 to bind to prostate cells.? I was assuming that Nolva would be good for this. I may have jumped the gun. Perhaps Adex is the better option here? Anyone know if Nolva prevents Estrogen from affecting prostate? It obviously works on pecks, but then again, I guess that is why it is a breast cancer drug??

Although I just got done saying that prostate cancer is androgen dependant, there's definitely reason to think that esterogen is inolved as well, as explained in reviews like this. I've mentioned to you before when looking into tamoxifen and cancer that nolva appears to be prescribed in cases of prostate cancer, so I would think that it could help prevent or at least treat prostate cancer.

All that said, keep in mind that I am not a doctor and I am in no way giving you medical advice. This is just my lay opinion.

 

[bigbench]

Why are you convinced of that? Prostate cancer is a classic example of an androgen-dependent tumor. Hormone therapy in later stages of prostate cancer involve lowering the levels of ANDROGENS in the body. If prostate cancer is a significant risk for you, you should go off anabolic/androgenic steroids and never take them again. Seriously.
Although I just got done saying that prostate cancer is androgen dependant, there's definitely reason to think that esterogen is inolved as well, as explained in reviews like this. I've mentioned to you before when looking into tamoxifen and cancer that nolva appears to be prescribed in cases of prostate cancer, so I would think that it could help prevent or at least treat prostate cancer.

All that said, keep in mind that I am not a doctor and I am in no way giving you medical advice. This is just my lay opinion.

You are right on the nose bro. Some of the very first treatment given to those with PC is either an androgen blocker or anti androgen and if that fails, then large doses of nolva are used with great success in not only stopping future growth, but also reversing the size of the tumor. Both androgens AND estrogen play a role in prostate cancer. If you have a history of that in your family, then maybe AAS are not for you bro

 

[BBC3]

It may just not be about androgens when it comes to prostate cancer. There is a lot of "chicken or egg" research out there supporting the idea that DHT is a saint in comparison to estrogens. the primary argument would be that YOU NEVER SEE A YOUNG GUY WITH PROSTATE CANCER. This of course is muddied by the fact that if a young man gets it he is dead overnight. HOWEVER, the whole cancer thing is about cells gone wild, or dying, depending on the type of cancer.. So did the prostate fail from years of androgen battering? or did the prostate fail because testosterone levels fell too low to support it.?? The results are FAR from in. While needless to say it is not responsible for anyone to use anything beyond moderation. My research is not directed toward steroid abuse as a cure. But I can get away with a little while young. It is my belief that an improper balance of hormones creates the problems for the prostate. I have genetically low testosterone. I look like two fathers ahead of me. Dont you think they had low testosterone.?? Well, then why did they both have some knifework done by the age of 50?? While I appreciate everyone's advice as far as my decision to supplement is concerned, I assure you guys, my plans go way beyond a simple juice up. this is what now brings me to how to control E2 while increasing test levels. How to change these proportions. No one here has any of these answers i am sure. But I do appreciate the sound back to help my think tank. Conciliator, you stated that some prostate cancers are treated with Nolva? Do you have any links for me. They would be appreciated. You have to concider just from that notion alone that there is now proof out there that estrogens may indeed by the culpret. I am early on in this of course so any help is always appreciated. the prostate is of course androgen dependent, but a sick prostate may just not know what to do with them anymore. I am trying to figure out how to keep it from getting sick..

Conciliator, one thing further. You asked "why am I convinced that E2 is a major cause of prostate cancer". I think I answered a bit up there. But the bottom line is that you have to admit, if my fathers before me were low T, or out of balance T to E ratios, then I have noting to loose. Doing something different like correcting the low test seems obviously logical.

 

[brang]

this is what now brings me to how to control E2 while increasing test levels. How to change these proportions. No one here has any of these answers i am sure.

That is exactly what an AI will do. The hard part would be getting your dosage right i suspect.
HGH will also help i think.

Regarding the CNS and its relation to the HPTA you asked about before; TBH i didnt really understand what you were asking directly.. Also, I'm not really knowledgeable enough to give you a good solid overview of the relationship between CNS and HPTA that i can back up with details if you wanted them.

However, i _think_ i have a reasonable understanding of the basics. Suffice to say that it'*s the Hypothalamus that is the controller of the messages that are sent, which control the secretion of hormones that are indirectly responsible for the production of Test and Estrogen.

I believe that it is the Pituitary which is the receptor that is the only player that's "listening" for messages that the hypothalamus uses to determine hormone levels. Other receptors such as the ones in breast tissue are responsible for acting in the locale of the messages received (eg) Grow tits.
As i said, i _think_ i know the basics but i would not be at all surprised if i have something arse about. So take this with a pinch of salt and read the real science from the source (the scientists and the scientific books .

I'd recommend you start by getting hold of a University level Human Biology text book and read about the Endocrine System and CNS, as it sounded like there is some confusion about these at a fundamental level.

HTH.

peace.
- b

 

[BBC3]

That is exactly what an AI will do. The hard part would be getting your dosage right i suspect.
HGH will also help i think.

Regarding the CNS and its relation to the HPTA you asked about before; TBH i didnt really understand what you were asking directly.. Also, I'm not really knowledgeable enough to give you a good solid overview of the relationship between CNS and HPTA that i can back up with details if you wanted them.

However, i _think_ i have a reasonable understanding of the basics. Suffice to say that it'*s the Hypothalamus that is the controller of the messages that are sent, which control the secretion of hormones that are indirectly responsible for the production of Test and Estrogen.

I believe that it is the Pituitary which is the receptor that is the only player that's "listening" for messages that the hypothalamus uses to determine hormone levels. Other receptors such as the ones in breast tissue are responsible for acting in the locale of the messages received (eg) Grow tits.
As i said, i _think_ i know the basics but i would not be at all surprised if i have something arse about. So take this with a pinch of salt and read the real science from the source (the scientists and the scientific books .

I'd recommend you start by getting hold of a University level Human Biology text book and read about the Endocrine System and CNS, as it sounded like there is some confusion about these at a fundamental level.

HTH.

peace.
- b

Yes, I am tending toward Adex for a first try. I was simply wondering if some of these SERMS out there may have effects that I am looking for. meaning preventing E2 from affecting the prostate in the same way it does breast tissue. And looking into other serms as well regarding this. I also have no doubt that finding a good dosing level on an AI is going to be trouble.

Regarding my inquiry with the CNS as it relates to the HPTA. What I am saying is that with regard to feedback loops and signaling, everyone wants to talk about how much of a hormone is in the bloodstream and moving past the "sensors". Before I dilute this with another ADHD ramble, I will simplify this post with one simple question. How does the body "detect" hormone levels??
IS IT: (a) the actual hormones in the blood stream are physically measured by the hypothalmus, or pituitary which then senses and makes adjustments.
(b) The Nerves in different areas of the body are reading measurements, or getting feedback from tissue that is affected by a hormone, and then sending a signal to the hypothalmus thru nerves telling it what to do?

There may very well be a fundamental problem with my understanding of the body. So please help me here. Which is it. I am leaning toward simple nervous system to a high degree. Considering healthy and unsupplemented circumstances, What causes the body to naturally raise or lower a hormone. For example, Marriage tends to lower male testosterone avg 2 -300 points. Why does it do this. Is was not the physical addition of a hormone to my body that caused it. Or another example, how does the body know to increase testosterone when put under a heavy physical load. It is probably sensing the fact that the mucscles are being straigned, CNS'ly speaking. OR is it some type chemical we put out from a sore muscle that is physically measured by the hypothalmus.

I dont know if I am making point clear. Am I having a great misunderstanding.? I personally believe that the CNS is completely discounted around here simply due to the fact that medicine knows about "jack shit" about it. It is difficult to measure and can not even be visually seen when referencing the skin for example, it feels, but if you cut a piece off you are not going to see a nerve. This whole thing got started in my mind due to an arguement last week regarding how Novadex works. We talk about the physical presence of hormones and chemicals in the body and everyone seems to want to assume it is a "direct physical relationship" of chemical sensors with no consequence for the actual nerves that are sensing and where they are actually located.

OK I went a little askew. But does anyone see the logic to my point and question? I am seeing a urologist in a week and I am going to ask him whick meds they are treating prostate cancer with these days. It should be interesting.

 

[Conciliator]

There is a lot of "chicken or egg" research out there supporting the idea that DHT is a saint in comparison to estrogens.

Research where? Why do they give finasteride (a 5-AR inhibitor, to prevent DHT) to those with prostate cancer? Why do they call it an androgen-dependant cancer and try to suppress androgens if DHT is a saint? Again, research where?

Conciliator, you stated that some prostate cancers are treated with Nolva? Do you have any links for me. They would be appreciated.

From what I see, the research is tentative. Here's one study that concluded "This preliminary study seems to justify further clinical research to confirm the potential efficacy of tamoxifen in the treatment of hormone-refractory prostate cancer." This study found that, "High-dose tamoxifen therapy was well tolerated and associated with micromolar concentrations of tamoxifen in human plasma, and it demonstrated activity, albeit limited, in a heavily pretreated patient cohort with hormone-refractory prostate cancer." However, this paper mentions another study in which "Growth inhibition was not dependent upon estrogenic activity" but rather other effects that tamoxifen has. The limited research I've seen doesn't seem to support taxmoxifen as a therapy because of any effect it has on estrogen. However, I haven't looked in depth. You can also google "tamoxifen prostate cancer" and you'll come up with a lot of leads.

You have to concider just from that notion alone that there is now proof out there that estrogens may indeed by the culpret.

It appears that androgens are the culprit, not estrogens (which probably play a less significant role).

Conciliator, one thing further. You asked "why am I convinced that E2 is a major cause of prostate cancer". I think I answered a bit up there. But the bottom line is that you have to admit, if my fathers before me were low T, or out of balance T to E ratios, then I have noting to loose. Doing something different like correcting the low test seems obviously logical.

No, I would not say that you have nothing to lose. That's not a logical conclusion. It's quite possible that your father and grandfather had a protective effect from the low testosterone, inhiting progression of the disease, and that had test levels been higher, problems would have advanced more rapidly. Neither possibility necessarily follows as a matter of logic.

 

[BBC3]

Research where? Why do they give finasteride (a 5-AR inhibitor, to prevent DHT) to those with prostate cancer? Why do they call it an androgen-dependant cancer and try to suppress androgens if DHT is a saint? Again, research where?

From what I see, the research is tentative. Here's one study that concluded "This preliminary study seems to justify further clinical research to confirm the potential efficacy of tamoxifen in the treatment of hormone-refractory prostate cancer." This study found that, "High-dose tamoxifen therapy was well tolerated and associated with micromolar concentrations of tamoxifen in human plasma, and it demonstrated activity, albeit limited, in a heavily pretreated patient cohort with hormone-refractory prostate cancer." However, this paper mentions another study in which "Growth inhibition was not dependent upon estrogenic activity" but rather other effects that tamoxifen has. The limited research I've seen doesn't seem to support taxmoxifen as a therapy because of any effect it has on estrogen. However, I haven't looked in depth. You can also google "tamoxifen prostate cancer" and you'll come up with a lot of leads.
It appears that androgens are the culprit, not estrogens (which probably play a less significant role).
No, I would not say that you have nothing to lose. That's not a logical conclusion. It's quite possible that your father and grandfather had a protective effect from the low testosterone, inhiting progression of the disease, and that had test levels been higher, problems would have advanced more rapidly. Neither possibility necessarily follows as a matter of logic.

See some of Dr. Eugene Shippen's studies. He is one of the up and comming fathers of TRT. I have put a little stock in him. I am not saying that estrogens are more directly a cause for sure. BUT I am saying that it does appear that an imbalance and improper t/e ratios are the cause. I appreciate you rhetoric, however, you are only quoting to same crap that US medicine has stated and goes by. This is why ones prostate is allowed to fail and then he is provided an insulting and inevitable degredation to end. TAKING AWAY ANDROGENS HAS CURED NOBODY!!. The prostate thrives on androgens as you stated, it is androgen dependent. This is a cancer that operates on more of a "growth and spread" principle. If you allow it to get sick, then of course it is going to go nuts. These TRT pioneers are all about supporting the prostate to keep it from even getting sick. Sure androgens make make it grow (like they do any muscle), but I believe they support it, there is no evidence to indicate that androgens are the CAUSE of cancer of failure. In fact the opposite as a lack of androgens are cause for sure failure of the prostate. CONSIDER THIS: if you starve any part or all of the body what does it do. It gets sick and diseased. If starved long enough it will get sick to the point that it can not even recover and die. What does the body grow on, hormones, more simply FOOD. Say one develops ANY TYPE of cancer, well guess what, that cancer lives off the same food the healthy cells do. They may even grow at a faster rate, and from what? eating a sandwich, burger, whatever to fuel the body to work. The priciple that Androgens CAUSE prostate cancer seems REDICULOUS. They support it. If you have a deficiency that will lead to blindness do you allow it to continue?? I think not. If you allow that deficiency to continue your eye may stop working and even die, then guess what, if that sick tissue (eye or prostate) is not removed once ill, you have cancer, rot, nasty growth. So what are you going to do. Not give that eye the support it needs so that it dies and further complicates, or give it what it THRIVES ON. There is no evidence to support androgens causing cancer. Sure they will feed it, but so does a cheeseburger, as it would feed any other type of cancer. Shippen states it is no coincidence that you only see older men with already low test levels diagnosed with prostate cancer. This is only proof that their prostate died due to lack of proper androgen support. I believe you are completely wrong. I think statements like "seriously you should never use AAS do to this are CLOSED MINDED. You are doing more harm to that community than good. DO YOU REALLY THINK THAT METHOD WORKS. Look around, you will find that it has raised many gravestones. You should not be so closed minded based on some articles you read. You OBVIOUSLY have read nothing from this perspective I am speaking of and it is poor judgement to publically make such definitive statements. I am starting to think you are either a fool or a doctor. Either way, most of them are identical. Come on Conciliator, work with me here.

No man is so foolish but he may sometimes give another good counsel, and no man so wise that he may not easily err if he takes no other counsel than his own. He that is taught only by himself has a fool for a master.
Hunter S. Thompson

 

[Conciliator]

See some of Dr. Eugene Shippen's studies.

What studies? Seriously. He has only one published study. It has nothing to do with prostate cancer, but endometriosis in women. See for yourself.

TAKING AWAY ANDROGENS HAS CURED NOBODY!!

The purpose of hormonal therapy is not to cure prostate cancer. It's to slow or halt growth of the cancer, as the cancer depends on androgens for growth.

The prostate thrives on androgens as you stated, it is androgen dependent.

Your reading comprehension is very poor. I said that prostate CANCER is androgen dependant. I've never seen, heard, or said anything about the prostate itself "thriving" on androgens or being more healthy because of androgens.

This is a cancer that operates on more of a "growth and spread" principle. If you allow it to get sick, then of course it is going to go nuts. These TRT pioneers are all about supporting the prostate to keep it from even getting sick. Sure androgens make make it grow (like they do any muscle), but I believe they support it, there is no evidence to indicate that androgens are the CAUSE of cancer of failure. In fact the opposite as a lack of androgens are cause for sure failure of the prostate.

Something that you probably don't comprehend is that correlation does not imply causation. The fact that the risk of heart disease and prostate cancer is higher in men with low testosterone does not entail that a lack of testosterone is what is causing it. It's definitely possible, but we won't know until studies on TRT directly examine the effect of testosterone replacement on prostate cancer rates, when compared to a control group.

The priciple that Androgens CAUSE prostate cancer seems REDICULOUS. They support it.

I never said that androgens cause cancer. I agree with you, however, that they support it.

Shippen states it is no coincidence that you only see older men with already low test levels diagnosed with prostate cancer. This is only proof that their prostate died due to lack of proper androgen support.

Wrong. That absolutely is not proof. As I said before, correlation does not imply causation. Look that up and try to understand what it means. It's important if you want to be able to look at this logically. As it stands now, you're making illogical conclusions.

I believe you are completely wrong. I think statements like "seriously you should never use AAS do to this are CLOSED MINDED. You are doing more harm to that community than good. DO YOU REALLY THINK THAT METHOD WORKS. Look around, you will find that it has raised many gravestones. You should not be so closed minded based on some articles you read. You OBVIOUSLY have read nothing from this perspective I am speaking of and it is poor judgement to publically make such definitive statements. I am starting to think you are either a fool or a doctor. Either way, most of them are identical. Come on Conciliator, work with me here.

I am trying to work with you. The problem is that you're slow to learn. Let me try to put this simply:

Low testosterone appears to correleate with prostate cancer (and cardiovascular disease). That does not mean that restoring testosterone levels to normal will prevent these. It's possible that a third variable (like a poor diet) is the cause of both. Second, even if low testosterone was the cause, it does not mean that the more testosterone the better. Often times, there is a U-shaped response curve. For example, research has shown that low testosterone increases insulin resistance. As you increase the level of testosterone, insulin resistance drops to a minimum, but as testosterone levels increase even higher than the normal range, insulin resistance increases again. So insulin resistance goes from high to low to high, as the testosterone dose increases. It's shaped like the letter U. This could also be the case with testosterone and prostate cancer, which means more is not always better.

My point is that when you're taking doses of steroids that are higher than found naturally, you're possibly increasing your risk for prostate cancer. And even if you're not increasing your risk, you still have a high risk because it runs in your family. So if you do develop it, it will spread more rapidly because of the high levels of androgens in your body.

 

[bigbench]

Just a side note, high doses of tomaxifen have been shown to stop the growth of prostate cancer cells as well as reduce the pain caused by it, and even to a higher degree than just an AI alone

 

[Conciliator]

Just a side note, high doses of tomaxifen have been shown to stop the growth of prostate cancer cells as well as reduce the pain caused by it, and even to a higher degree than just an AI alone

Reference?

 

[bigbench]

Reference?

Lol, damn it. I KNEW you were going to ask that. I was actually reading up on something completely different and ran across it. I will search my history and find it. It was a 12 month study showing that after anti-androgen (androgen blockers) had been used and either had little to no effect, or had stopped progression that nolva was used for 6-12 weeks followed by an AI and either the cells had stayed the same size, or shrunk a bit. Andro levels were that of a castrated male as well.

This isnt the full study I read, but this is a small one on it that was in the archives:
Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

BACKGROUND: Inhibition of protein kinase C (PKC) and modulation of transforming growth factor-beta (TGF-beta) are both associated with tamoxifen treatment, and both appear to be important in the regulation of prostate cancer cell growth. Investigations were performed which sought to measure the efficacy, and to elucidate the mechanism of growth inhibition by tamoxifen, in hormone-refractory prostate cancer. METHODS: Growth assays were performed on PC3, PC3-M, and DU145 prostate cancer cells. TGF-beta was measured by ELISA; p21(waf1/cip1) and retinoblastoma (Rb) protein levels were measured by Western blot; PKC activity was measured by kinase assay; and effects upon cell cycle were measured by flow cytometric analysis. RESULTS: IC50s for growth inhibition ranged from 5.5-10 microM, and were not affected by estrogen. Tamoxifen-mediated growth inhibition was not associated with induction of TGF-beta. However, tamoxifen treatment was associated with inhibition of PKC, which was followed by induction of p21(waf1/cip1), Rb dephosphorylation, and G1/S phase cell cycle arrest. Similar effects were observed with the known PKC inhibitor, Ro31-8220. CONCLUSIONS: These data suggest that micromolar concentrations of tamoxifen inhibit prostate cancer cell growth by inhibition of PKC, resulting in induction of the p21(waf1/cip1) protein.

 

[TZTARZAN2000]

you guys crack me up! [)]

 

[bigbench]

Lol, I think I should have wrote the whole things about blocking andros so that Conc knew I was BACKING what he was stating in this one... Or maybe he just likes reading these studies like me.. how lame am I?

 

[Conciliator]

Lol, damn it. I KNEW you were going to ask that. I was actually reading up on something completely different and ran across it. I will search my history and find it. It was a 12 month study showing that after anti-androgen (androgen blockers) had been used and either had little to no effect, or had stopped progression that nolva was used for 6-12 weeks followed by an AI and either the cells had stayed the same size, or shrunk a bit. Andro levels were that of a castrated male as well.

I believe you. I'm not trying to call you out. I'd just like to read the actual study. If you can find it, please post it.

This isnt the full study I read, but this is a small one on it that was in the archives:
Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

The second link I gave in post #12 is pretty much this same research, performed by this same group, one year later. They say pretty much the same thing: tamoxifen can inhibit prostate cancer cell growth, not by blocking estrogen, but by inhibiting PKC. As the full text of the paper explains: "Growth inhibition was not dependent upon estrogenic activity. It was, however, associated with inhibition of PKC3 (a known effect of tamoxifen), and direct activation of the TGF- signaling pathway, including induction of the cell cycle-inhibitory protein, p21waf1/cip1."