MESO-Rx Exclusive Primobolan and/or Equipoise Symptoms of Low vs. High Estrogens, Explained

MESO-Rx Administrator

Administrator
Staff member
10+ Year Member
20+ Year Member
There has been a lot of discussion in recent years from members seemingly experiencing symptoms of low estrogens when using Primobolan and/or Equipoise, even when combined with moderately aromatizing AAS like testosterone, etc. So I asked @Type-IIx if he would spend some time researching and explaining this phenomena. He sent me this comprehensive, albeit a little bit technical article, presenting his thesis to explain in detail plus information on making choices when encountering such estrogen-related issues. I am please to announce the publication last week of this article on MESO. Feel free to ask any questions about the article in the current thread.

 
Amazing stuff!

Does dieting down from a high bodyfat not affect hormonal profile then due to still having the same number of adipocytes?

Or are there other hormonal benefits apart from aromatisation?
 
Amazing stuff!

Does dieting down from a high bodyfat not affect hormonal profile then due to still having the same number of adipocytes?

Or are there other hormonal benefits apart from aromatisation?
Hah, I knew that statement about maintaining lifelong low body fat levels in order to keep a high T/E2 ratio by reduced aromatase activity would prove controversial. It's good that you are reading attentively and with a critical eye.

I make this assertion despite the existence of evidence that caloric restriction increases T/E2 ratio by, in part, reduced aromatase activity because it seems to me that mechanistically adipocyte # is what "must" be related to aromatase # because of the richness of fat cells, rather than lipid contents, in aromatase expression. Yet, there is undeniably still that very, albeit limited, evidence that adipocyte size is a good predictor of E2/T elevations. Admittedly, then, it is an intuitive leap that I have made here, in a form that can lead to errors by relying on notions of "common sense" ("it must," "it follows," or "it speaks for itself").

The best explanation that I have for the association between increased E2/T ratio and adipocyte size independent from adipocyte # is that this "must" be mediated by adipokine signaling (which we, and certainly I, do not fully understand at present) and its effects on the hypothalamo-pituitary-gonadal axis; i.e., primarily by reducing T.

The only viable alternative explanation that I can foresee is that besides the # of adipocytes, increasing cross-sectional area of the adipocytes (cell swelling by lipid) may permit a greater # of aromatase on the adipocyte.

I am very keen to see a good argument that maintaining lifelong low b.f. or destruction of the adipocyte (e.g., chemical lysing, freezing, liposuction) is not superior to caloric restriction (to cause lipid content reduction, thereby decreasing adipocyte size, but not #) to keep aromatase activity low.
 
I enjoy this level of autism! The more technical, the better. It can always be diluted and made more "reader friendly" later on.

So far, I like it, although I didn't finish reading it yet, because I need some more peace and quiet.

I have a request/suggestion: I think DHB may fit in similarity in this analysis, but I'd like to see an edit that includes a special analysis section for DHB, and if there are any special properties of DHB that may explain its effect on estrogen, although it is probably similar enough to Primo in effect. Plus, mentioning DHB may get more attention/clicks on article since it seems to be getting more popular nowadays, and people are researching DHB in tandem with primo and/or estrogen control.

And it is true: the number of adipocytes appears to be the biggest problem when it comes to aromatase activity, and you can easily see this proven by looking at overweight children. Look at siblings where one child is overweight and one is thin, due to differences in eating, and then look at them as adults. You will see the thin sibling stay thin and the formerly overweight child always cycling up and down in weight. Once a child is overweight before perhaps....7 years old when their level of adipocytes is set, they will have weight problems for life and if you talk to guys, even those who are lean or ripped, if they were even slightly chubby or overweight as children, they are generally always more susceptible to aromatization and estrogen effects/gyno, unless they stay at very low body fat levels. There seems to be a cut off where the fat cells, due to dryness perhaps, have reduced aromatase activity.

Also, please reconsider your use of the word "trope". I know it's a trendy word, but I seriously hate this word and I'm not alone. It's being used everywhere and it just cheapens everything.
 
Last edited:
I enjoy this level of autism! The more technical, the better. It can always be diluted and made more "reader friendly" later on.

So far, I like it, although I didn't finish reading it yet, because I need some more peace and quiet.

I have a request/suggestion: I think DHB may fit in similarity in this analysis, but I'd like to see an edit that includes a special analysis section for DHB, and if there are any special properties of DHB that may explain its effect on estrogen, although it is probably similar enough to Primo in effect. Plus, mentioning DHB may get more attention/clicks on article since it seems to be getting more popular nowadays, and people are researching DHB in tandem with primo and/or estrogen control.

And it is true: the number of adipocytes appears to be the biggest problem when it comes to aromatase activity, and you can easily see this proven by looking at overweight children. Look at siblings where one child is overweight and one is thin, due to differences in eating, and then look at them as adults. You will see the thin sibling stay thin and the formerly overweight child always cycling up and down in weight. Once a child is overweight before perhaps....7 years old when their level of adipocytes is set, they will have weight problems for life and if you talk to guys, even those who are lean or ripped, if they were even slightly chubby or overweight as children, they are generally always more susceptible to aromatization and estrogen effects/gyno, unless they stay at very low body fat levels. There seems to be a cut off where the fat cells, due to dryness perhaps, have reduced aromatase activity.

Also, please reconsider your use of the word "trope". I know it's a trendy word, but I seriously hate this word and I'm not alone. It's being used everywhere and it just cheapens everything.
Bro, this kind of backhanded compliment is totally insulting. Detail-oriented is not equivalent to autistic. I'll be polite about this here because I don't think you are being intentionally ignorant, but do sit there for a moment and reflect on the total lack of tact you demonstrate by equating attention to detail with a form of mental retardation. It's derogatory and, in fact, since we're communicating our assessments of one another's social skills, pretty goddamn socially inept.

I don't mean that to be as harsh as it might come off initially; but I do want to convey a point, that it's harmful to deride, even if well-intentioned, detailed technical writing with some sort of disorder; not merely on a personal level, but a societal one. If people are dissuaded from this sort of writing, think about the harm that brings for the societal good of an educated populace, something that, e.g., democracy depends on.

I've written about 1-Test before ("DHB"). See DHB (misnomer, it is 1-Testosterone) versus Tren: is it more like Primo or a "Tren lite"? [Author: Type-IIx]

You're correct that 1-Test can be packed in with EQ & Primo in a discussion about estrogenicity. I actually had a section discussing 1-Test in addition to Primo & EQ in the original long form of this article, but removed it for readability during the editing process.

1-Test & Primo are functionally equivalent not only in the context of this article (estrogenicity) but across all dimensions of practical use. However, interestingly (and the reason that it is an excellent edge case for thinking about the individualized [per-user] factors contributing to symptoms of low estrogenicity), 1-Test increases DHT almost certainly by acting as a 17β-HSD1 inhibitor.
 
Last edited:
Hah, I knew that statement about maintaining lifelong low body fat levels in order to keep a high T/E2 ratio by reduced aromatase activity would prove controversial. It's good that you are reading attentively and with a critical eye.

I make this assertion despite the existence of evidence that caloric restriction increases T/E2 ratio by, in part, reduced aromatase activity because it seems to me that mechanistically adipocyte # is what "must" be related to aromatase # because of the richness of fat cells, rather than lipid contents, in aromatase expression. Yet, there is undeniably still that very, albeit limited, evidence that adipocyte size is a good predictor of E2/T elevations. Admittedly, then, it is an intuitive leap that I have made here, in a form that can lead to errors by relying on notions of "common sense" ("it must," "it follows," or "it speaks for itself").

The best explanation that I have for the association between increased E2/T ratio and adipocyte size independent from adipocyte # is that this "must" be mediated by adipokine signaling (which we, and certainly I, do not fully understand at present) and its effects on the hypothalamo-pituitary-gonadal axis; i.e., primarily by reducing T.

The only viable alternative explanation that I can foresee is that besides the # of adipocytes, increasing cross-sectional area of the adipocytes (cell swelling by lipid) may permit a greater # of aromatase on the adipocyte.

I am very keen to see a good argument that maintaining lifelong low b.f. or destruction of the adipocyte (e.g., chemical lysing, freezing, liposuction) is not superior to caloric restriction (to cause lipid content reduction, thereby decreasing adipocyte size, but not #) to keep aromatase activity low.
I agree with your alternative. I'm leaning more towards the state of the adipocyte affecting lepin and other peptide signalling so consequently aromatase and the HPTA than # of adipocytes given how one can transform the body composition of mice so quickly knocking out the leptin gene and reintroducing it. I think that number of adipocytes will affect the speed at which changes happen given what environment and signalling the adiopocytes are experiencing. However I'm struggling to tell whether this is just personal bias because I was a fat kid whose always struggled with body fat and don't want to face up to permenant alterations in hormone levels from past poor dietary choices or actual objective reasoning.

Paper attached with interesting reading on the subject.
 

Attachments

Bro, this kind of backhanded compliment is totally insulting. Detail-oriented is not equivalent to autistic. I'll be polite about this here because I don't think you are being intentionally ignorant, but do sit there for a moment and reflect on the total lack of tact you demonstrate by equating attention to detail with a form of mental retardation. It's derogatory and, in fact, since we're communicating our assessments of one another's social skills, pretty goddamn socially inept.

I don't mean that to be as harsh as it might come off initially; but I do want to convey a point, that it's harmful to deride, even if well-intentioned, detailed technical writing with some sort of disorder; not merely on a personal level, but a societal one. If people are dissuaded from this sort of writing, think about the harm that brings for the societal good of an educated populace, something that, e.g., democracy depends on.

I've written about 1-Test before ("DHB"). See DHB (misnomer, it is 1-Testosterone) versus Tren: is it more like Primo or a "Tren lite"? [Author: Type-IIx]

You're correct that 1-Test can be packed in with EQ & Primo in a discussion about estrogenicity. I actually had a section discussing 1-Test in addition to Primo & EQ in the original long form of this article, but removed it for readability during the editing process.

1-Test & Primo are functionally equivalent not only in the context of this article (estrogenicity) but across all dimensions of practical use. However, interestingly (and the reason that it is an excellent edge case for thinking about the individualized [per-user] factors contributing to symptoms of low estrogenicity), 1-Test increases DHT almost certainly by acting as a 17β-HSD1 inhibitor.
That's not what I meant though and you know it, or you're pretending to know it, so why don't you just take the compliment in a positive way? And if you don't know that the comment was positive, then forgive me, and I will explain. If you don't know that the word "autism" is regularly used to describe excellent work in society in 2023 and the last decade atleast, then you probably are autistic and as a result, are completely misinterpreting the social cues that you are receiving, which is why you'd feel insulted. My comment wasn't backhanded at all, I assure you. "Autism" used to describe good work, is a positive thing. Every hear of terms like "weaponized autism"? Whether one is autistic or not, the word is used to compliment good work. End of story.

And next time, don't go so extreme with the edits. You're first instinct on including DHB was probably the correct instinct. I'd have appreciated still seeing it included in the article even though you've already written about DHB before.
 
This thread is desined for arguing I guess...

The more knowledgeable people research such complicated things the more arguments there will be from anecdotal experience.

I think we should appreciate his opinion on the matter and learn something useful from reading his articles, regardless I think the most important point here is that he is not forcing his point of view and opinion on to us, more so he wants to educate us and share his knowledge, what we do with this information is up to us at the end of the day.

Personally, I don't feel any low estrogen symptoms when stacking Testosterone with equipoise, and no ratio or dosages doesn't change anything for me either T/EQ 200/400, 300/300, 400/400, 400/600 and so on...

He says it is an individual thing like with most drugs, we are all different. We can't argue that.
 
This thread is desined for arguing I guess...

The more knowledgeable people research such complicated things the more arguments there will be from anecdotal experience.

I think we should appreciate his opinion on the matter and learn something useful from reading his articles, regardless I think the most important point here is that he is not forcing his point of view and opinion on to us, more so he wants to educate us and share his knowledge, what we do with this information is up to us at the end of the day.

Personally, I don't feel any low estrogen symptoms when stacking Testosterone with equipoise, and no ratio or dosages doesn't change anything for me either T/EQ 200/400, 300/300, 400/400, 400/600 and so on...

He says it is an individual thing like with most drugs, we are all different. We can't argue that.
Thank you bro; that's exactly how the article is intended to be viewed.
 
That's not what I meant though and you know it, or you're pretending to know it, so why don't you just take the compliment in a positive way? And if you don't know that the comment was positive, then forgive me, and I will explain. If you don't know that the word "autism" is regularly used to describe excellent work in society in 2023 and the last decade atleast, then you probably are autistic and as a result, are completely misinterpreting the social cues that you are receiving, which is why you'd feel insulted. My comment wasn't backhanded at all, I assure you. "Autism" used to describe good work, is a positive thing. Every hear of terms like "weaponized autism"? Whether one is autistic or not, the word is used to compliment good work. End of story.

And next time, don't go so extreme with the edits. You're first instinct on including DHB was probably the correct instinct. I'd have appreciated still seeing it included in the article even though you've already written about DHB before.
I really didn't want to argue about it, but I've been called autistic and never as a compliment on these boards for the sort of writings that I think are fair contributions, but curiously, never in person or face to face.

Sure had friends of mine call others autistic in disgust plenty of times.

I note the doubling down to construe me as autistic because I find it, reasonably, insulting, speaks volumes, however.
 
I agree with your alternative. I'm leaning more towards the state of the adipocyte affecting lepin and other peptide signalling so consequently aromatase and the HPTA than # of adipocytes given how one can transform the body composition of mice so quickly knocking out the leptin gene and reintroducing it. I think that number of adipocytes will affect the speed at which changes happen given what environment and signalling the adiopocytes are experiencing. However I'm struggling to tell whether this is just personal bias because I was a fat kid whose always struggled with body fat and don't want to face up to permenant alterations in hormone levels from past poor dietary choices or actual objective reasoning.

Paper attached with interesting reading on the subject.
Interesting, that's very much in line with my thinking as well. I think that permanent alterations as a consequence of childhood obesity in (adipokine & hormone activity, satiation, etc.) are very real and leptin falls squarely within that. I don't think you're expressing any bias here whatsoever; but it's also good to see that as your first instinct, to question your reasoning because of potential bias.
 
I really didn't want to argue about it, but I've been called autistic and never as a compliment on these boards for the sort of writings that I think are fair contributions, but curiously, never in person or face to face.

Sure had friends of mine call others autistic in disgust plenty of times.

I note the doubling down to construe me as autistic because I find it, reasonably, insulting, speaks volumes, however.
I assure you that I do not play games. I'm not being passive aggressive. In my world, being called autistic is mostly a positive thing, atleast these days. Being called autistic can also be negative, but my comment certainly wasn't intended to be negative. Nor did I think or assume or know for sure if you were autistic. Maybe you are. I'm starting to think you might be or that you have some other problem that causes you difficulties with understanding social cues. Either way, I did not mean to imply that in my initial comment in this thread, when I positivity called the work "autism I like". If you find this insulting, I don't care. I really don't know what you are or aren't. It's a word that is thrown around a lot nowadays, in my world, and it's usually complimentary. What else can I say? I think you overreacted. Next time you encounter a similar situation, maybe you should privately ask if someone is trying to be negative or not.


I wish all these comments could be deleted so that the original topic doesn't get sidelined by stupid arguments.
 
Last edited:
I assure you that I do not play games. I'm not being passive aggressive. In my world, being called autistic is mostly a positive thing, atleast these days.
That's interesting to me, honestly it's totally different from my social circles, but I believe you. I have seen younger kids using it kind of ironically as a backhanded compliment mostly. But "nerd" used to be derogatory, and now is sort of en vogue. Perhaps that's going to happen with this term.
Being called autistic can also be negative, but my comment certainly wasn't intended to be negative. Nor did I think or assume or know for sure if you were autistic. Maybe you are. I'm starting to think you might be or that you have some other problem that causes you difficulties with understanding social cues. Either way, I did not mean to imply that in my initial comment in this thread, when I positivity called the work "autism I like". If you find this insulting, I don't care. I really don't know what you are or aren't. It's a word that is thrown around a lot nowadays, in my world, and it's usually complimentary. What else can I say? I think you overreacted. Next time you encounter a similar situation, maybe you should privately ask if someone is trying to be negative or not.
I tried to give some push back without appearing overly miffed, and obviously in your case it appears I failed.
I wish all these comments could be deleted so that the original topic doesn't get sidelined by stupid arguments.
Maybe, @Millard I am fine with this.
 
Just curious was the estrone testing done with the lc/ms (ultra sensitive ) method?
It does show higher reading on the regular tests thats why i am asking .
 
Just curious was the estrone testing done with the lc/ms (ultra sensitive ) method?
It does show higher reading on the regular tests thats why i am asking .
I believe that it was direct immunoassay. It's crazy high regardless, in this assay the reference range is < 250 pmol/L for men, so about 5.5-fold the upper limit of the reference range.
 
Very cool.
I just ran 2nd test/primo cycle and actually felt shitty compared to first round.
First was 2:1
600 T / 300 P

Went to 600 / 400 and definitely saw less gains, and had some low estrogen sides.

I just went woth it as all the cystic acne Anadrol gave last round was basically pushed out of my face.
Skins amazing lol

Can't wait to find time to read this...
 
I believe that it was direct immunoassay. It's crazy high regardless, in this assay the reference range is < 250 pmol/L for men, so about 5.5-fold the upper limit of the reference range.
I remembered reading a mpmd article on this whit similar results for estrone and they retested with ultra sensitive estrone test end it came back in range .
I don't know if it matters or not but the conclusion was that it aromatizes to some other synthetic estrogen that is being cross detected by the regular test .
 
I remembered reading a mpmd article on this whit similar results for estrone and they retested with ultra sensitive estrone test end it came back in range .
I don't know if it matters or not but the conclusion was that it aromatizes to some other synthetic estrogen that is being cross detected by the regular test .
Well that's a remarkably dumb conclusion.

If you read my article here, you'll see that one should distinguish between endocrinology & intracrinology.

If the estrone direct immunoassay is cross-reactive of anything significant, it's sulfated portions (estrone sulfate).

At the end of the day, we don't really give a fuck anyway because what matters is the local activity of estrogens that even ultrasensitive estrone values do not reflect.

Local estrone fatty acyl ester activity would start to get us somewhere. Find me a private laboratory measure for that.

But, for the sake of argument, let us assume that 100% of this estrone DIA measurement was free estrone (bioactive E1). Then, 1,352 pmol/L would (at 2% of estradiol's estrogenic potency) be as bioactive as 7.3 pg/mL of free estradiol (free E2). This is an insignificant estradiol concentration that is well within the normal male reference range, and as such, not biologically or clinically relevant.

The point of this article was, if anything, to illustrate the low value of bloodwork measures, and to provide a practical flowchart that practically dispenses with them because symptoms should dictate decisionmaking over some arbitrary value.

Believe it or not, no value is usually better than a bullshit value; and judging by the way people order up and interpret bloodwork (including "authorities" like MPMD) so badly, it's fair to say that the overwhelming bulk of bloodwork value interpretations laypeople make from self-ordered laboratory measures constitutes bullshit.
 
Back
Top