Today I got my endocrenologist to perscribe tamoxifen for me to try to get rid of the mild case of gyno ive had for roughly 3-4 years now.
im just wondering since im gonna be on this stuff are there side effects I can take advantage of from a body building aspect such as increased fat loss, decrease in subcataneous water etc…? Any type of body composition changes that would be easier to achieve while im on this stuff?
[quote]vicktimised wrote:
Today I got my endocrenologist to perscribe tamoxifen for me to try to get rid of the mild case of gyno ive had for roughly 3-4 years now.
im just wondering since im gonna be on this stuff are there side effects I can take advantage of from a body building aspect such as increased fat loss, decrease in subcataneous water etc…? Any type of body composition changes that would be easier to achieve while im on this stuff?[/quote]
It’s been said that a 20mg dose of tamoxifen can boost your T levels by 150%, but I don’t think very many people would recommend you base a training agenda on an SERM.
Nolva is also supposed to help a little with your LDL to HDL ratio.
I notice that i retain less water when on it which I guess can be good and bad.
It will lower the effects of E on some tissues and not on others… it is selective.
I have wondered about the fat aspect and I do not know if there would be an effect as one would get with a true reduction of E or an improvement of the T:E ratio.
If you have a long term issue with fat or fat patterns, then you might want to try a longer term low dose of AI. A typical dose of anastrozole for guys on TRT is 1mg/wk. If you are significantly heavier than most older guys, say 150-160 pounds, you might want to make a weight adjusted increase in that dose. When someone is taking TRT or gear, the dose of anastrozole has to be increased with the T load to get the expected benefits.
With E lowered, you can expect some fat loss and fat pattern remodelling. That takes time, so your AI trial would need to be longer term. You could get E2 blood work and aim for E2 of 17-20 which seems to be healthy and optimal from a libido point of view.
Longer term gyno needs longer term treatment as the tissue changes get sticky with time. So don’t expect a complete change in a short amount of time. The breast gland tissue needs to wither away. You want more than the short term shrinkage, you need the tissue to change significantly.
Do you have E2 blood work? T:E is also important and if T is low, that is a problem too. If I had a gyno issue, I would want to do a SERM and AI to lower E2 as well.
Did you know that for most, when a SERM is introduced, E2 levels increase and stay high[er]? With SERM introduced increases in T, E production will rise. It is not understood [that I can find] how the body responds to the uncreased E when the SERM acts only on some tissues to reduce the effect of the E selectively.
One also has to taper off of a SERM as the HPTA would otherwise perceive a huge increase in E effects and you would go through a HPTA shutdown. Using an AI during that transition would have obvious effects.
There will be /can be effects on the mind and libido. Lowering E with AI can increase libido and other related aspects. I do not know how a SERM compares in that regard.
You might need to have a discussion with your endo about E2 blood work, AI and E2 level targets for dosing.
If you have a script for tamox and the cost of the drug is an issue, you can follow the prescribed amount and get your tamox at a research chem supplier. You can get the anastrozole there as well. Feel free to PM if you have any questions.
[quote]KSman wrote:
It will lower the effects of E on some tissues and not on others… it is selective.
I have wondered about the fat aspect and I do not know if there would be an effect as one would get with a true reduction of E or an improvement of the T:E ratio.
If you have a long term issue with fat or fat patterns, then you might want to try a longer term low dose of AI. A typical dose of anastrozole for guys on TRT is 1mg/wk. If you are significantly heavier than most older guys, say 150-160 pounds, you might want to make a weight adjusted increase in that dose. When someone is taking TRT or gear, the dose of anastrozole has to be increased with the T load to get the expected benefits.
With E lowered, you can expect some fat loss and fat pattern remodelling. That takes time, so your AI trial would need to be longer term. You could get E2 blood work and aim for E2 of 17-20 which seems to be healthy and optimal from a libido point of view.
Longer term gyno needs longer term treatment as the tissue changes get sticky with time. So don’t expect a complete change in a short amount of time. The breast gland tissue needs to wither away. You want more than the short term shrinkage, you need the tissue to change significantly.
Do you have E2 blood work? T:E is also important and if T is low, that is a problem too. If I had a gyno issue, I would want to do a SERM and AI to lower E2 as well.
Did you know that for most, when a SERM is introduced, E2 levels increase and stay high[er]? With SERM introduced increases in T, E production will rise. It is not understood [that I can find] how the body responds to the uncreased E when the SERM acts only on some tissues to reduce the effect of the E selectively.
One also has to taper off of a SERM as the HPTA would otherwise perceive a huge increase in E effects and you would go through a HPTA shutdown. Using an AI during that transition would have obvious effects.
There will be /can be effects on the mind and libido. Lowering E with AI can increase libido and other related aspects. I do not know how a SERM compares in that regard.
You might need to have a discussion with your endo about E2 blood work, AI and E2 level targets for dosing.
If you have a script for tamox and the cost of the drug is an issue, you can follow the prescribed amount and get your tamox at a research chem supplier. You can get the anastrozole there as well. Feel free to PM if you have any questions.[/quote]
Wow thanks a lot for the info. My T:E levels were within the normal range everytime we did blood tests, and the tamox was perscribed by an endocronologist. Most likely the gyno arose due to hyperthyroidism which ive had for a while, got rid of with treatment and now arose again since it throws a lot of the bodys hormones out of wack. Ive only taken it for about 3-4 days now and already seem to have noticed a bit of a change.
And now that you mention it my libido definatly rose cuz the other day i was far more sensitive in a good way then usual when i was with my girl. The endo said i would be taking the drug for 4 months. right now im taking a 10 mg pill twice a day.
A couple of points and issues with KSman.
Serms do cause a ‘true’ reduction in the amount of endogenous estrogen production.
1mg of Arimidex is not a standard dose for people on trt.
Arimidex dosage has much more to do with aromatization than it does bodyweight. Bodyfat levels and physical excertion is a much more telling tale than test levels.
Agree with the 17-20 level of E2, but that is a very, very tight range. I personally shoot for 10-30 as a change in 10+ is common thoughout a single day.
Curious as to why you would want an AI and a serm? Wouldn’t an AI make taking an SERM senseless?
SERMS increase Testosterone by the hypothalmus sensing a rise in estrogen from the nolvadex. Nolvadex does not cause a rise in endogenous estrogen by causing more to be produced or aromatized. If anything the extra estrogen (nolvadex) would cause less to be produced.
uhhhhhh. You have to explain that!
Lowering Estrogen through an AI for someone not running large amounts of exogenous testosterone or other aromatizing steroids would more than likely cause a DECREASE in libido, possible to cause an increase IF he has an suppressed libido now caused by high estrogen otherwise…NO. Serms usually cause an decrease in libido caused by the extra estrogen (the SERM, not endogenously produced estrogen)
Also long-term AI + SERM use would not be recommended for health at all. The AI more than likely is going to throw off your cholesterol levels and the SERM is going to mess up your tiglyercides - basically completely screwing up your blood lipids.
[quote]TheBeat wrote:
A couple of points and issues with KSman.
Serms do cause a ‘true’ reduction in the amount of endogenous estrogen production.
1mg of Arimidex is not a standard dose for people on trt.
Arimidex dosage has much more to do with aromatization than it does bodyweight. Bodyfat levels and physical excertion is a much more telling tale than test levels.
Agree with the 17-20 level of E2, but that is a very, very tight range. I personally shoot for 10-30 as a change in 10+ is common thoughout a single day.
Curious as to why you would want an AI and a serm? Wouldn’t an AI make taking an SERM senseless?
SERMS increase Testosterone by the hypothalmus sensing a rise in estrogen from the nolvadex. Nolvadex does not cause a rise in endogenous estrogen by causing more to be produced or aromatized. If anything the extra estrogen (nolvadex) would cause less to be produced.
One also has to taper off of a SERM as the HPTA would otherwise perceive a huge increase in E effects and you would go through a HPTA shutdown. Using an AI during that transition would have obvious effects.
uhhhhhh. You have to explain that!
Lowering Estrogen through an AI for someone not running large amounts of exogenous testosterone or other aromatizing steroids would more than likely cause a DECREASE in libido, possible to cause an increase IF he has an suppressed libido now caused by high estrogen otherwise…NO. Serms usually cause an decrease in libido caused by the extra estrogen (the SERM, not endogenously produced estrogen)
Also long-term AI + SERM use would not be recommended for health at all. The AI more than likely is going to throw off your cholesterol levels and the SERM is going to mess up your tiglyercides - basically completely screwing up your blood lipids.[/quote]
I fully agree with this post. Estrogen plays a large role in male physiology when it comes to sex drive and performance. From personal experience ,even when running a decent dosage of testosterone, nolvadex will reduce my sex drive and an AI like A-dex will completely shut it off.
I don’t feel like you are seriously considering the negative mental health aspects of this either. Tamoxafin (sp)? was created to help fight breast cancer in women. Before treatment most doctors will warn their patients that after treatment they will most likely fight depression for a long period of time due to the effects on their hormone profile. Just something to take into consideration.
Guys… too many issues that need to be better understood.
SERMs do lead to higher E. Because they blind the feedback receptors in the HPTA to the serum levels of E. So the negative feedback from the levels of E are largely eliminated. This leads to more LH t more T to more T–>E aromatization.
An AI like arimidex will not take your E levels low enough to reduce E to the extent that lipid or libido will be adversely affected. Arimidex is self limiting.
1mg/wk is typical for TRT use. 1mg/day is something that was discussed in a research setting and does not apply to TRT dosing… but did show the self limiting effect of arimidex. Note that femara is a different class of action for an AI and small doses can clobber E levels and create problems.
You would use an AI to reduce E when on a SERM that would otherwise lead to higher E. When on gear, the E can get quite high as well.
When on a SERM for recovery, your E levels will be high - from the SERM. If you stop the SERM suddenly, the SERM will wash out and the PHTA will then see the higher levels of E, that were there all the time and that non-unmasked E will partially shutdown the HPTA just as you are trying to recover.
Please understand the above and reread my post. The other points of concern should then mostly be cleared up for you.
Responses to SERMs are very individualistic. SERMs can act like E and for some the SERM could directly lower libido.
In my case, 1mg/wk anastrozole, lowering E2 from 37–>22 greatly increased libido.
Lipid problems with low E seem to be confined to body builders getting into sub 10% body fat range. Don’t take those extremes as universal truths.
[quote]KSman wrote:
Guys… too many issues that need to be better understood.
SERMs do lead to higher E. Because they blind the feedback receptors in the HPTA to the serum levels of E. So the negative feedback from the levels of E are largely eliminated. This leads to more LH t more T to more T–>E aromatization.
An AI like arimidex will not take your E levels low enough to reduce E to the extent that lipid or libido will be adversely affected. Arimidex is self limiting.
1mg/wk is typical for TRT use. 1mg/day is something that was discussed in a research setting and does not apply to TRT dosing… but did show the self limiting effect of arimidex. Note that femara is a different class of action for an AI and small doses can clobber E levels and create problems.
You would use an AI to reduce E when on a SERM that would otherwise lead to higher E. When on gear, the E can get quite high as well.
When on a SERM for recovery, your E levels will be high - from the SERM. If you stop the SERM suddenly, the SERM will wash out and the PHTA will then see the higher levels of E, that were there all the time and that non-unmasked E will partially shutdown the HPTA just as you are trying to recover.
Please understand the above and reread my post. The other points of concern should then mostly be cleared up for you.
Responses to SERMs are very individualistic. SERMs can act like E and for some the SERM could directly lower libido.
In my case, 1mg/wk anastrozole, lowering E2 from 37–>22 greatly increased libido.
Lipid problems with low E seem to be confined to body builders getting into sub 10% body fat range. Don’t take those extremes as universal truths.[/quote]
Where do you come up with this crap!?! Post some studies to pack your crazy claims. Particularly about: Arimidex being self limiting, Serms directly raising estrogen, Serms causing shutdown, 1mg of arimidex being standard for hrt (try .588mg), etc, basically everything you are saying please.
I have never heard this from anyone but you and have never seen any studies or anedotal evidence, empirical experience that backs what you say. I might be wrong, but I think your taking a couple of truths, mixing in some theory and a whole lot of bullshit. I’d dig up some studies if needed, otherwise let’s let this play out how it may.
ok here are some quotes to point you in the right direction. You obviously do know some, and maybe even alot, about what you are talking about, but seem to get some things confused. You had much good things to say and got me thinking about some of it, but again some issues are confused. It’s random and not put together, but I do not have the desire right now to write an article.
Few users really understand how clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up.
Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody’s best interest to bring back natural test as soon as humanly possible.
Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That’s basically how the mechanism works, nothing more, nothing less.
Nolvadex and Clomid - Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall endogenous estrogen (not completely true as endogenous estrogen actually stays the same - neither lowered or RAISED)
Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it
blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to, ultimately leading to the destruction of estrogen and less produced as the hypothalamus senses the SERM as an estrogen and lowers production
Estrogen helps determine sexual aggression - too high and too low effects sexual aggression and libido.
Some clinicians expressed preference for an estradiol of around 32 pg/ml for optimal libido in men. However, this will depend on all the factors that determine libido. Some need more. Some need less.
An added risk of using an AI is of driving estrogen levels too low, with deleterious consequences for the lipid profile, calcium deposition, libido, etc
male patients who suffer E2 elevations above the top of normal range are placed on 0.25mg of Arimidex every third day
It is important to not lower estrogen too far, which is easy to do with an AI, as doing so has disastrous effects on the Lipid Profile, bone deposition, libido, etc. I prefer to maintain E in mid-range.
These results may indicate that the negative effects of estrogen deprivation in men only become manifest when the concentration falls below the levels induced by our intervention with anastrozole (77 pmol/l). This assumption is supported by the observation in the anastrozole group that, although effects of the reduction of serum E(2) on vascular parameters could not be demonstrated in subjects as a group, there was a correlation between individual serum E(2) and several vascular parameters.
a significant decrease in flow-mediated dilation was observed in subjects taking anastrozole [median, 6.1% (range, 5.2 to 13.4) to 3.5% (2.0 to 5.7), P=0.034] but not in the placebo group
Here is a place where you can see real-life experiences with Arimidex, most are women, but you will see that empiricaly it can cause estrogen to get too low and effect libido among other things - askapatient.com/viewrating.asp?drug=20541&name=ARIMIDEX
IF YOU CAN FIND SOME INFO ON ARIMIDEX BEING SELF-LIMITING TO THE POINT OF NOT LOWERING ESTROGEN TOO MUCH I WOULD LOVE IT! I’ve been using bunk stuff and would love to get my hands on this wonder drug - Arimidex!!!
References and research areas:
Circ Res. 2003 Nov 28;93(11):1127-33. Epub 2003 Oct 30
Eur J Endocrinol. 2006 Apr;154(4):569-75
Exp Physiol. 2006 Mar;91(2):445-56. Epub 2005 Dec 19.
John Crisler, DO
1: Cancer Res. 2002 May 1;62(9):2474-7
Fertil Steril. 1978 Mar;29(3):320-7.
J Clin Endocrinol Metab. 2000 Sep;85(9):3027-35
[quote]TheBeat wrote:
ok here are some quotes to point you in the right direction. You obviously do know some, and maybe even alot, about what you are talking about, but seem to get some things confused. You had much good things to say and got me thinking about some of it, but again some issues are confused. It’s random and not put together, but I do not have the desire right now to write an article.
Few users really understand how clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up.
Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody’s best interest to bring back natural test as soon as humanly possible.
Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That’s basically how the mechanism works, nothing more, nothing less.
Nolvadex and Clomid - Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall endogenous estrogen (not completely true as endogenous estrogen actually stays the same - neither lowered or RAISED)
Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it
blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to, ultimately leading to the destruction of estrogen and less produced as the hypothalamus senses the SERM as an estrogen and lowers production
Estrogen helps determine sexual aggression - too high and too low effects sexual aggression and libido.
Some clinicians expressed preference for an estradiol of around 32 pg/ml for optimal libido in men. However, this will depend on all the factors that determine libido. Some need more. Some need less.
An added risk of using an AI is of driving estrogen levels too low, with deleterious consequences for the lipid profile, calcium deposition, libido, etc
male patients who suffer E2 elevations above the top of normal range are placed on 0.25mg of Arimidex every third day
It is important to not lower estrogen too far, which is easy to do with an AI, as doing so has disastrous effects on the Lipid Profile, bone deposition, libido, etc. I prefer to maintain E in mid-range.
These results may indicate that the negative effects of estrogen deprivation in men only become manifest when the concentration falls below the levels induced by our intervention with anastrozole (77 pmol/l). This assumption is supported by the observation in the anastrozole group that, although effects of the reduction of serum E(2) on vascular parameters could not be demonstrated in subjects as a group, there was a correlation between individual serum E(2) and several vascular parameters.
a significant decrease in flow-mediated dilation was observed in subjects taking anastrozole [median, 6.1% (range, 5.2 to 13.4) to 3.5% (2.0 to 5.7), P=0.034] but not in the placebo group
Here is a place where you can see real-life experiences with Arimidex, most are women, but you will see that empiricaly it can cause estrogen to get too low and effect libido among other things - askapatient.com/viewrating.asp?drug=20541&name=ARIMIDEX
IF YOU CAN FIND SOME INFO ON ARIMIDEX BEING SELF-LIMITING TO THE POINT OF NOT LOWERING ESTROGEN TOO MUCH I WOULD LOVE IT! I’ve been using bunk stuff and would love to get my hands on this wonder drug - Arimidex!!!
References and research areas:
Circ Res. 2003 Nov 28;93(11):1127-33. Epub 2003 Oct 30
Eur J Endocrinol. 2006 Apr;154(4):569-75
Exp Physiol. 2006 Mar;91(2):445-56. Epub 2005 Dec 19.
John Crisler, DO
1: Cancer Res. 2002 May 1;62(9):2474-7
Fertil Steril. 1978 Mar;29(3):320-7.
J Clin Endocrinol Metab. 2000 Sep;85(9):3027-35
[/quote]
I am very happy you posted this
thank you
Good discussion.
All I have to offer are some blood test results from using a SERM (Clomid) + an AI (Arimidex) either: 1. Clomid only…2. Clomid + Arimidex.
I’m not going to state numbers or dosages, but I can say the trend was interesting. On Clomid only, my test levels definitely went up. And I already have reasonably high endogeneous test levels when I’m “clean” (i.e. no steroids. Yes, I am a steroid user).
After 3 months on Clomid only, my estrogen went up (estrodiol) and my test went down to normal levels. This was not good!
Add in the Arimidex. This lowered my estrogen (estrodiol) and brought my test back up to some pretty good levels (NOTE: NOT supraphysical levels, but on very top “natural” levels spouted by the medical profession).
Personally, I think anyone who wants to dabble in a little “chemistry” should get blood tests. It’s the ONLY way to know how YOUR physiology reacts to whatever protocol you’re using.
I don’t claim at all to be an expert in any of this; I think experimentation (wait, scratch that…what I mean is INTELLIGENT experimentation) is the only way to really know.
Good thread. Go to the front page.