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Community Research Equipoise Boldenone and Estrogen Control

Threads marked with the 'Community Research' prefix involve ongoing research, high-quality logs, or in-depth community discussions backed by experience, data, or expert input.

LevButlerov

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Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/
serum levels of LH, FSH, and E2 hormones were significantly (p < 0.001) decreased in both BOL and BOL+Vit-C treated rats compared to control ones.

My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
 
I would so far, agree with the first theory. That EQ aromatises into E1 and competes for Aromatase at a much higher rate than Test.

In my anecdotal experience, a higher EQ dose to test eventually led to sore feet, sore joints and crazy brain fog.
Good feedback :D I also have a feeling the e1 is the issue deep down @Doctakay
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
Brother this is sensational 👏

I truly love and appreciate the commitment to diving deeper for the benefit of the community, especially around how people can sometimes get caught up in the way certain mechanistic pathways are explained or understood regarding the influence a compound may have.

Like Equipoise and the way people often describe it as having a “Ai like” influence on oestradiol, when the reality and underlying mechanisms can be a lot more nuanced than that as you have brought to the table.

It is strange though as studies show that testosterone has the higher affinity tp the aromatase enzyme over eq yet anecdotal evidence in some cases reflects otherwise through blood work with lcms "e2" test being conducted.

Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
It would show the levels of e1 if the specific lcms e1 testing was requested. As most dont consider the need to know where e1 levels are at due estrone not having a significant influence on males at the levels we would see from eq use. Would be cool to compare though and have both e2 and e1 lcms conducted to see how much cross activity can be present.

However a costly comparison for what would really be a individual specific case.
EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
This gets discussed alot and though we wont see a scientific case study to prove this now, being eq is no longer approved for human use, however there is continuous anecdotal evidence to support.
Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
I agree brother this probably makes the most practical sense.

Though as mentioned earlier, it does become a little tricky because testosterone is essentially the “preferred” substrate for aromatase, meaning conversion to oestradiol occurs relatively readily.

It would actually be a really interesting concept to test properly.

For example, someone could first run a testosterone only cycle at a fixed dose, with pre cycle and mid cycle bloodwork assessing:

total testosterone
dht
sensitive lcms oestradiol
estrone

We know testosterone can convert to oestradiol via aromatase, while it also converts to dht via 5 alpha reductase.

Then in the second phase, the exact same testosterone dose is used again, but with the addition of eq. Bloodwork is repeated under the same conditions, again assessing dht, lcms e2, and e1 levels.

The interesting part would be observing whether dht levels increase relative to the testosterone only phase. In theory, if eq is competing more aggressively for aromatase activity, less testosterone may be converted toward oestrogenic pathways, potentially leaving a greater proportion available for 5 alpha reduction into dht.

Of course, this wouldn’t definitively prove “stronger affinity” in isolation because enzyme kinetics, tissue specific activity, androgen receptor interactions and downstream metabolites all complicate the picture. But it could still provide some interesting indirect insight into substrate competition dynamics between testosterone and eq at the aromatase enzyme.

This is definitely more of a mechanistic thought experiment than a hard conclusion but still a genuinely interesting concept to think about 😂😂😂


Well you have definitely got me hook line and sinker here with this thread brother @LevButlerov 😂💪🤌

This thread is awesome work bro 🤜🏼🤛🏼💙
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
This is a great write up @LevButlerov , and does raise a lot of very good theories.
We did briefly touch on this in my podcast with @stevesmi and @Mobster and it was noted that quite a few Australian brothers run Eq and find it reduces e2.
I am an example of this. I run 750mg of Test E per week and 700mg of Eq. My blood test taken mid cycle a month ago showed no e2 issues at all.
I may be one of the fortunate ones in this regard however your conclusion seem to entirely with merit 🩵
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
But it’s great you brought this up, because from my experience EQ can act as a kind of “masking” of E2 — and like you said, they interact with each other in a way. EQ seems to occupy aromatase more quickly, which changes how testosterone is being converted.


But I’d add something else here — @Mobster also mentioned this: genetic factors and individual body type matter a lot. This is extremely important when it comes to how someone responds to compounds like boldenone. It’s not one-size-fits-all.


People who naturally have low E2 levels may react worse to EQ, especially if testosterone dosing is not properly balanced. Another important factor is how each individual converts testosterone into different metabolic pathways — this varies greatly from person to person.


Also worth noting, EQ is not a DHT derivative — it is a testosterone-derived compound — which affects how it interacts with aromatase and why it can influence E2 dynamics so strongly.


To summarise: when it comes to using EQ as an E2 “support” or regulator, it is highly individual. Genetics, current hormonal state, and overall health all play a major role. That’s why bloodwork during EQ use is so important, so dosing can be adjusted properly and issues avoided.


Because while EQ can be a very effective compound, it can also cause significant problems if E2 becomes suppressed for too long — and chronically low estrogen levels can have serious negative effects on health.
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
This was an amazing read! Very precise and well laid out @LevButlerov. And @Allupfromhere you can always make it move for me with your geeky feedback, I love nerd in you that you like to try and hide with those arms! :p

It may shift estrogen toward estrone, not estradiol:
Like I discussed after the horse estrogen post, of the e1-e4 options I think what's going on is that e1 is winning here.

We know testosterone can convert to oestradiol via aromatase, while it also converts to dht via 5 alpha reductase.
Similarly EQ converts to DHB this way too, albeit in a very small ratio. EQ has a poor affinity for 5 alpha reductase so DHB is but a minor metabolite. Just wanted this out there for the community. I mentioned this very briefly in my first podcast but didn't impress upon it enough. It's arguable that, depending on your goals, it's better to just run a lower dose DHB vs. EQ if estrogen isn't the reason one is running EQ.
 
It's arguable that, depending on your goals, it's better to just run a lower dose DHB vs. EQ if estrogen isn't the reason one is running EQ.
You should give much more context to this 😂😂😂

The next guy that reads this is just going to think, “ok, so dhb is better than eq lol.”

Dhb may have its place, but personally I see it more as a preference based compound rather than something most people genuinely 'need' to use. In my opinion, it makes more sense comparing dhb to something like tren, rather than comparing it directly to eq itself.

Logically, any compound that starts interfering with our ability to eat, sleep, recover, or maintain overall performance is often going to become counterproductive outside of specific scenarios.

That’s exactly why compounds like tren are usually viewed as a later stage contest prep tool, essentially a final lever to pull when pushing for that extreme look, rather than something ideal for building quality progress long term.
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
I swear there is a gap in the Aussie members and the American and North American members when it comes to this. I really believe that the North American members are more prone to estrogen than the Aussies, and it has to do with the quality of food that we grew up with.
 
I swear there is a gap in the Aussie members and the American and North American members when it comes to this. I really believe that the North American members are more prone to estrogen than the Aussies, and it has to do with the quality of food that we grew up with.
Wow, Didn't even think about that as a concept. Very profound brother 🩵
 
I swear there is a gap in the Aussie members and the American and North American members when it comes to this. I really believe that the North American members are more prone to estrogen than the Aussies, and it has to do with the quality of food that we grew up with.
💯 agree ... most of the food in the US is purposely poisoned to make us fat and dependent on big pharma 😪

Check out these perfect examples 😪😪
 

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I swear there is a gap in the Aussie members and the American and North American members when it comes to this. I really believe that the North American members are more prone to estrogen than the Aussies, and it has to do with the quality of food that we grew up with.
You think so? more estrogen in our food? it could be true but you would think more metabolites to stimulate estrogen receptors is what you mean? @stevesmi
 
💯 agree ... most of the food in the US is purposely poisoned to make us fat and dependent on big pharma 😪

Check out these perfect examples 😪😪
dont hate on mcdonalds lol :P
 
Brother this is sensational 👏

I truly love and appreciate the commitment to diving deeper for the benefit of the community, especially around how people can sometimes get caught up in the way certain mechanistic pathways are explained or understood regarding the influence a compound may have.

Like Equipoise and the way people often describe it as having a “Ai like” influence on oestradiol, when the reality and underlying mechanisms can be a lot more nuanced than that as you have brought to the table.

It is strange though as studies show that testosterone has the higher affinity tp the aromatase enzyme over eq yet anecdotal evidence in some cases reflects otherwise through blood work with lcms "e2" test being conducted.


It would show the levels of e1 if the specific lcms e1 testing was requested. As most dont consider the need to know where e1 levels are at due estrone not having a significant influence on males at the levels we would see from eq use. Would be cool to compare though and have both e2 and e1 lcms conducted to see how much cross activity can be present.

However a costly comparison for what would really be a individual specific case.

This gets discussed alot and though we wont see a scientific case study to prove this now, being eq is no longer approved for human use, however there is continuous anecdotal evidence to support.

I agree brother this probably makes the most practical sense.

Though as mentioned earlier, it does become a little tricky because testosterone is essentially the “preferred” substrate for aromatase, meaning conversion to oestradiol occurs relatively readily.

It would actually be a really interesting concept to test properly.

For example, someone could first run a testosterone only cycle at a fixed dose, with pre cycle and mid cycle bloodwork assessing:

total testosterone
dht
sensitive lcms oestradiol
estrone

We know testosterone can convert to oestradiol via aromatase, while it also converts to dht via 5 alpha reductase.

Then in the second phase, the exact same testosterone dose is used again, but with the addition of eq. Bloodwork is repeated under the same conditions, again assessing dht, lcms e2, and e1 levels.

The interesting part would be observing whether dht levels increase relative to the testosterone only phase. In theory, if eq is competing more aggressively for aromatase activity, less testosterone may be converted toward oestrogenic pathways, potentially leaving a greater proportion available for 5 alpha reduction into dht.

Of course, this wouldn’t definitively prove “stronger affinity” in isolation because enzyme kinetics, tissue specific activity, androgen receptor interactions and downstream metabolites all complicate the picture. But it could still provide some interesting indirect insight into substrate competition dynamics between testosterone and eq at the aromatase enzyme.

This is definitely more of a mechanistic thought experiment than a hard conclusion but still a genuinely interesting concept to think about 😂😂😂


Well you have definitely got me hook line and sinker here with this thread brother @LevButlerov 😂💪🤌

This thread is awesome work bro 🤜🏼🤛🏼💙
Brother this is sensational 👏

I truly love and appreciate the commitment to diving deeper for the benefit of the community, especially around how people can sometimes get caught up in the way certain mechanistic pathways are explained or understood regarding the influence a compound may have.

Like Equipoise and the way people often describe it as having a “Ai like” influence on oestradiol, when the reality and underlying mechanisms can be a lot more nuanced than that as you have brought to the table.

It is strange though as studies show that testosterone has the higher affinity tp the aromatase enzyme over eq yet anecdotal evidence in some cases reflects otherwise through blood work with lcms "e2" test being conducted.
I think equipoise and estrogen control is like the tren and estrogen of 5 years ago :D @Allupfromhere though we should get that thread up as well how trenbolone appears as e2 on bloods.
It would show the levels of e1 if the specific lcms e1 testing was requested. As most dont consider the need to know where e1 levels are at due estrone not having a significant influence on males at the levels we would see from eq use. Would be cool to compare though and have both e2 and e1 lcms conducted to see how much cross activity can be present.

However a costly comparison for what would really be a individual specific case.
Fair point and I agree, if you request specific LCMS estrone testing then yes you could see e1 directly, but most guys only pull e2 and even then most are not using sensitive LCMS. I was just talking with @wye about his high estrogen labs in his Log update with bloods here.

That is where the confusion starts, because people say EQ crashed estrogen when really we may only be looking at one part of the estrogen picture. I also agree estrone probably is not driving massive male symptoms at normal levels, but on a cycle with EQ, testosterone, maybe AI use, and different doses, it would be interesting to see e1 and e2 side by side. Cost is the issue though, and like you said it may only explain that one person’s response.
This gets discussed alot and though we wont see a scientific case study to prove this now, being eq is no longer approved for human use, however there is continuous anecdotal evidence to support.
I agree, and thats the hard part with EQ. We are not going to get clean human studies with EQ use, because boldenone is not approved for human use so nobody is funding that kind of trial. Imagine the news, horse steroid on humans trial lol :P
So we are stuck with animal data, mechanism theory, bloodwork patterns, and years of anecdotal cycle reports. Anecdotal evidence is not perfect proof I think we all agree, but when enough guys keep showing lower e2 symptoms or lower LCMS e2 after adding EQ, it becomes hard to ignore.
The mistake is when people turn that into EQ is an AI. It is not. It just seems to affect estrogen balance in some users through aromatase competition, weaker conversion, and individual response. It's by far not an ai.
I agree brother this probably makes the most practical sense.

Though as mentioned earlier, it does become a little tricky because testosterone is essentially the “preferred” substrate for aromatase, meaning conversion to oestradiol occurs relatively readily.

It would actually be a really interesting concept to test properly.

For example, someone could first run a testosterone only cycle at a fixed dose, with pre cycle and mid cycle bloodwork assessing:

total testosterone
dht
sensitive lcms oestradiol
estrone

We know testosterone can convert to oestradiol via aromatase, while it also converts to dht via 5 alpha reductase.

Then in the second phase, the exact same testosterone dose is used again, but with the addition of eq. Bloodwork is repeated under the same conditions, again assessing dht, lcms e2, and e1 levels.

The interesting part would be observing whether dht levels increase relative to the testosterone only phase. In theory, if eq is competing more aggressively for aromatase activity, less testosterone may be converted toward oestrogenic pathways, potentially leaving a greater proportion available for 5 alpha reduction into dht.

Of course, this wouldn’t definitively prove “stronger affinity” in isolation because enzyme kinetics, tissue specific activity, androgen receptor interactions and downstream metabolites all complicate the picture. But it could still provide some interesting indirect insight into substrate competition dynamics between testosterone and eq at the aromatase enzyme.

This is definitely more of a mechanistic thought experiment than a hard conclusion but still a genuinely interesting concept to think about 😂😂😂
Yes brother that would be the cleanest way to test it, but not sure if practical right? :D
You would need a true baseline first with test only, same dose, same injection schedule, same lab timing, same diet, same AI use or no AI use, then repeat with EQ added and compare sensitive LCMS e2, e1, dht, total test and free test.
The dht angle is interesting because if less testosterone is being pushed through aromatase, you could theoretically see more available for 5 alpha reduction, but like you said that still does not prove direct affinity by itself. Too many moving parts with tissue activity and metabolites imo. If we could pull this study off it could be the 1st study in steroid forum history!
Well you have definitely got me hook line and sinker here with this thread brother @LevButlerov 😂💪🤌

This thread is awesome work bro 🤜🏼🤛🏼💙
I hope this thread grows and we can add to it :D
 
You should give much more context to this 😂😂😂

The next guy that reads this is just going to think, “ok, so dhb is better than eq lol.”

Dhb may have its place, but personally I see it more as a preference based compound rather than something most people genuinely 'need' to use. In my opinion, it makes more sense comparing dhb to something like tren, rather than comparing it directly to eq itself.

Logically, any compound that starts interfering with our ability to eat, sleep, recover, or maintain overall performance is often going to become counterproductive outside of specific scenarios.

That’s exactly why compounds like tren are usually viewed as a later stage contest prep tool, essentially a final lever to pull when pushing for that extreme look, rather than something ideal for building quality progress long term.
Agreed, DHB is more like an "off-season tren" and it's definitely not "better than EQ" I definitely should have clarified that.

It's not so much comparable to EQ in its function it's moreso for the folk that want to run EQ simply due to what they know they get out of the downstream conversion of it to DHB. This type of finicky preference is but the 1% out of we the 5% of the population who are either into bodybuilding or bodybuilders ourselves which makes my comment likely for too small a crowd and it definitely could have been interpreted poorly. Agreed!
 
Anecdotal evidence is not perfect proof I think we all agree, but when enough guys keep showing lower e2 symptoms or lower LCMS e2 after adding EQ, it becomes hard to ignore.
Here is not only my own personal example of the profound impact of EQ on e2 but the power of and difference in testing using LCMS vs. standard labs.

Running the following cycle with only 105mg EQ (along with 400mg Test and 70 Mast)
This is a 4:1 ratio of Test/EQ!
  • 330mg Sust
  • 70mg TestP
  • 70mg MastP
  • 105mg EQ
This cycle and more specifically the bloodwork can be found in my January-April 2026 log here ➡️ https://www.evolutionary.org/forums...transformation-log.108526/page-7#post-2029770
The e2 LCMS (came a week later) and pic is here ➡️ https://www.evolutionary.org/forums...transformation-log.108526/page-8#post-2052962

My standard lab test (non-LCMS) of e2 on the above cycle using that dose of EQ was 78 pmol/L (see pic) or, said differently, this equates to 21 pg/mL.

One would normally just stop there and consider their e2 at 21 pg/mL.

After having an LCMS test done on the these same bloods the LCMS e2 results that came back were 5.5 pg/mL (see pic)

Therefore two things:
  • EQ lowered my standard lab test of e2 to 21 pg/mL (not the true result as we'll see) while running 400mg of Test using ED pinning
  • EQ in fact profoundly lowered e2 to a more accurate marker of 5.5 pg/mL upon further testing via LCMS
Bottom line:
  • EQ profoundly lowered my LCMS e2 on 400mg of Test at a 4:1 ratio
  • Standard testing vs. LCMS testing was a difference of 21 pg/mL vs. 5.5 pg/mL
Note: for e2 the formula is pmol/L=pg/mL x 3.671

See pics below showing standard lab test of e2 and then subsequent LCMS test of e2 from same blood for comparison - this all using a 4:1 ratio of Test/EQ (with the Mast) on ED dosing
30Mar Blood4 partial.webp

25Apr e2 sensitive bloodwork.webp


The mistake is when people turn that into EQ is an AI. It is not.
Agreed. EQ is not a direct "aromatase inhibitor".
 
Im currently waiting for my E2 LC/MS back after adding 200mg EQ but heres my previous bloods.

Cycle at the time was
250mg Sustanon weekly, EOD pins
40mg Anavar daily
Screenshot_20260516-235412.Moto App Launcher.webp


I then added 200mg EQ weekly (EOD pins) without changing any other variables to confirm effects for future cycle planning.
Screenshot_20260516-235306.Moto App Launcher.webp
Screenshot_20260516-235330.Moto App Launcher.webp

I am currently waiting on the E2 LC/MS for this bloodwork to confirm EQ effect. Thoigh we can see by adding 200mg of EQ, my free test went up by 367 pmol/l.

Will post here with E2 sensitive when testing is back.
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
Awesome write-up mate! Very interesting!
 
You think so? more estrogen in our food? it could be true but you would think more metabolites to stimulate estrogen receptors is what you mean? @stevesmi
More chems, poorer quality and so on

I touched upon how your average Ozzy member handles stress way better than most. Stress hormones make a difference

And, to back up @stevesmi, the food etc when young

But I'll also back up @US-pharmacies it's NOT a 1 size fits all approach
 
You think so? more estrogen in our food? it could be true but you would think more metabolites to stimulate estrogen receptors is what you mean? @stevesmi
Don’t know. Probably a combo of all.
Farming practices are not the same
 
💯 agree ... most of the food in the US is purposely poisoned to make us fat and dependent on big pharma 😪

Check out these perfect examples 😪😪
Our salt even has anti caking agents.
And every fast food joint and restaurant drenches food with it
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
I think at the end of the day the blood work does not lie. You can get your own blood work and see for yourself. Then you'll know the answer 100%.
 
From what I’ve seen on forums etc, always best to start with a lower than necessary dose, especially if not using the cyp ester. I’ve seen guys run 800mg and only needing 50mg eq weekly, anything above that, dry joints, fatigue etc kick in.

Definitely is a compound that should be approached with caution and blood work before and after any dose changes are made.
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


@Allupfromhere @Pigsy @waggat @Trenhead3cc @Kopite67 @Nasser1997o2 @fatboy999
@Grumpy @LH5515 @Yuri @Doctakay @catdadironman @bss @Shakey @MarshMonsta
@trenAMP @Nood @RawCutlery @liftedlivingwithlegacy @catdadironman @Jro
@BigVelvetG @floridaman1984 @Noah Wixx @MarkNV @US-pharmacies @Mobster
I've always viewed equipoise as a very versatile steroid. You can do everything with it. I think a lot of people react differently to them, but there's definitely a tren when it comes to individual experiences and estrogen.
 
Im currently waiting for my E2 LC/MS back after adding 200mg EQ but heres my previous bloods.

Cycle at the time was
250mg Sustanon weekly, EOD pins
40mg Anavar daily
View attachment 232028

I then added 200mg EQ weekly (EOD pins) without changing any other variables to confirm effects for future cycle planning.
View attachment 232029View attachment 232030
I am currently waiting on the E2 LC/MS for this bloodwork to confirm EQ effect. Thoigh we can see by adding 200mg of EQ, my free test went up by 367 pmol/l.

Will post here with E2 sensitive when testing is back.
This will be good data for the research article I'd post it here when you get LCMS back.

Personally I'm only ever getting LCMS moving forward. The difference from standard to LCMS is nuts sometimes!
 
The only issue I see here is that our body constantly changes. What happens on a previous cycle may not apply on a future cycle. That's the frustrating thing about it and why anecdotal evidence sometimes is just not helpful.
 
This will be good data for the research article I'd post it here when you get LCMS back.

Personally I'm only ever getting LCMS moving forward. The difference from standard to LCMS is nuts sometimes!
This is the same bloods sample for both the standard immunoassay and lcms e2 tests..

Almost a 20% difference i had at the start of the year.
Screenshot_20260505_111809_Gallery.webp
Screenshot_20260505_111716_Gallery.webp
 
The question is what molecule is cross reacting with the standard immunoassay testing for e2?

The IA testing is using an antibody/antigen binding mechanism and using fluorescence activated by the binding to produce a flouerscence with an intensity relative to the number of molecules.

So if its producing more fluoresce the test isnt wrong, its just not specific and theres something causing cross reaction.

Its plausible (and likely) that another form of estrogen that binds to the antigen for e2 (but differs in a way that effects e2 active site binding on the cell membrane in vivo) is binding and causing the signal.

What is the cause of that?

Because LCMS uses mass to charge, so if is looking for a specific mass thats all they noted results. The other shit is ignored but if you had the raw data it would be helpful if theres other peaks in the mass spec.

So if there is a molecule binding to IA tests (which has to be or the signal would not be elevated) and not showing up in LCMS, then there is a 2nd e2 antigen biding analog in the (blood) sample.

That other thing is what "molecular" is calling preloquin or whatever. He did this using RDkit which isnt like an LLM thats essentially a kickass chatbot. Its probably accurate and I wouldnt be surprised if its real (i dont trust LLM's).

Off topic- but wouldnt this be way sicker if clavicular did it?

Back on topic... I dont find his speculation unreasonable.

As @US-pharmacies stated - genetic individuality plays a huge role in the end result, and even bigger picture we may be able to use these pathways and personal reactions to different androgens to predict responses to others based on structure and likely enzyme activity deduced by an individuals response to other known molecules and pathways.

In the end this is a big mental jerk off session so we can sound smart and rationalize using drugs to look better before we die and our planet gets absorbed by the sun and the universe cools and contracts untill the next big bang explodes us outward and we do it all over again.

Pizza is one of the best answers.
 
In the end this is a big mental jerk off session so we can sound smart and rationalize using drugs to look better before we die and our planet gets absorbed by the sun and the universe cools and contracts untill the next big bang explodes us outward and we do it all over again.

Pizza is one of the best answers.
😂😂😂 this was good lol.
 
@LevButlerov asked me to post in the community research section my upcoming 14 week cycle, not sure why my best guess i have always had the pure luck of controlling estrogen with either primo, mast or eq.

I also might try a subq experiment for this run as ive never ran a cycle subq before.

Anyway this will be the first time i will BE attempting a cycle designed in this manner.

i am trying to compete this year if possible, i have untill October to see if i have done enough to be show ready and to bring my best, this cycle will be helping me push into that best.

I also have AI on hand for a last ditch shit is seriously wrong need to fix it kind of deal, will be holding off as long as i can to see how we are looking. I have had E2 as high as 90 before no sides symptoms or issues, i prefer between 25-50 range somewhere in that ball park.

Goal first 10 weeks control E2 with EQ utilizing long ester compounds.

Ciliais all 14 weeks
Tirzepatide all 14 weeks
Bpc/tb500 combo run daily 14 weeks

In-between the first 10 weeks 5 weeks of var will be run 30-40mg then dropped
Last 4 weeks switch into Test Prop, Mast Prop
GW501156 will be run the last 4 weeks to aid in endurance and potential fat loss

Here it is

Weeks 1-10 lean Mass Phase
Monday

Test E — 150 mg
NPP — 60 mg
EQ -- 50 mg

Tuesday

Off

Wednesday
Test E — 150 mg
NPP — 60 mg

Thursday
Off

Friday
Test E — 150 mg
NPP — 60 mg
EQ --- 50 mg

Saturday

Off

Sunday
NPP — 60 mg

Weeks 5-10
Daily orals

Anavar
3040 mg daily

Weeks 8-12
HCG
250 IU EOD


Weeks 10-14

Monday

Test Prop — 100 mg
Masteron Prop — 100 mg

Tuesday
Off

Wednesday
Test Prop — 100 mg
Masteron Prop — 100 mg

Thursday
Off

Friday
Test Prop — 100 mg
Masteron Prop — 100 mg

Saturday
Off

Sunday
Test Prop — 100 mg
Masteron Prop — 100 mg

Daily Support
Weeks 10-14

GW501516
20 mg daily

Weeks 1-14
Cialis
10 mg daily

Weeks 1-14
Tirzepatide
2 mg weekly

Bloodwork Week 3
Testosterone
Free Testosterone
E2
Prolactin
CBC
Liver Panel
Lipids
Kidney Function
Blood Pressure
 
In the end this is a big mental jerk off session so we can sound smart and rationalize using drugs to look better before we die and our planet gets absorbed by the sun and the universe cools and contracts untill the next big bang explodes us outward and we do it all over again.

Pizza is one of the best answers.
Perfect closer comment! Slammed it home! :p:p:ROFLMAO::ROFLMAO:
 
@LevButlerov asked me to post in the community research section my upcoming 14 week cycle, not sure why my best guess i have always had the pure luck of controlling estrogen with either primo, mast or eq.

I also might try a subq experiment for this run as ive never ran a cycle subq before.

Anyway this will be the first time i will BE attempting a cycle designed in this manner.

i am trying to compete this year if possible, i have untill October to see if i have done enough to be show ready and to bring my best, this cycle will be helping me push into that best.

I also have AI on hand for a last ditch shit is seriously wrong need to fix it kind of deal, will be holding off as long as i can to see how we are looking. I have had E2 as high as 90 before no sides symptoms or issues, i prefer between 25-50 range somewhere in that ball park.

Goal first 10 weeks control E2 with EQ utilizing long ester compounds.

Ciliais all 14 weeks
Tirzepatide all 14 weeks
Bpc/tb500 combo run daily 14 weeks

In-between the first 10 weeks 5 weeks of var will be run 30-40mg then dropped
Last 4 weeks switch into Test Prop, Mast Prop
GW501156 will be run the last 4 weeks to aid in endurance and potential fat loss

Here it is

Weeks 1-10 lean Mass Phase
Monday

Test E — 150 mg
NPP — 60 mg
EQ -- 50 mg

Tuesday

Off

Wednesday
Test E — 150 mg
NPP — 60 mg

Thursday
Off

Friday
Test E — 150 mg
NPP — 60 mg
EQ --- 50 mg

Saturday

Off

Sunday
NPP — 60 mg

Weeks 5-10
Daily orals

Anavar
3040 mg daily

Weeks 8-12
HCG
250 IU EOD


Weeks 10-14

Monday

Test Prop — 100 mg
Masteron Prop — 100 mg

Tuesday
Off

Wednesday
Test Prop — 100 mg
Masteron Prop — 100 mg

Thursday
Off

Friday
Test Prop — 100 mg
Masteron Prop — 100 mg

Saturday
Off

Sunday
Test Prop — 100 mg
Masteron Prop — 100 mg

Daily Support
Weeks 10-14

GW501516
20 mg daily

Weeks 1-14
Cialis
10 mg daily

Weeks 1-14
Tirzepatide
2 mg weekly

Bloodwork Week 3
Testosterone
Free Testosterone
E2
Prolactin
CBC
Liver Panel
Lipids
Kidney Function
Blood Pressure
Good plan for the research article to do bloods at 3 weeks.

Goal first 10 weeks control E2 with EQ utilizing long ester compounds.
It will be good data for the research thread to post e2 bloodwork here both at your 3 week mark as planned and beyond. You'll be at a 3:1 ratio so we can get some insight then learn more for anecdotal research as you adjust.
 
Good plan for the research article to do bloods at 3 weeks.
Always got to stay ontop of bloods its critical imo
It will be good data for the research thread to post e2 bloodwork here both at your 3 week mark as planned and beyond. You'll be at a 3:1 ratio so we can get some insight then learn more for anecdotal research as you adjust.
Be the first time ive run a 3:1 myself so i will be learning as well as i go, typically i am at a 1:1 ratio, so yes overall this will show alot of new data for myself and other people.
 
@catdadironman was using sustanon and equipoise in his log and estrogen dropped to 6 in LCMS!
https://www.evolutionary.org/forums...og-sustanon-eq-and-anavar.110504/post-2079563
Well the E2 came in this morning - and EQ seems to have slammed it like the Rock doing the peoples elbow! A bit unexpected as I haven’t noticed a classical low E2 symptoms.

View attachment 235331

After consulting with @HarleyGuy the following action plan is being implemented:

  • Bump to 500/w Sustanon
  • Lower EQ to 100/w
  • Add in Mast at 200/w
  • Redo bloods in 4 weeks

Any other suggestions are welcome!

@trenAMP @RawCutlery @LevButlerov @HarleyGuy @Mobster @MarkNV @James Creeper
1779460448694-webp.235331
 
@Shakey reported in his Log, he ran a 4 week cycle sustanon anavar hgh; he had estradiol levels 267 (BEFORE Equipoise EQ)
screenshot_20260523-223214_adobe-acrobat-webp.236135

https://www.evolutionary.org/forums...g-log-with-team-oxygen-o2.111010/post-2081000
Week 4 of rehab cycle - 250mg sust, 40mg var and 6iu gh. E2 was high,

After introducing 200mgs of equipoise to the cycle for 4 weeks his Estradiol E2 dropped to 78
screenshot_20260523-223901_adobe-acrobat-webp.236146

https://www.evolutionary.org/forums...g-log-with-team-oxygen-o2.111010/post-2081001
so added 200mg eq.
4 weeks after EQ - kept all other variables the same to check effects on bloodwork.
 
@Shakey reported in his Log, he ran a 4 week cycle sustanon anavar hgh; he had estradiol levels 267 (BEFORE Equipoise EQ)
screenshot_20260523-223214_adobe-acrobat-webp.236135

https://www.evolutionary.org/forums...g-log-with-team-oxygen-o2.111010/post-2081000


After introducing 200mgs of equipoise to the cycle for 4 weeks his Estradiol E2 dropped to 78
screenshot_20260523-223901_adobe-acrobat-webp.236146

https://www.evolutionary.org/forums...g-log-with-team-oxygen-o2.111010/post-2081001
Im still awaiting lcms currently, so i will post that here as well when i get it. @HarleyGuy said it took 2 weeks for his.
 
Im still awaiting lcms currently, so i will post that here as well when i get it. @HarleyGuy said it took 2 weeks for his.
This is really perfect for this community research thread on EQ and e2 thank you :D @Shakey
 
@catdadironman was using sustanon and equipoise in his log and estrogen dropped to 6 in LCMS!
https://www.evolutionary.org/forums...og-sustanon-eq-and-anavar.110504/post-2079563

1779460448694-webp.235331

@Shakey reported in his Log, he ran a 4 week cycle sustanon anavar hgh; he had estradiol levels 267 (BEFORE Equipoise EQ)
screenshot_20260523-223214_adobe-acrobat-webp.236135

https://www.evolutionary.org/forums...g-log-with-team-oxygen-o2.111010/post-2081000


After introducing 200mgs of equipoise to the cycle for 4 weeks his Estradiol E2 dropped to 78
screenshot_20260523-223901_adobe-acrobat-webp.236146

https://www.evolutionary.org/forums...g-log-with-team-oxygen-o2.111010/post-2081001
@LevButlerov This is some top notch eagle eye watcher lookout for data for this thread. "The Entity" always in full gear!

Ill have bloods for both test:eq 5:4 and 2:1(in 4 weeks or so)
5:4 vs. 2:1 will be amazing data @Shakey this is great work!

Trending toward EQ being the e2 soul crusher!

I may start recommending members start out at 4 or even 5:1 after I consult with @LevButlerov. @BertaBoy was advised in a group DM by @LevButlerov (group DM with me Lev and Berta) to start at 6:1 in fact! Low and slow with EQ with all we're finding out.
 
@LevButlerov This is some top notch eagle eye watcher lookout for data for this thread. "The Entity" always in full gear!


5:4 vs. 2:1 will be amazing data @Shakey this is great work!

Trending toward EQ being the e2 soul crusher!

I may start recommending members start out at 4 or even 5:1 after I consult with @LevButlerov. @BertaBoy was advised in a group DM by @LevButlerov (group DM with me Lev and Berta) to start at 6:1 in fact! Low and slow with EQ with all we're finding out.
Im super new on learning about eq but I'll run labs at 4 weeks and we shall see what that ratio does 😁
 
@LevButlerov This is some top notch eagle eye watcher lookout for data for this thread. "The Entity" always in full gear!


5:4 vs. 2:1 will be amazing data @Shakey this is great work!

Trending toward EQ being the e2 soul crusher!

I may start recommending members start out at 4 or even 5:1 after I consult with @LevButlerov. @BertaBoy was advised in a group DM by @LevButlerov (group DM with me Lev and Berta) to start at 6:1 in fact! Low and slow with EQ with all we're finding out.
This 2:1 test will have deca in the mix aswell. And i did start an ai with the full @OxygenPharm stack, but for the sake of testing , i will be pulling arimidex 14days before testing. Thatll allow for full drug clearance and a return to untreated aromatase activity e2 levels. Wont pull deca though. ;)
 
Im super new on learning about eq but I'll run labs at 4 weeks and we shall see what that ratio does 😁
You're in the right place to learn bro, and where better to start than on your own self too!
 
This 2:1 test will have deca in the mix aswell. And i did start an ai with the full @OxygenPharm stack, but for the sake of testing , i will be pulling arimidex 14days before testing. Thatll allow for full drug clearance and a return to untreated aromatase activity e2 levels. Wont pull deca though. ;)
It will be good data for all but especially for you for future cycles.
 
Not super thrilled about the results - but I am happy that it can add some insight for those looking to run EQ. Eq doesnt play around!
eq is serious for sure :D
 
I may start recommending members start out at 4 or even 5:1

For my next cycle (July 1st start) I’m planning Test, EQ, NPP, and proviron.

Im wondering if the EQ is getting pushed down to 5:1 or 6:1 of test, is it still worth running? Are you getting the full benefit of EQ? Why not just add more test until you can’t tolerate it, and manage with an AI?

What is the minimum effective dose of EQ (from AAS standpoint, not estrogen management)?

The other logistical issue I’m curious about is that the half life of EQ is so long. So in a 4 month cycle you don’t have much time to adjust dosages and see the response.
 
For my next cycle (July 1st start) I’m planning Test, EQ, NPP, and proviron.

Im wondering if the EQ is getting pushed down to 5:1 or 6:1 of test, is it still worth running? Are you getting the full benefit of EQ? Why not just add more test until you can’t tolerate it, and manage with an AI?

What is the minimum effective dose of EQ (from AAS standpoint, not estrogen management)?

The other logistical issue I’m curious about is that the half life of EQ is so long. So in a 4 month cycle you don’t have much time to adjust dosages and see the response.
I'd rather have my E2 managed by EQ than by an AI regardless of how little is required to do that.

As for the long half life, get yourself some boldenone ace from @Gold Standard Labs and dial in your test:EQ ratio much quicker :)
 
For my next cycle (July 1st start) I’m planning Test, EQ, NPP, and proviron.

Im wondering if the EQ is getting pushed down to 5:1 or 6:1 of test, is it still worth running? Are you getting the full benefit of EQ? Why not just add more test until you can’t tolerate it, and manage with an AI?

What is the minimum effective dose of EQ (from AAS standpoint, not estrogen management)?

The other logistical issue I’m curious about is that the half life of EQ is so long. So in a 4 month cycle you don’t have much time to adjust dosages and see the response.
Depends when or if you plan to get bloods. My ratio was almost 5:1 and it tanked my e2 and now the shoulder issue I thought was from training is in the other shoulder and now I know it’s from low e2. Elbows too now. If I could go back I woulda done bloods every 3 weeks to get ahead of this.

I’d start at very minimum 3:1 ratio if not 5:1 and do bloods 3 weeks later then every 3 weeks after that.

An effective dose of EQ not considering what it can do to e2 is 200mg+. So you’re kinda stuck running it low dose to start until you see how your e2 responds to it. My dose was 100mg of EQ and it shut my e2 down hard
 
Depends when or if you plan to get bloods. My ratio was almost 5:1 and it tanked my e2 and now the shoulder issue I thought was from training is in the other shoulder and now I know it’s from low e2. Elbows too now. If I could go back I woulda done bloods every 3 weeks to get ahead of this.

I’d start at very minimum 3:1 ratio if not 5:1 and do bloods 3 weeks later then every 3 weeks after that.

An effective dose of EQ not considering what it can do to e2 is 200mg+. So you’re kinda stuck running it low dose to start until you see how your e2 responds to it. My dose was 100mg of EQ and it shut my e2 down hard
I see, I could get estrogen checked as frequently as weekly if needed be.

Maybe I’ll just start off higher 600 test, 200 EQ 200 NPP. I’d really like to run 300+ NPP that’s where it seemed to really feel good for me, but would put me starting over a gram. The other option I suppose is pulling the NPP entirely ( or EQ I suppose).
 
Original thread on this is here: https://www.evolutionary.org/forums...tios-a-study-of-equipoise-and-estrogen.105375
We were discussing Equipoise and how it can lower e2 in some EVO brothers. Recently, @James Creeper and @Mobster @stevesmi were discussing it in our group chat as well. I heard Steve mentioned it on the podcast a few times as well when he was on with @HarleyGuy and EVO Aussie brothers. After this a video is circulating online talking about eq being horse estrogen, very little evidence of this btw. The hype is too much so I had to write this.

IMO eq is not a clean AI like aromasin. Basically, equipoise can reduce the amount of testosterone being converted into estradiol, while also creating a different estrogen profile, so bloodwork may show lower e2 even though the body is not estrogen free by any means. Though, I have seen LCMS e2 tests after eq which do show some estrogen control, but it makes me wonder is this related to masking like we have with trenbolone. For new guys, Trenbolone can show up as E2 on bloods.

Why e2 can drop on EQ? My theories on this. I'm open to being corrected :D
  • Substrate competition: This is what @stevesmi was saying on multiple podcasts. Testosterone and boldenone related metabolites are fighting for the same aromatase system. If EQ is occupying aromatase, less testosterone may convert into e2. That is the competition theory, and it makes the most sense practically tbh.
  • EQ aromatizes weaker than testosterone: Mg for mg, EQ does not behave like testosterone for estrogen conversion. So if someone runs high EQ with lower test, e2 often trends down because the stack has less strong e2 producing ability. Though I have seen this wrong where lower test causes eq to completely crash e2 with symptoms.
  • It may shift estrogen toward estrone, not estradiol: A lot of the EQ estrogen confusion comes from e1 vs e2. You may not get much e2, but there can still be estrogenic metabolites or estrone pathway activity. That is why some guys feel low e2 while bloods or symptoms dont feel like low e2 or high e2 for that matter. It's the e1 vs e2 issue.
  • Blood testing can be misleading: Regular bloods are not ideal for low E2 ranges. You'd have to get sensitive LCMS for e2 each time, which is complex. And makes me think would it show the e1 issue? seems not.
I did check studies on this. Some data does show boldenone can reduce e2. In a rat study, boldenone treatment significantly lowered LH, FSH, and e2, with e2 dropping from about 58 to 28pg/mL in the boldenone group. But we are not rats lol

https://pmc.ncbi.nlm.nih.gov/articles/PMC7694087/


My open ended conclusion right now. EQ lowers e2 by competing at aromatase level, aromatizing less strongly than testosterone, shifting estrogen metabolites, and sometimes confusing standard e2 testing. This is why high EQ with low test can crash e2 hard in some guys, while others barely see any issues.


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Very well written @LevButlerov. It’s certainly not a straight forward AAS. It’s great that you are being open minded. there’s a lot of different conjecture on eq out there and for me being new to the space, it’s pretty good to have something here on evo with some sources to back up the data!

With limited studies in humans, I’d presume those with the most knowledge would be coaches that regularly read bloodwork. No doubt there’d be correlated findings for those that had eq in their protocol that you wouldn’t find elsewhere. 👍

I’m currently running 450 test 250 eq. Hoping this lands me in good range!
 
Very well written @LevButlerov. It’s certainly not a straight forward AAS. It’s great that you are being open minded. there’s a lot of different conjecture on eq out there and for me being new to the space, it’s pretty good to have something here on evo with some sources to back up the data!

With limited studies in humans, I’d presume those with the most knowledge would be coaches that regularly read bloodwork. No doubt there’d be correlated findings for those that had eq in their protocol that you wouldn’t find elsewhere. 👍

I’m currently running 450 test 250 eq. Hoping this lands me in good range!
You'll see lowered e2 from EQ and the video implies an increase in e1 instead which we don't look for on bloods except in menopausal or post menopausal women most times. But equilin, I'm not buying it yet.

450 Test and 250 EQ would crush my e2 but everyone is different. Post your results here for research bro.
 
You'll see lowered e2 from EQ and the video implies an increase in e1 instead which we don't look for on bloods except in menopausal or post menopausal women most times. But equilin, I'm not buying it yet.

450 Test and 250 EQ would crush my e2 but everyone is different. Post your results here for research bro.
What video is it? I’ve seen videos saying one to one ratio abd other saying start at a 1:7 ratio. It’s unreal how different it is for different people.

week 3 for me atm, I’m looking at week 6 for bloods. I’ll be sure to post the results here
 
Just a though.

The estrone argument may be less relevant than we think due to the 17beta-hydroxysteroid dehydrogenases, specifically type 1 which continuously converts e1 into e2.

Also, probably due to the fact that Boldenone doesnt aromatise very efficiently to estrogen, it will shift the androgen to estrogen ratio in the body when paired with testosterone, simply by outpacing estrogen. This is why some people can measure that dht-derivates lower or ameliorate estrogen symptoms - not because it always physically lowers e2 levels in the body (nuance) - but just because it shifts the androgen/est ratio.

But thats why you can still get high estrogen symptoms with boldenone, due to the interconversion of e1 - e2.
 
Very well written @LevButlerov. It’s certainly not a straight forward AAS. It’s great that you are being open minded. there’s a lot of different conjecture on eq out there and for me being new to the space, it’s pretty good to have something here on evo with some sources to back up the data!

With limited studies in humans, I’d presume those with the most knowledge would be coaches that regularly read bloodwork. No doubt there’d be correlated findings for those that had eq in their protocol that you wouldn’t find elsewhere. 👍

I’m currently running 450 test 250 eq. Hoping this lands me in good range!
I think most of the knowledge on this is mainly anecdotal and we have a lot of logs to back this up :D @jenkemj
 
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