Why you should NOT take estrogens (Exogenous E2 ≠ Test's aromatic product)

[Type-IIx]

Estrogens are in fact vital to male functioning: estrogens are integral to lipid management, male sexual functioning, bone growth, glucose & lipid metabolism, skeletal muscle function (strength and mass)[1][2].


Men produce estrogens via the process of aromatization (Aromatase enzyme). Testrosterone produces E2 (17β-estradiol; a potent estrogen). These products of Aromatase ("Aromatic products") can be increased by increasing the dose of aromatizing androgen (e.g., Test, Deca, EQ, Dbol, MENT), which serves to maintain a positive androgen/estrogen ratio: a positive androgen/estrogen ratio dictates male sexual functioning and prevents gynecomastia [1].


Conversely, exogenous estrogens (estrogens consumed orally, transdermally, intramuscularly, or via whichever conceivable route of administration) pose great harm to men. Indeed, these hormones should only be used by men committed to transitioning (transwomen).

Exogenous estrogens:
✖ cause male reproductive pathologies [1] - even when exposure is to environmental estrogens, far less potent than E2 and in very low concentrations
✖cause an increase in IGFBP-1, decreasing IGF-I bioavailability [3]
✖cause a dramatic increase in SHBG (reducing T bioavailability) [4]


Aromatic products ✓ (positive effects)
Exogenous estrogens ✖ (negative effects)
______________________________
References:
[1] Cooke PS, Nanjappa MK, Ko C, Prins GS, Hess RA. Estrogens in Male Physiology. Physiol Rev. 2017 Jul 1;97(3): 995-1043. doi:10.1152/physrev.00018.2016.
[2] Chidi-Ogbolu N, Baar K. Effect of Estrogen on Musculoskeletal Performance and Injury Risk. Front Physiol. 2019;9:1834. Published 2019 Jan 15. doi:10.3389/fphys.2018.01834
[3] He, X., & Barkan, A. L. (2020). Growth hormone therapy in adults with growth hormone deficiency: a critical assessment of the literature. Pituitary. doi:10.1007/s11102-020-01031-5
[4] Damewood MD, Bellantoni JJ, Bachorik PS, Kimball AW Jr, Rock JA. Exogenous estrogen effect on lipid/lipoprotein cholesterol in transsexual males. J Endocrinol Invest. 1989 Jul-Aug;12(7):449-54. doi:10.1007/BF03350728.

 

[Canine]

Estrogens are in fact vital to male functioning: estrogens are integral to lipid management, male sexual functioning, bone growth, glucose & lipid metabolism, skeletal muscle function (strength and mass)[1][2].


Men produce estrogens via the process of aromatization (Aromatase enzyme). Testrosterone produces E2 (17β-estradiol; a potent estrogen). These products of Aromatase ("Aromatic products") can be increased by increasing the dose of aromatizing androgen (e.g., Test, Deca, EQ, Dbol, MENT), which serves to maintain a positive androgen/estrogen ratio: a positive androgen/estrogen ratio dictates male sexual functioning and prevents gynecomastia [1].


Conversely, exogenous estrogens (estrogens consumed orally, transdermally, intramuscularly, or via whichever conceivable route of administration) pose great harm to men. Indeed, these hormones should only be used by men committed to transitioning (transwomen).

Exogenous estrogens:
✖ cause male reproductive pathologies [1] - even when exposure is to environmental estrogens, far less potent than E2 and in very low concentrations
✖cause an increase in IGFBP-1, decreasing IGF-I bioavailability [3]
✖cause a dramatic increase in SHBG (reducing T bioavailability) [4]


Aromatic products ✓ (positive effects)
Exogenous estrogens ✖ (negative effects)
______________________________
References:
[1] Cooke PS, Nanjappa MK, Ko C, Prins GS, Hess RA. Estrogens in Male Physiology. Physiol Rev. 2017 Jul 1;97(3): 995-1043. doi:10.1152/physrev.00018.2016.
[2] Chidi-Ogbolu N, Baar K. Effect of Estrogen on Musculoskeletal Performance and Injury Risk. Front Physiol. 2019;9:1834. Published 2019 Jan 15. doi:10.3389/fphys.2018.01834
[3] He, X., & Barkan, A. L. (2020). Growth hormone therapy in adults with growth hormone deficiency: a critical assessment of the literature. Pituitary. doi:10.1007/s11102-020-01031-5
[4] Damewood MD, Bellantoni JJ, Bachorik PS, Kimball AW Jr, Rock JA. Exogenous estrogen effect on lipid/lipoprotein cholesterol in transsexual males. J Endocrinol Invest. 1989 Jul-Aug;12(7):449-54. doi:10.1007/BF03350728.

What about when using non-aromatizing compounds? eg. Deca Only. <-- dumb but people do it. Also I would asume the behavior, and response of your endocrine system will be completely different if you're already taking other exoegous compounds vs, taking estrogens on their own (which these studies seem to look at).

 

[T&H]

Estrogens are in fact vital to male functioning: estrogens are integral to lipid management, male sexual functioning, bone growth, glucose & lipid metabolism, skeletal muscle function (strength and mass)[1][2].


Men produce estrogens via the process of aromatization (Aromatase enzyme). Testrosterone produces E2 (17β-estradiol; a potent estrogen). These products of Aromatase ("Aromatic products") can be increased by increasing the dose of aromatizing androgen (e.g., Test, Deca, EQ, Dbol, MENT), which serves to maintain a positive androgen/estrogen ratio: a positive androgen/estrogen ratio dictates male sexual functioning and prevents gynecomastia [1].


Conversely, exogenous estrogens (estrogens consumed orally, transdermally, intramuscularly, or via whichever conceivable route of administration) pose great harm to men. Indeed, these hormones should only be used by men committed to transitioning (transwomen).

Exogenous estrogens:
✖ cause male reproductive pathologies [1] - even when exposure is to environmental estrogens, far less potent than E2 and in very low concentrations
✖cause an increase in IGFBP-1, decreasing IGF-I bioavailability [3]
✖cause a dramatic increase in SHBG (reducing T bioavailability) [4]


Aromatic products ✓ (positive effects)
Exogenous estrogens ✖ (negative effects)
______________________________
References:
[1] Cooke PS, Nanjappa MK, Ko C, Prins GS, Hess RA. Estrogens in Male Physiology. Physiol Rev. 2017 Jul 1;97(3): 995-1043. doi:10.1152/physrev.00018.2016.
[2] Chidi-Ogbolu N, Baar K. Effect of Estrogen on Musculoskeletal Performance and Injury Risk. Front Physiol. 2019;9:1834. Published 2019 Jan 15. doi:10.3389/fphys.2018.01834
[3] He, X., & Barkan, A. L. (2020). Growth hormone therapy in adults with growth hormone deficiency: a critical assessment of the literature. Pituitary. doi:10.1007/s11102-020-01031-5
[4] Damewood MD, Bellantoni JJ, Bachorik PS, Kimball AW Jr, Rock JA. Exogenous estrogen effect on lipid/lipoprotein cholesterol in transsexual males. J Endocrinol Invest. 1989 Jul-Aug;12(7):449-54. doi:10.1007/BF03350728.

Thank you for this. I had a few questions regarding estrogen so perfect timing.

It's often stated people should get to minimum 15% body fat before cycling. I personally think that's broscience started forever ago. The only reason given is because higher BF causes excessive estrogen production.

I know it is true extra bf levels cause more estrogen, not disputing that. However I have read many logs where low bf guys have high aromatization production running test. I then stumbled upon the Below article which is hard for me to fully comprehend. It seems like to a point, estrogen production running compounds that aromatize is almost unique to the individual and not so much a certain bf level. I could be wrong.

Can you read this and provide your thoughts on this whole 15% BF thing before using AAS? Even if it's true, would 15% and say 25% BF really cause a big difference in estrogen?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835337/

 

[Type-IIx]

What about when using non-aromatizing compounds? eg. Deca Only. <-- dumb but people do it. Also I would asume the behavior, and response of your endocrine system will be completely different if you're already taking other exoegous compounds vs, taking estrogens on their own (which these studies seem to look at).

Deca is actually an aromatizing androgen. It just tends to cause sub-normal estrogen concentrations at low - moderate doses. You can, therefore, increase Deca dose or use it in combination with other aromatizing androgens. Another consideration exists with the use of the aromatizing androgen-progestins (that is, estrogens upregulate PR & progestins enhance the effect of estradiol on breast tissues).

 

[Type-IIx]

Thank you for this. I had a few questions regarding estrogen so perfect timing.

It's often stated people should get to minimum 15% body fat before cycling. I personally think that's broscience started forever ago. The only reason given is because higher BF causes excessive estrogen production.

I know it is true extra bf levels cause more estrogen, not disputing that. However I have read many logs where low bf guys have high aromatization production running test. I then stumbled upon the Below article which is hard for me to fully comprehend. It seems like to a point, estrogen production running compounds that aromatize is almost unique to the individual and not so much a certain bf level. I could be wrong.

Can you read this and provide your thoughts on this whole 15% BF thing before using AAS? Even if it's true, would 15% and say 25% BF really cause a big difference in estrogen?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835337/

Yes, any hard value for when aromatization may be considered excessive is definitely bro-science. While it is true that Aromatase is expressed in adipose tissue, it is ubiquitously expressed as well in skeletal muscle (and other tissues). Beyond this, there is wide inter-individual variation in estrogen metabolism & circulating estrogens are not even the sole determinant of tissue estrogen levels.

 

[Canine]

Deca is actually an aromatizing androgen. It just tends to cause sub-normal estrogen concentrations at low - moderate doses. You can, therefore, increase Deca dose or use it in combination with other aromatizing androgens. Another consideration exists with the use of the aromatizing androgen-progestins (that is, estrogens upregulate PR & enhance the effect of estradiol on breast tissues).

Right, I've just seen people try to use very high doses of deca solo, and still experience low e sides, then supplement with exogenous e, and feel better. Seems like aromatized deca is not sufficiently estrogenic enough especially at hrt doses, which justifies exogenous estrogen use, and If your estrogen levels are within physiologic range, I don't see how it's much different, then what you would have naturally if something is aromatizing at close to physiologically normal levels.

 

[Type-IIx]

Right, I've just seen people try to use very high doses of deca solo, and still experience low e sides, then supplement with exogenous e, and feel better. Seems like aromatized deca is not sufficiently estrogenic enough especially at hrt doses, which justifies exogenous estrogen use, and If your estrogen levels are within physiologic range, I don't see how it's much different, then what you would have naturally if something is aromatizing at close to physiologically normal levels.

I guess you didn't actually read the original post...

 

[Canine]

I guess you didn't actually read the original post...

I did, and I read through the studies, I was just responding to this part:

Conversely, exogenous estrogens (estrogens consumed orally, transdermally, intramuscularly, or via whichever conceivable route of administration) pose great harm to men. Indeed, these hormones should only be used by men committed to transitioning (transwomen).

This is not always the case, and the studies you referenced are not on individuals supplementing with exogenous androgens which reduce estrogen serum concentrations, and as a result have inadequate estrogen levels. I really don't think from the studies you mentioned, you can make the conclusion that injectable estradiol especially, is automatically bad in every circumstance for men.

One study was on women's estrogen levels, who have very different hormone profiles and biology then men. Another study on mtf transitioners, only supplementing with estrogen, with no exogenous androgen's, another study on growth hormone, and another study on male hormone profiles who are not using exogenous androgens. In fact your 2nd refrence supports the idea of female HRT and the bennefits of higher estrogen levels, having bennefits on muscle mass,tendon strength and collagen synthesis etc.

I guess what I'm saying is I'm failing to understand how you reached the conclusion that exogenous estrogen is just bad from these studies. I could see the argument for naturals who decide to use estrogens on their own and only on their own potentially having non desirable effects, but again for people on a steroid forum, who are using multiple other compounds in combination, I fail to see how these studies apply to the situations in which we'd be using exogenous estrogens.

 

[Type-IIx]

I did, and I read through the studies, I was just responding to this part:

This is not always the case, and the studies you referenced are not on individuals supplementing with exogenous androgens which reduce estrogen serum concentrations, and as a result have inadequate estrogen levels. I really don't think from the studies you mentioned, you can make the conclusion that injectable estradiol especially, is automatically bad in every circumstance for men.

One study was on women's estrogen levels, who have very different hormone profiles and biology then men. Another study on mtf transitioners, only supplementing with estrogen, with no exogenous androgen's, another study on growth hormone, and another study on male hormone profiles who are not using exogenous androgens. In fact your 2nd refrence supports the idea of female HRT and the bennefits of higher estrogen levels, having bennefits on muscle mass,tendon strength and collagen synthesis etc.

I guess what I'm saying is I'm failing to understand how you reached the conclusion that exogenous estrogen is just bad from these studies. I could see the argument for naturals who decide to use estrogens on their own and only on their own potentially having non desirable effects, but again for people on a steroid forum, who are using multiple other compounds in combination, I fail to see how these studies apply to the situations in which we'd be using exogenous estrogens.

Sorry, an error was made in Footnote 3. The correct reference is Veldhuis, J. D., & Bowers, C. Y. (2003). Human GH pulsatility: An ensemble property regulated by age and gender. Journal of Endocrinological Investigation, 26(9), 799–813. doi:10.1007/bf03345229

Get back after digesting all the references. If you conclude that exogenous estrogens are equivalent to aromatic products of androgens then we can sit with your reading comprehension & logic being the problem!

P.S. Exogenous androgens do not reduce estrogens & the second paper support ERT in post-menopausal women.

 

[Canine]

This is exactly what I just said?

the second paper support ERT in post-menopausal women.

Also I'm not saying it's identical in action, just as TRT is not identical to natural production. I'm asking why you are just straight up saying exogenous estradiol is just bad always if you're a man, and then your source for that statement is a study that supports estrogen supplementation in not just post-menopausal women, but even some evidence that oral estrogens reduce risk of injury in pre-menopausal women.

I'm genuinely trying to understand your logic. I'm not trying to fight, I just want to understand where you're coming with from this, instead you're not addressing the points I've made and instead just go to insult me?

Also primobolan, has very strong anecdotal evidence of reducing e2 levels, most likely via a machanism of partially blocking the aromatase enzyme. Granted no literature has been published on this, neither has ERT been studied in combination with TRT or other HRT compounds.

 

[Type-IIx]

This is exactly what I just said?


Also I'm not saying it's identical in action, just as TRT is not identical to natural production. I'm asking why you are just straight up saying exogenous estradiol is just bad always if you're a man, and then your source for that statement is a study that supports estrogen supplementation in not just post-menopausal women, but even some evidence that oral estrogens reduce risk of injury in pre-menopausal women.

I'm genuinely trying to understand your logic. I'm not trying to fight, I just want to understand where you're coming with from this, instead you're not addressing the points I've made and instead just go to insult me?

Also primobolan, has very strong anecdotal evidence of reducing e2 levels, most likely via a machanism of partially blocking the aromatase enzyme. Granted no literature has been published on this, neither has ERT been studied in combination with TRT or other HRT compounds.

No, you did not state specifically that ERT is beneficial for post-menopausal women. It's clear you didn't actually read the study, because it does not show improved tendon strength from estrogens (quite opposite).

You are going to need to bring more than a cursory reading of these linked studies to debate me on this. My logic is succinctly explained in the title post: Why you should NOT take estrogens (Exogenous E2 ≠ Test's aromatic product)

I really think you need to give it a slow read. Then try reading slowly and perhaps taking notes on the cited literature.

If you have even a cursory familiarity with the literature on environmental estrogen exposure (characterized by very low concentrations) and harms in men, you will know that E2 is a far more potent estrogen than these compounds. It follows that exogenous E2 in practice is more harmful than these environmental estrogens in human male functioning.

Seriously, read the title post. Therein lies my logic. Then read the papers. Then take notes. Then think about them. Then read the title post again. And relate the notes and your understanding to the title post.

Only then, apparently, will you understand the logic. Hopefully.

 

[Canine]

No, you did not state specifically that ERT is beneficial for post-menopausal women. It's clear you didn't actually read the study, because it does not show improved tendon strength from estrogens (quite opposite).

You are going to need to bring more than a cursory reading of these linked studies to debate me on this. My logic is succinctly explained in the title post: Why you should NOT take estrogens (Exogenous E2 ≠ Test's aromatic product)

I really think you need to give it a slow read. Then try reading slowly and perhaps taking notes on the cited literature.

If you have even a cursory familiarity with the literature on environmental estrogen exposure (characterized by very low concentrations) and harms in men, you will know that E2 is a far more potent estrogen than these compounds. It follows that exogenous E2 in practice is more harmful than these environmental estrogens in human male functioning.

Seriously, read the title post. Therein lies my logic. Then read the papers. Then take notes. Then think about them. Then read the title post again. And relate the notes and your understanding to the title post.

Only then, apparently, will you understand the logic. Hopefully.

From your own source:

"In these other musculoskeletal tissues, estrogen improves muscle mass and strength, and increases the collagen content of connective tissues. However, unlike bone and muscle where estrogen improves function, in tendons and ligaments estrogen decreases stiffness, and this directly affects performance and injury rates."

"Interestingly, women suffer fewer muscle injuries, and more ligament ruptures than men (Arendt and Dick, 1995; Sewright et al., 2008; Hägglund et al., 2009; Edouard et al., 2016; Leblanc et al., 2017). These observations are consistent with lower sinew stiffness in women than men. Since knee laxity changes with estrogen levels through the menstrual cycle (Shultz et al., 2005), estrogen is believed to decrease sinew stiffness."

And here's the quote wich shows oral estrogens reducing risk of injury:

"Further, Rahr-Wagner et al. found a 20% higher relative risk (RR) value of ACL injury in women who had never used OCs than in women who were long-term users (Rahr-Wagner et al., 2014). Together, these data suggest that ACL laxity changes through the cycle and eliminating the changes in estrogen using oral contraceptives decreases the risk of ACL rupture."

 

[Type-IIx]

From your own source:

"In these other musculoskeletal tissues, estrogen improves muscle mass and strength, and increases the collagen content of connective tissues. However, unlike bone and muscle where estrogen improves function, in tendons and ligaments estrogen decreases stiffness, and this directly affects performance and injury rates."

"Interestingly, women suffer fewer muscle injuries, and more ligament ruptures than men (Arendt and Dick, 1995; Sewright et al., 2008; Hägglund et al., 2009; Edouard et al., 2016; Leblanc et al., 2017). These observations are consistent with lower sinew stiffness in women than men. Since knee laxity changes with estrogen levels through the menstrual cycle (Shultz et al., 2005), estrogen is believed to decrease sinew stiffness."

And here's the quote wich shows oral estrogens reducing risk of injury:

"Further, Rahr-Wagner et al. found a 20% higher relative risk (RR) value of ACL injury in women who had never used OCs than in women who were long-term users (Rahr-Wagner et al., 2014). Together, these data suggest that ACL laxity changes through the cycle and eliminating the changes in estrogen using oral contraceptives decreases the risk of ACL rupture."

Now I know you have sought from the outset to distort & confront, to hell with what these data tell us.

Because you stated,

your 2nd refrence supports the idea of female HRT and the bennefits of higher estrogen levels, having bennefits on muscle mass,tendon strength and collagen synthesis etc.

The second reference shows a clear effect of estrogen in reducing tendon strength: it shows that estrogens decrease stiffness in tendons, thereby reducing strains and pulls (due to laxity) and decreases performance/power/strength.

Here's the kicker: It ALSO shows EXOGENOUS estrogens as oral contraceptives perversely increasing injury risk, muscle damage, & DOMS. And decreasing collagen synthesis.

Ligaments ≠ Tendons. Like Exogenous E2 ≠ Test's aromatic product.

 

[Type-IIx]

@Canine BTW: allow me to give you some context that you may not be aware of. Keith Baar, one of the authors of that paper you've decided to hyper-focus on, coaches girls sports. You're focusing on a paper that is aimed at prescribing training and competition recommendations to young women.

Try looking at all the data, not the stuff that's for girl's volleyball.

If you look again to the title post, look at where the little "[2]"s are. Those are the sentences that are relevant to the Baar paper.

 

[Canine]

Now I know you have sought from the outset to distort & confront, to hell with what these data tell us.

Because you stated,


The second reference shows a clear effect of estrogen in reducing tendon strength: it shows that estrogens decrease stiffness in tendons, thereby reducing strains and pulls (due to laxity) and decreases performance/power/strength.

Here's the kicker: It ALSO shows EXOGENOUS estrogens as oral contraceptives perversely increasing injury risk, muscle damage, & DOMS. And decreasing collagen synthesis.

Ligaments ≠ Tendons. Like Exogenous E2 ≠ Test's aromatic product.

Hey man, again, I just want to say, I didn't reply to your post because I wanted to insult you, or your intelligence. I just wanted to have a discussion, I have read many of your posts, and your knowledge of the subject is a value to the community, and I was neither trying to discredit you, nor undercut you.

I feel like you may have taken my input of the literature as something of more hostile, rather than a contribution to discussion. The literature regarding hormones, I have read much of, and not just these studies, but others specifically in the relation estrogen and connective tissue behavior. On reason in particular being I myself had an injury I was trying to heal, and what I had come to understand through my review is that estrogen could be very beneficial, if used properly. I am currently mid-experiment, and while I am a sample size of 1 and merely offering anecdotal evidence from my situation, the higher E2 levels I have sought out have appeared to have been helpful. Again I'm not finished with my self-experiment, but I will hopefully write a full post on my thoughts, cumulative evidence from other studies, and my results.

Also most literature specifically on the subject is highly conflicting, some showing great benefits other showing detriments, and our overall understanding of physiology in relation to hormone levels and ratios is still quite primitive especially when at supraphysiological levels and the ways in which we use them (within bodybuilding), and I hope much more attention is given to this area of biology in academia.

I'm not trying to fight, merely discuss and potentially learn from each other, as I'm sure we have both found studies the other has not heard of. Otherwise, I do enjoy reading your posts, and again finding previous literature I was unaware of. Hopefully we can coexist, I'd hate to not get along.

 

[Type-IIx]

Hey man, again, I just want to say, I didn't reply to your post because I wanted to insult you, or your intelligence. I just wanted to have a discussion, I have read many of your posts, and your knowledge of the subject is a value to the community, and I was neither trying to discredit you, nor undercut you.

I feel like you may have taken my input of the literature as something of more hostile, rather than a contribution to discussion. The literature regarding hormones, I have read much of, and not just these studies, but others specifically in the relation estrogen and connective tissue behavior. On reason in particular being I myself had an injury I was trying to heal, and what I had come to understand through my review is that estrogen could be very beneficial, if used properly. I am currently mid-experiment, and while I am a sample size of 1 and merely offering anecdotal evidence from my situation, the higher E2 levels I have sought out have appeared to have been helpful. Again I'm not finished with my self-experiment, but I will hopefully write a full post on my thoughts, cumulative evidence from other studies, and my results.

Also most literature specifically on the subject is highly conflicting, some showing great benefits other showing detriments, and our overall understanding of physiology in relation to hormone levels and ratios is still quite primitive especially when at supraphysiological levels and the ways in which we use them (within bodybuilding), and I hope much more attention is given to this area of biology in academia.

I'm not trying to fight, merely discuss and potentially learn from each other, as I'm sure we have both found studies the other has not heard of. Otherwise, I do enjoy reading your posts, and again finding previous literature I was unaware of. Hopefully we can coexist, I'd hate to not get along.

This is so reasonable.

Excuse me for seeing your claim that you "did [read the title post], and... read through the studies" (Why you should NOT take estrogens (Exogenous E2 ≠ Test's aromatic product)) as less than forthright. Judging by the timestamps, you claimed to have consumed the entirety of the citations in an hour and a half. With a clairvoyance to see my post the second it hit the internet, time to mistakenly claim Deca is a non-aromatizing androgen, and with time to spare.

In that post, you continue, that because no literature exists on supplemental estrogens for men on supraphysiological androgens, that we cannot know anything (a perfect solution fallacy).

Then, you continued debating me haphazardly still without properly reading the title post nor its references in any manner... Literally copy and pasting from a paper that was cited merely in support of estrogen having a positive effect on muscle function, about endogenous estrogens and connective tissue, for girl's volleyball athletes.

Understand that:
A) the literature does not contain studies where researchers administered exogenous estrogens to men unless they are committed to transitioning (transwomen) for a reason
and
B) the very reason for this thread is the conflicting literature on estrogens: I want to clarify for people (I posted it in the steroid harm reduction subforum) that exogenous estrogens are particularly harmful whereas endogenous estrogens are largely beneficial even in men.

There will NEVER be a legitimate study on supplemental estrogens in supraphysiological androgen users. We can STILL know things though. We can still make applicable extrapolations.

My hope was that anyone engaging me in a debate would first thoroughly read and comprehend the data cited.

Perhaps your early adversarial tone is rooted in your trial of 1 FEELZ (you feel better with exogenous estrogens, right? so they must not be harmful?)

So: if you want to extend an olive branch, I'd simply like you to show me that you've actually reasoned through the full data before you actually discuss it and copy and paste from the cited data.

That's all that's owed. Not a mea culpa.

I appreciate the gesture. But my ego isn't so big as to need massaging. I really just want an intelligent conversation about the data if anything.

 

[Canine]

Hey man, your ego does seem a bit bruised, literally I pointed out a few things you say that are potentially wrong and you go off. We can sit here all day and say what the other said was false. Just like you falsely said exogenous androgens do not ever reduce estrogens, some clearly do have downstream effects eg. masteron and primobolan.

You keep trying to twist my words. I said that because no data exist for the situations in which we use them, it is difficult to make a claim such as you did, that says exogenous estrogens are ALWAYS bad for men.

If someone is as smart as you make yourself seem to be you should understand, a womans ovulatory cycle and its associated hormonal fluctuations do not necessarily translate to men. You should also know the ratios of hormones matter, meaning in some cases testosterone can be neurotoxic, and in other cases it is not, which is something moderated by estrogen levels.

If you site a source you should understand the full discussion of said source, but you complain when I quote your source, which contains data that directly counter the assumptions you are making about the data. Your own source says the data from multiple studies is conflicting and that further research on the subject is needed to understand what is actually happening! Yet you are somehow more sure of what is actually happening then the researchers with PhD's are, maybe you should write your own paper then.

All of these points I have made are valid criticisms of your position, and if you were in academia, you would fully understand why I am asking these questions.

Have you ever written a research paper? Have you ever had to deal with reviewers? They will grill you so hard, you will start to question your own research you were working on for months.

Also reading the abstracts alone in your sources was enough for me to understand the conclusion you got from them was probably a bit stretched, before I later dug into them deeper.

Also this as you say is a harm reduction forum, and that is a place which should foster discussion, I again clearly pointed out faults in your reasoning, which you just respond with saying I'm wrong, and that's it and procede to insult me instead of actually telling me which exact data you made your conclusion from, and tell me if i don't understand I didn't read. I did read and your sources are not substantial enough to make the claim you just did, you just can't fathom someone disagreeing with you.

Again I recomend you take a reasearch methods course if you can't understand the faults in your own data interpretation for this situation. Most universities allow members of the public to drop in on lectures for free.

 

[zg0136]

What about when using non-aromatizing compounds? eg. Deca Only. <-- dumb but people do it. Also I would asume the behavior, and response of your endocrine system will be completely different if you're already taking other exoegous compounds vs, taking estrogens on their own (which these studies seem to look at).

You’ll get enough estrogen on deca only.. actually you may need an AI at high doses. Nandrolone has direct ER activity as well as converting into a lot of estrone while still converting into a sufficient amount of estradiol

 

[Canine]

You’ll get enough estrogen on deca only.. actually you may need an AI at high doses. Nandrolone has direct ER activity as well as converting into a lot of estrone while still converting into a sufficient amount of estradiol

Brother, I've looked at peoples bloodwork doing it, and how they felt, for some, it clearly was not estrogenic enough. Theory being Deca only could be used as TRT, and potentially lessen hair loss sides, but it's not very good on your overall markers long term. Deca was merely an example on why you may want to run estrogen while running specific protocols. People mistakenly think estrogen is the devil.

While IIx is on the side that exogenous estrogen is always bad and automatized is the only good way, I clearly disagree. If you're not aromatizing sufficiently at a given level of androgens, in some situations you may not want to take higher doses of androgens to compensate. Instead you can use injectable estradiol to bring your levels to within physiological range. Just because you use a small dose of estrogens, is not going to all of the sudden make you a transvestite if you're within normal levels, as he makes it seem in his original post.

 

[Type-IIx]

Hey man, your ego does seem a bit bruised, literally I pointed out a few things you say that are potentially wrong and you go off. We can sit here all day and say what the other said was false. Just like you falsely said exogenous androgens do not ever reduce estrogens, some clearly do have downstream effects eg. masteron and primobolan.

You keep trying to twist my words. I said that because no data exist for the situations in which we use them, it is difficult to make a claim such as you did, that says exogenous estrogens are ALWAYS bad for men.

If someone is as smart as you make yourself seem to be you should understand, a womans ovulatory cycle and its associated hormonal fluctuations do not necessarily translate to men. You should also know the ratios of hormones matter, meaning in some cases testosterone can be neurotoxic, and in other cases it is not, which is something moderated by estrogen levels.

If you site a source you should understand the full discussion of said source, but you complain when I quote your source, which contains data that directly counter the assumptions you are making about the data. Your own source says the data from multiple studies is conflicting and that further research on the subject is needed to understand what is actually happening! Yet you are somehow more sure of what is actually happening then the researchers with PhD's are, maybe you should write your own paper then.

All of these points I have made are valid criticisms of your position, and if you were in academia, you would fully understand why I am asking these questions.

Have you ever written a research paper? Have you ever had to deal with reviewers? They will grill you so hard, you will start to question your own research you were working on for months.

Also reading the abstracts alone in your sources was enough for me to understand the conclusion you got from them was probably a bit stretched, before I later dug into them deeper.

Also this as you say is a harm reduction forum, and that is a place which should foster discussion, I again clearly pointed out faults in your reasoning, which you just respond with saying I'm wrong, and that's it and procede to insult me instead of actually telling me which exact data you made your conclusion from, and tell me if i don't understand I didn't read. I did read and your sources are not substantial enough to make the claim you just did, you just can't fathom someone disagreeing with you.

Again I recomend you take a reasearch methods course if you can't understand the faults in your own data interpretation for this situation. Most universities allow members of the public to drop in on lectures for free.

[chuckle] my Achilles heel. You found it: my education. I should go back and retake my research methods course from undergrad. I must have forgotten the section where they taught us that if it's not stated as a Conclusion or in the first sentence of the Abstract there's nothing to be gleaned. Maybe I'll stop by my local community college and see if I can get office hours with an adjunct prof and go over my findings and where I went wrong. This is why I love these anonymous forums, you have no fucking idea who you're talking to.