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Using nolvadex on cycle as an ai with certain compounds?

Jswole220

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I know back in the day a lot of guys used nolva as an ai but lately I’ve been hearing about adding nolva with your other ai such as arimidex or Aromasin with certain compounds and specifically Anadrol. I can’t seem to find any actual information other than just add it in. If anyone has any info on this please share I would really appreciate it.
 
Nolva isn’t an AI so that makes zero sense. People use it to prevent gyno on cycle but if you’re estrogen isn’t elevated because you’re using an actual AI it isn’t needed. Using nolva will block the estrogen but it’s still there
 
That’s exactly what I thought but I’ve herd a lot lately using it specifically with Anadrol as an “extra ai”
 
If it isn’t from e2 then nolva won’t help. I haven’t heard of this mysterious anadrol gyno before but if it’s true then who knows, I don’t think anyone would have an answer
 
The use of AIs is a fairly recent thing honestly. They all ran gear with 20-40mg of nolvadex to prevent gyno. That's it. I also think there's merit to this. There's a reason most all guys always blew the fuck up on gear back then, not just the genetic freaks. I think it has to do with serum estradiol levels. Estrogen is essential is hypertrophy. I'm seriously considering my next blast to use no AI at all, just 40mg nolva daily. With of course exceptions when I want my dick to work better than just Cialis can do. Of course if my fiancee is on any gear I'll have to run AIs or else she'd probably murder me if my D isn't down for at least twice a day minimum. Anyhow,I'm gonna try it I think. I'll report how it goes. It'll be probably March before I do that though
 
and that’s what I understand as well and was told take nolva to combat it but I just can’t get a solid reason on why or how it works
If it isn’t from e2 then nolva won’t help. I haven’t heard of this mysterious anadrol gyno before but if it’s true then who knows, I don’t think anyone would have an answer
Sure it could.

E2 can be in range and you can still have gyno flare ups especially if you have some prexisting tissue there.
 
The use of AIs is a fairly recent thing honestly. They all ran gear with 20-40mg of nolvadex to prevent gyno. That's it. I also think there's merit to this. There's a reason most all guys always blew the fuck up on gear back then, not just the genetic freaks. I think it has to do with serum estradiol levels. Estrogen is essential is hypertrophy. I'm seriously considering my next blast to use no AI at all, just 40mg nolva daily. With of course exceptions when I want my dick to work better than just Cialis can do. Of course if my fiancee is on any gear I'll have to run AIs or else she'd probably murder me if my D isn't down for at least twice a day minimum. Anyhow,I'm gonna try it I think. I'll report how it goes. It'll be probably March before I do that though
So it’s common practice to run an AI throughout the cycle from start to finish? You said using an AI is a more recent thing, back when I first ran gear we had bag of nova & clomid but only worried about issues during pct. I have adex on hand just in case though. Is there another benefit to running the AI weather you have gyno symptoms or not?
 
Drol "can" exhibit similar chitter chat with E1/E2 estrogen receptors (ERα, ERβ, mERs (e.g., GPER, others), although that's NOT its intented target, biologically it can initate similar chitter chat that E1/E2 naturally is instructed to do..When people experience prolactin (gyno, glandular duct inflammation) it's plausible to the PR activation by way of ER's being fooled into a mimicking response.. This is rare, but when there is issues this is suspected to be a potential of the cause and effect.. Hormones can be weird with their unintentional mimicking or simulating the hormonal structures or even activations of other hormones, much like cross-reactivity with Trenbolone being recognized as estradiol on blood work.. all those lab testing doesn't always possess the abilities to see and recognize the difference is like our body does, sometimes the body just as well can be dictated and manipulated..

This is why Nandrolone, Drol, EQ and even Tren can give false positives with either cellular chitter chat or even lab work..
 
Bump for more info please

As mentioned prior estrogen is extremely pivotal with not only growth but also other functions throughout the body.. on paper and by theory that makes perfect sense to have a lower-end estrogen, but the reality is when at supraphysiological hormonal levels and Beyond I prefer my estrogen a little bit on the higher-end then normal, 60-64'ish is where I like to be..In fact that's not high at all considering the ratio of all of the other AAS.. employing an anti estrogen does not have to be aggressive, sometimes less can be more just to keep things at an even balance . What's important is including tamoxifen, because this is what will bind aggressively in Target to multiple ER's found throughout skeletal/glandular tissue..
Estrogen is extremely important with so many functions..

People try to treat the symptoms with a very aggressive anti estrogen and hopes to minimize estrogenic symptoms especially in the glandular duct issue of the breasts. Tamoxifen is very underrated, and it's actually 1 of 2 drugs that will Target Target Target The receptors and will help suppress inflammation, meanwhile the addition of an anti estrogen working in the background to control future blood serum circulation will be complimentary..

Not everyone needs this combination, but it is recommended for those sensitive individuals or those that are least attempting to have a higher presence of estrogen at the same time without experiencing the dreaded gynecomastia..
 
As mentioned prior estrogen is extremely pivotal with not only growth but also other functions throughout the body.. on paper and by theory that makes perfect sense to have a lower-end estrogen, but the reality is when at supraphysiological hormonal levels and Beyond I prefer my estrogen a little bit on the higher-end then normal, 60-64'ish is where I like to be..In fact that's not high at all considering the ratio of all of the other AAS.. employing an anti estrogen does not have to be aggressive, sometimes less can be more just to keep things at an even balance . What's important is including tamoxifen, because this is what will bind aggressively in Target to multiple ER's found throughout skeletal/glandular tissue..
Estrogen is extremely important with so many functions..

People try to treat the symptoms with a very aggressive anti estrogen and hopes to minimize estrogenic symptoms especially in the glandular duct issue of the breasts. Tamoxifen is very underrated, and it's actually 1 of 2 drugs that will Target Target Target The receptors and will help suppress inflammation, meanwhile the addition of an anti estrogen working in the background to control future blood serum circulation will be complimentary..

Not everyone needs this combination, but it is recommended for those sensitive individuals or those that are least attempting to have a higher presence of estrogen at the same time without experiencing the dreaded gynecomastia..

So if a person has never had an issue with gyno, when do you personally start taking nolvadex ?
Example: 16 weeks of Test 500mg,Deca 300mg weekly and zero symptoms of gyno and good sex drive. ??? Just wondering your opinions. Thx


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So if a person has never had an issue with gyno, when do you personally start taking nolvadex ?
Example: 16 weeks of Test 500mg,Deca 300mg weekly and zero symptoms of gyno and good sex drive. ??? Just wondering your opinions. Thx


Sent from my iPhone using Tapatalk
I definitely wouldn't use nolvadex unless you need it. Nolvadex is proven to suppress IGF-1 and natural GH production...I'm assuming hand in hand since IGF-1 levels are directly correlated to GH levels. Keep your IGF-1 as high as possible unless you have gyno symptoms, then you can throw in the tamoxifen
 
So if a person has never had an issue with gyno, when do you personally start taking nolvadex ?
Example: 16 weeks of Test 500mg,Deca 300mg weekly and zero symptoms of gyno and good sex drive. ??? Just wondering your opinions. Thx


Sent from my iPhone using Tapatalk

I myself personally start taking it when I notice symptoms, I use it as a symptom treating compound. Much like an aspirin when you get a headache. I won't take an aspirin and hopes not to get a headache but rather when I feel it coming on.

Tamoxifen can actually be fast acting much quicker than people would think. There is quite a few different protocols someone could attempt to use such as being proactive by taking a low to moderate dose daily or even every other day for that matter from the start of their blast or cycle.. and others can employ it when needed during their cycle or blast if they feel it's necessary.. you will hear so many different theories and arguments across the board.. but the reality is it's appropriate usage all comes down to what the user feels is adequate enough for their specific protocol..
 
Thx! I ask because I hate to take another compound when I’m not having any symptoms. I totally believe in a proper pct protocol and do one every cycle. I want to make that clear -because a lot of people need these compounds during and after a cycle. Very important subject here. (Nolvadex, clomid, proviron, hcg, adex,aromasin) even cyclofenil and older compounds can help a lot )


Sent from my iPhone using Tapatalk
 
I definitely wouldn't use nolvadex unless you need it. Nolvadex is proven to suppress IGF-1 and natural GH production...I'm assuming hand in hand since IGF-1 levels are directly correlated to GH levels. Keep your IGF-1 as high as possible unless you have gyno symptoms, then you can throw in the tamoxifen

This is where the complex interplay is suggested that itcould happen..It may actually reduces HGRH the hormone responsible for releasing GH, this is where the beauty of peptides come into play that possess the ability to stimulate HGRH levels, such as ghrp-6, ghrp-2, CJC, cjc-1295 with DAC, ipamorelin, sermorelin and other peptides.. it's found that chronic usage and long-term treatment with tamoxifen have made the suggestion with these levels being affected through GH and IGF levels by way of HGRH suppression..

Tamoxifen was almost a staple item for decades and decades, and I'll tell you what I don't see anybody getting skinny from using it..lol..

This goes back to something I was saying earlier in a different topic, it's amazing how so many drugs and hormones can have an indirect effect on certain people but not others.. at the same time we are constantly and desperately looking for drugs to counteract other drugs that counteract that drug.. such a cat and mouse game.. will there ever be simplicity in the synthetic lifestyle aside from just eating, training and sleeping?!?!?
 
This is where the complex interplay is suggested that itcould happen..It may actually reduces HGRH the hormone responsible for releasing GH, this is where the beauty of peptides come into play that possess the ability to stimulate HGRH levels, such as ghrp-6, ghrp-2, CJC, cjc-1295 with DAC, ipamorelin, sermorelin and other peptides.. it's found that chronic usage and long-term treatment with tamoxifen have made the suggestion with these levels being affected through GH and IGF levels by way of HGRH suppression..

Tamoxifen was almost a staple item for decades and decades, and I'll tell you what I don't see anybody getting skinny from using it..lol..

This goes back to something I was saying earlier in a different topic, it's amazing how so many drugs and hormones can have an indirect effect on certain people but not others.. at the same time we are constantly and desperately looking for drugs to counteract other drugs that counteract that drug.. such a cat and mouse game.. will there ever be simplicity in the synthetic lifestyle aside from just eating, training and sleeping?!?!?

For myself, it took decades to figure things out going through the aging process. I do know that after 25 years of training, my go to compounds are:

1.Testosterone
2.Deca
3.GH
PCT, and one AI (if needed)

I spend the most time figuring out my meals and preparation of food. From Larry Scott to Sergio Oliva to Arnold to Frank Zane to Ronnie Coleman to Bob Paris to Shawn Ray to Jay Cutler to Phil Heath to Kai Greene, all of these individuals were incredible bodybuilders. It has shown me that some of the compounds we have now weren’t around in the 50’s and 60’s but it never stopped these men from achieving outrageously awesome physiques! The thing we need to spend our time on is consistency in our training, diet and beliefs! I really believe that.








Sent from my iPhone using Tapatalk
 
This is where the complex interplay is suggested that itcould happen..It may actually reduces HGRH the hormone responsible for releasing GH, this is where the beauty of peptides come into play that possess the ability to stimulate HGRH levels, such as ghrp-6, ghrp-2, CJC, cjc-1295 with DAC, ipamorelin, sermorelin and other peptides.. it's found that chronic usage and long-term treatment with tamoxifen have made the suggestion with these levels being affected through GH and IGF levels by way of HGRH suppression..

Tamoxifen was almost a staple item for decades and decades, and I'll tell you what I don't see anybody getting skinny from using it..lol..

This goes back to something I was saying earlier in a different topic, it's amazing how so many drugs and hormones can have an indirect effect on certain people but not others.. at the same time we are constantly and desperately looking for drugs to counteract other drugs that counteract that drug.. such a cat and mouse game.. will there ever be simplicity in the synthetic lifestyle aside from just eating, training and sleeping?!?!?
See this is what I was thinking is the way it lowers it. So realistically...if one was using GH or GH releasing peptides, the nolvadex shouldn't have much if any impact on IGF-1!

This explains a lot to me. Most of the biggest guys rarely, if ever, use any AIs while on. They mostly use nolva just to control gyno. Pretty much all of them are on GH, using IGF-1, peptides, etc. This, other than better genetics, explains why they grow better when using gear compared to most guys these days. For the most part, everyone that comes on these forums runs an AI alongside their blast.

Recently, I've stopped using any AIs at all to let my e2 rebound and help with the healing process. I've also started growing a lot while still in a caloric deficit. Much more than I did while running AIs. Obviously I'm no genetic gift when it comes to putting on muscle, but I've gained a lot more since I stopped all AI use. I retain water easier (especially when cheating), but that's easily remedied with increased water intake and clean diet. Rarely I'll throw in a little bit of HCTZ if it makes my blood pressure high. The only other issue is that the 'ol D doesn't like to work as well, but that's also easily remedied with my 5mg cialis daily that I take anyways to be able to piss. Sure there's less sensitivity, but whatever.

Next blast I think I'm going to run no AI and see how much I grow compared to the past. I have the feeling it'll be a pretty significant difference. Especially considering I've been gaining muscle while in a pretty decent caloric deficit.
 
SB Labs
See this is what I was thinking is the way it lowers it. So realistically...if one was using GH or GH releasing peptides, the nolvadex shouldn't have much if any impact on IGF-1!

This explains a lot to me. Most of the biggest guys rarely, if ever, use any AIs while on. They mostly use nolva just to control gyno. Pretty much all of them are on GH, using IGF-1, peptides, etc. This, other than better genetics, explains why they grow better when using gear compared to most guys these days. For the most part, everyone that comes on these forums runs an AI alongside their blast.

Recently, I've stopped using any AIs at all to let my e2 rebound and help with the healing process. I've also started growing a lot while still in a caloric deficit. Much more than I did while running AIs. Obviously I'm no genetic gift when it comes to putting on muscle, but I've gained a lot more since I stopped all AI use. I retain water easier (especially when cheating), but that's easily remedied with increased water intake and clean diet. Rarely I'll throw in a little bit of HCTZ if it makes my blood pressure high. The only other issue is that the 'ol D doesn't like to work as well, but that's also easily remedied with my 5mg cialis daily that I take anyways to be able to piss. Sure there's less sensitivity, but whatever.

Next blast I think I'm going to run no AI and see how much I grow compared to the past. I have the feeling it'll be a pretty significant difference. Especially considering I've been gaining muscle while in a pretty decent caloric deficit.
Man, I wish I had an answer for that.. By theory and on paper it seems that as long as there's an exogenous source providing a pulse/secretion than IGF levels should be impervious to any detrimental influences stemming from Tamox effecting endogenous releases of HGRH and natty GH pulses. virtually no blunting so to speak.. Let's take a gander and some of the older timers that paved the way for us, from the 70's and 80's..These guys had chests that you could hang picture frames from and traps that would make them deaf by blocking their hearing.. Did they use AI's? and Tamox has been one of the longest estro combatants in the game yet we still see mass monsters throughout the ages..

IMO, I think Tamox usages has minimal effects on IGF, now if used at 40 mgs daily for months on end in some sort of therapeutic treatment like these studies explain, that's where they seen blunting with decreased levels, but none of these subjects are on AAS or anything at supraphysiologic levels such as Testosterone and so on from what I gather, in fact if they were on anything the synthesis of IGF-1 wouldn't have mitigated..
 
Man, I wish I had an answer for that.. By theory and on paper it seems that as long as there's an exogenous source providing a pulse/secretion than IGF levels should be impervious to any detrimental influences stemming from Tamox effecting endogenous releases of HGRH and natty GH pulses. virtually no blunting so to speak.. Let's take a gander and some of the older timers that paved the way for us, from the 70's and 80's..These guys had chests that you could hang picture frames from and traps that would make them deaf by blocking their hearing.. Did they use AI's? and Tamox has been one of the longest estro combatants in the game yet we still see mass monsters throughout the ages..

IMO, I think Tamox usages has minimal effects on IGF, now if used at 40 mgs daily for months on end in some sort of therapeutic treatment like these studies explain, that's where they seen blunting with decreased levels, but none of these subjects are on AAS or anything at supraphysiologic levels such as Testosterone and so on from what I gather, in fact if they were on anything the synthesis of IGF-1 wouldn't have mitigated..
Exactly. I completely agree. One of these days I need to test my serum IGF-1 during similar periods, say running the same dosages of AAS and GH, but one on tamoxifen for a while and the other off. It's only one sample but a fairly definitive one for myself. Be kinda interesting
 
Exactly. I completely agree. One of these days I need to test my serum IGF-1 during similar periods, say running the same dosages of AAS and GH, but one on tamoxifen for a while and the other off. It's only one sample but a fairly definitive one for myself. Be kinda interesting

Maybe when time is free on your end in the future PSL can sponsor you with conducting a bro-study... that would be super!!!! :winkfinger:
 
Maybe when time is free on your end in the future PSL can sponsor you with conducting a bro-study... that would be super!!!! :winkfinger:
That would be awesome! If really like to disprove the nolva/IGF-1 theory if possible! I really have the feeling, like you said, that it doesn't apply to people on supraphysiological levels of test and exogenous GH. That could be a game changer in the bro science world! Lol
 
Nolva definitely decreases igf.

Even if you're using gh, your baseline will still decrease which will in turn reduce total igf.
 
Nolva definitely decreases igf.

Even if you're using gh, your baseline will still decrease which will in turn reduce total igf.

natty base lines, sure.. But when there's synthetically "enhanced digits" aggrandized by an exogenous source providing higher serums, how detrimental can it be especially if there's GHRH stimulation in lieu of suppression?
I don't think anyone is disputing the effects of tamox on IGF, but these experimental studies are not only limited, but most if not all subjects that participate are in long term treatments, anything associated with a decrease is on solely endogenous levels that have nothing to bolster or buff expression of IGF.. I personally haven't seen anything regarding tamox effecting IGF while on hgh or TRT, if anything all I see is studies supporting igf expressions are through the roof with no mention of tamox.. Just how much could tamox blunt if it can at all while at
supraphysiologic levels???
 
natty base lines, sure.. But when there's synthetically "enhanced digits" aggrandized by an exogenous source providing higher serums, how detrimental can it be especially if there's GHRH stimulation in lieu of suppression?
I don't think anyone is disputing the effects of tamox on IGF, but these experimental studies are not only limited, but most if not all subjects that participate are in long term treatments, anything associated with a decrease is on solely endogenous levels that have nothing to bolster or buff expression of IGF.. I personally haven't seen anything regarding tamox effecting IGF while on hgh or TRT, if anything all I see is studies supporting igf expressions are through the roof with no mention of tamox.. Just how much could tamox blunt if it can at all while at
supraphysiologic levels???
20%.
 
Nolva definitely decreases igf.

Even if you're using gh, your baseline will still decrease which will in turn reduce total igf.
According to what study on enhanced athletes? As far as I know there's literally none, so this would be an assumption when referring to someone that's injecting exogenous GH and other IGF-1 increasing compounds like ghrps, ghrhs, nandrolone, etc.

It is known that tamoxifen decreases igf-1, but it looks to be directly correlated to the decrease in natural GH production that occurs. That said, someone over 30 isn't producing much anyways...and someone over 40 isn't producing hardly anything at all. So the overall probably isn't 20% in an enhanced person. Maybe in someone that's natural and has been inclused in these studies, but not someone that is using multiple compounds that dramatically increase IGF-1 production like nandrolone, GH, testosterone, etc. It's most likely very minimal overall.

Back on to my original point, if we can increase growth potential a lot by increasing serum e2 levels, the difference in growth potential from the lowered IGF-1 might be negligible and not even worth worrying about at all.

Anyhow, the only way to figure this out definitively is by doing our own controlled studies. Otherwise NONE of us can say for sure that it's going to make X amount of difference. There's simply no real data to analyze given the factors we're referring to.
 
I read somewhere about certain compounds causing peripheral gyno, even when e2 is in range. even people getting gyno on peptides. the AI and serm is a 2 prong approach that is pretty smart if your gyno prone
 

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