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Thoughts on Nolva for stand-alone estrogen control on TRT?

Agreed, I just didn't want anyone to think it was free of side effects, most of us turned to AIs decades ago because they had a better safety profile than nolvadex, which everyone was using.

I personally don't think nolva is that bad, but when we are considering long term (rest of life) use I think this has to be considered. I'd rather be on a very low dose AI for 30 years than be on nolvadex for 30 years.

i completely agree. In fact many men who are not on TRT could probably benefit from that.
 
If you are on a test dose that will results in elevated E2 levels ( more then normal range) then nolva alone is not only not adequate it would be potentially dangerous to your health

If you have higher E2 due to testosterone and you're not on other compounds id always go with tamoxifen tbh. Every E2 related problem I had, it has fixed it and quick Too. I have seen that with many others too. In general, ive seen more problems with ai's than tamoxifen.

Both AI's and serms could potentially be dangerous for your health, Same goes for any AAS which no one seems to bat an eye from.
 
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If you have higher E2 due to testosterone and you're not on other compounds id always go with tamoxifen tbh. Every E2 related problem I had, it has fixed it and quick Too. I have seen that with many others too. In general, ive seen more problems with ai's than tamoxifen.

Both AI's and serms could potentially be dangerous for your health, Same goes for any AAS which no one seems to bat an eye from.

If you have higher E2 due to testosterone and you're not on other compounds id always go with tamoxifen tbh. Every E2 related problem I had, it has fixed it and quick Too. I have seen that with many others too. In general, ive seen more problems with ai's than tamoxifen.

Both AI's and serms could potentially be dangerous for your health, Same goes for any AAS which no one seems to bat an eye from.

that is not a good idea at all... you are simply refering to tamox blocking the E2 binding that results in noticable size effects which is about appearance/feeling not health!

and how is tamox going to block prolonged elevated E2 levels on the liver?

I would almost always suggest an AI to keep E2 levels in range ( not bottomed out which causes issues) Tamox can be used for acute sympomatic flairs as it works on selective target tissues but not long term.

SERMS like clomid can be used long term at a low dose when off AAS although id prefer enclo mostly due to the estro effects of zuclo isomer
 
If you have higher E2 due to testosterone and you're not on other compounds id always go with tamoxifen tbh. Every E2 related problem I had, it has fixed it and quick Too. I have seen that with many others too. In general, ive seen more problems with ai's than tamoxifen.

Both AI's and serms could potentially be dangerous for your health, Same goes for any AAS which no one seems to bat an eye from.

I would agree with that... if not used properly the correct dose or for the appropriate indication they could both have side effects which could be dangerous. I discussed my position at length about AI's on another board but this whole AI's if used wrong is dangerous thing isnt new...its just understanding how they work. Same goes from SERMS if not used correctly.
 
that is not a good idea at all... you are simply refering to tamox blocking the E2 binding that results in noticable size effects which is about appearance/feeling not health!

and how is tamox going to block prolonged elevated E2 levels on the liver?

I would almost always suggest an AI to keep E2 levels in range ( not bottomed out which causes issues) Tamox can be used for acute sympomatic flairs as it works on selective target tissues but not long term.

SERMS like clomid can be used long term at a low dose when off AAS although id prefer enclo mostly due to the estro effects of zuclo isomer

I thought recent findings were that tamoxifen's metabolites act as aromatase inhibitors; https://www.ncbi.nlm.nih.gov/m/pubmed/21814747/

e2 within range with supraphysiologic levels of test won't 'work' for everyone (for Some will). I had a buddy on test deca with aromasin & caber, e2 and prolactin in range but still had massive gyno. A good A:E ratio is key, although imo, there is no standard A:E for everyone so it is a matter of finding what works for you.

But I agree, elevated e2 levels for a long time will probably not benefit you. Since I do rather mild stuff I havnt really searched for extreme consequences of prolonged high e2
 
I thought recent findings were that tamoxifen's metabolites act as aromatase inhibitors; https://www.ncbi.nlm.nih.gov/m/pubmed/21814747/

e2 within range with supraphysiologic levels of test won't 'work' for everyone (for Some will). I had a buddy on test deca with aromasin & caber, e2 and prolactin in range but still had massive gyno. A good A:E ratio is key, although imo, there is no standard A:E for everyone so it is a matter of finding what works for you.

But I agree, elevated e2 levels for a long time will probably not benefit you. Since I do rather mild stuff I havnt really searched for extreme consequences of prolonged high e2

I thought recent findings were that tamoxifen's metabolites act as aromatase inhibitors; https://www.ncbi.nlm.nih.gov/m/pubmed/21814747/

e2 within range with supraphysiologic levels of test won't 'work' for everyone (for Some will). I had a buddy on test deca with aromasin & caber, e2 and prolactin in range but still had massive gyno. A good A:E ratio is key, although imo, there is no standard A:E for everyone so it is a matter of finding what works for you.

But I agree, elevated e2 levels for a long time will probably not benefit you. Since I do rather mild stuff I havnt really searched for extreme consequences of prolonged high e2

thank you for the link. I was not aware of it. interesting that it MAY help to a degree but unfortunately i think that taking the amount of AAS that many do it just overwhelms its ability to limit the conversion thus we see so many gets with very high E2 levels while taking tamox but maybe it would be even higher if they hadnt taken it.

Its funny...a buddy of mine had a similar issue with gyno... he can occasionally get a flair even though his E2 levels are in range but i think like all things its a range and maybe being on the upper level of normal it still messes him up since he has preexisting gyno. he will take tamox short to to get it under control...take his e2 levels lower for a bit then go back to his normal AI dose and is good.
 
tamox certainly has its role in TRT and AAS usage i just dont think its enough for the vast majority of guys and certainly not using long term for estrogen control which is the OPs question
 
thank you for the link. I was not aware of it. interesting that it MAY help to a degree but unfortunately i think that taking the amount of AAS that many do it just overwhelms its ability to limit the conversion thus we see so many gets with very high E2 levels while taking tamox but maybe it would be even higher if they hadnt taken it.

Its funny...a buddy of mine had a similar issue with gyno... he can occasionally get a flair even though his E2 levels are in range but i think like all things its a range and maybe being on the upper level of normal it still messes him up since he has preexisting gyno. he will take tamox short to to get it under control...take his e2 levels lower for a bit then go back to his normal AI dose and is good.
Agree that if lowering e2 is the goal, tamoxifen will probably be inferior than any AI for this job.

Weird how the body works, I'm lucky I'm not really gyno prone. My stance on ai/serms could be different if I was more prone to gyno I guess
 
I thought recent findings were that tamoxifen's metabolites act as aromatase inhibitors; https://www.ncbi.nlm.nih.gov/m/pubmed/21814747/

e2 within range with supraphysiologic levels of test won't 'work' for everyone (for Some will). I had a buddy on test deca with aromasin & caber, e2 and prolactin in range but still had massive gyno. A good A:E ratio is key, although imo, there is no standard A:E for everyone so it is a matter of finding what works for you.

But I agree, elevated e2 levels for a long time will probably not benefit you. Since I do rather mild stuff I havnt really searched for extreme consequences of prolonged high e2

Your buddy with the prolactin gyno doesn't count, deca doesn't "raise" prolactin, it activates the prolactin receptor itself with a 20% affinity.

The "AI" effect of some tamoxifen metabolites is pretty minimal, especially since most AIs can't even reach all male aromatase.

Tamoxifen has a place in contest prep, gyno, and perhaps some cycles, but not in TRT.

The shit makes many people depressed as hell also btw...
 
Your buddy with the prolactin gyno doesn't count, deca doesn't "raise" prolactin, it activates the prolactin receptor itself with a 20% affinity.

The "AI" effect of some tamoxifen metabolites is pretty minimal, especially since most AIs can't even reach all male aromatase.

Tamoxifen has a place in contest prep, gyno, and perhaps some cycles, but not in TRT.

The shit makes many people depressed as hell also btw...

I heard from Some pretty knowledgeable guys (like one who writes scientific papers) that prolactine gyno doesn't exist and that all gyno is caused by estrogen. I dont have enough knowledge to support his claims tho. Some anecdotal 'evidence' show different I know.

Not sure if there were studies done on how strong tamoxifen's metabolites could inhibit aromatase, but I'm not doubting that AI's will probably be stronger.

Id only use either one in case of problems, never preventive, unless if I would know I'm prone to a e2 related Side effect.

Plenty of people are feeling depressed on AI's too, and Yes that's probably due to miss use but I think ai's are easy to overdo it with vs tamoxifen were overdoing it is less 'easy'
 
Your buddy with the prolactin gyno doesn't count, deca doesn't "raise" prolactin, it activates the prolactin receptor itself with a 20% affinity.

The "AI" effect of some tamoxifen metabolites is pretty minimal, especially since most AIs can't even reach all male aromatase.

Tamoxifen has a place in contest prep, gyno, and perhaps some cycles, but not in TRT.

The shit makes many people depressed as hell also btw...

When I brought that up a few years ago about Tamoxifen being a prodrug, and the miniscule abilities through its metabolites acting as aromatase inhibitors was more trivial than absolute. Although the context of it today through conversation is that it acts in tandem as an aromatase inhibitor. Which isn't the case, as pharmaceutical companies have isolated these metabolites and have used them directly as a aromatase inhibitors, with fail.

I personally wouldn't use nolvadex from some of the findings that I've seen on its capabilities on impairing cholesterol efflux ---reverse cholesterol transport (RCT). Even then the capacity of RCT is determined on the particle size of HDL, small particle size being more efficient.
 
I was running arimadex with my TRT for a couple years. It lowered my HDL and increased my LDL by about 20% each respectively. I also have had on and off side effects of low E2. I dropped my AI for TRT and when blasting I use 10mg Nolva ED. Since that, my cholesterol numbers have improved drastically and no low E2 symptoms (labs show normal E2 now). Just my anecdotal experience.
 
that is not a good idea at all... you are simply refering to tamox blocking the E2 binding that results in noticable size effects which is about appearance/feeling not health!

and how is tamox going to block prolonged elevated E2 levels on the liver?

I would almost always suggest an AI to keep E2 levels in range ( not bottomed out which causes issues) Tamox can be used for acute sympomatic flairs as it works on selective target tissues but not long term.

SERMS like clomid can be used long term at a low dose when off AAS although id prefer enclo mostly due to the estro effects of zuclo isomer

Can you even get enclo? I've heard of it and it sounds great but I've never seen it anywhere and even then would it be legit?? I know it never made it to market
 
I heard from Some pretty knowledgeable guys (like one who writes scientific papers) that prolactine gyno doesn't exist and that all gyno is caused by estrogen. I dont have enough knowledge to support his claims tho. Some anecdotal 'evidence' show different I know.

Not sure if there were studies done on how strong tamoxifen's metabolites could inhibit aromatase, but I'm not doubting that AI's will probably be stronger.

Id only use either one in case of problems, never preventive, unless if I would know I'm prone to a e2 related Side effect.

Plenty of people are feeling depressed on AI's too, and Yes that's probably due to miss use but I think ai's are easy to overdo it with vs tamoxifen were overdoing it is less 'easy'

If you think prolactin gyno doesn't exist, you don't understand how prolactin works. Your "pretty knowledgable guys, like one's that write scientific papers" are just spreading the typical misinformed broscience that has been going around about 19-nor based gyno for decades.

Now you could debate if the prolactin effect is from the prolactin receptor itself or from some kind co-binding factor involving estradiol and maybe progesterone, THAT part is debatable.

Why throw around so may guesses and blind secondhand info? It misinforms people.

I was running arimadex with my TRT for a couple years. It lowered my HDL and increased my LDL by about 20% each respectively. I also have had on and off side effects of low E2. I dropped my AI for TRT and when blasting I use 10mg Nolva ED. Since that, my cholesterol numbers have improved drastically and no low E2 symptoms (labs show normal E2 now). Just my anecdotal experience.

There is no doubt that tamoxifen will raise your HDL, as will anything that increase estrogen and it is great for symptoms of high E2, but that doesn't have anything to do with it's long term application in TRT.
 
If you think prolactin gyno doesn't exist, you don't understand how prolactin works. Your "pretty knowledgable guys, like one's that write scientific papers" are just spreading the typical misinformed broscience that has been going around about 19-nor based gyno for decades.

Now you could debate if the prolactin effect is from the prolactin receptor itself or from some kind co-binding factor involving estradiol and maybe progesterone, THAT part is debatable.

Why throw around so may guesses and blind secondhand info? It misinforms people.

He explained it why it isn't possible but uses Some difficult jargon which I dont understand a 100% in my native language, let alone in English. But he isn't Some random dumb Guy which is Why I tend to believe him.

He wrote a paper on AAS and hepatoxity, ill send you a Pm with it :)
 
When I brought that up a few years ago about Tamoxifen being a prodrug, and the miniscule abilities through its metabolites acting as aromatase inhibitors was more trivial than absolute. Although the context of it today through conversation is that it acts in tandem as an aromatase inhibitor. Which isn't the case, as pharmaceutical companies have isolated these metabolites and have used them directly as a aromatase inhibitors, with fail.

I personally wouldn't use nolvadex from some of the findings that I've seen on its capabilities on impairing cholesterol efflux ---reverse cholesterol transport (RCT). Even then the capacity of RCT is determined on the particle size of HDL, small particle size being more efficient.

To add a bit to this on the lipid discussion. If one has dire interests on their application approaches to lower Lp(a), nolvadex has been suggested to be a therapeutic in this regards unlike aromatase inhibitors that increase Lp(a). The caveat is that nolvadex can increase triglycerides.
 
I cruise on a high trt dose of 300mg a week and .5 mg arimidex a week works perfect for me, and alot cheaper than daily nolva. But everyone is different

Sent from my LGMP450 using Tapatalk
 
He explained it why it isn't possible but uses Some difficult jargon which I dont understand a 100% in my native language, let alone in English. But he isn't Some random dumb Guy which is Why I tend to believe him.

He wrote a paper on AAS and hepatoxity, ill send you a Pm with it :)

This is the standard dogma, it can't be prolactin, etc. It might not be prolactin directly, it maybe a progesterone/prolactin co-binding factor but the exact mechanics of it are moot, drugs that lower your prolactin levels stop these side effects, and the sides are independent of estradiol. And there are plenty of studies showing the affinity these AAS have for these receptors, so it's a moot point.
 
Fukking phenomenal thread!:headbang:
 
To add a bit to this on the lipid discussion. If one has dire interests on their application approaches to lower Lp(a), nolvadex has been suggested to be a therapeutic in this regards unlike aromatase inhibitors that increase Lp(a). The caveat is that nolvadex can increase triglycerides.

I used to use short, 1 month runs of nolvadex to raise my HDL a couple times a year, it was fairly effective. But ultimately I think just not tanking your E2 level is also somewhat effective at keeping HDL from going too low. Androgens just seem to raise LDL and estrogens raise HDL, probably pointless unless inflammation factors also change or there is a genetic disposition for CAD.
 

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