Aromatase Inhibitors Fix the Number but Break the System, open discussion.

[BALLISTIC]

Estrogen Balance Relative to Androgen Load I think suppression deserves scrutiny.

I think it’s time we seriously re examine the default tendency toward estrogen over suppression. This topic keeps resurfacing, and much of the confusion seems to come from treating estrogen as a number to minimize, rather than a regulatory system that operates relative to androgen load.

I’m not anti AI and I’m not “proestrogen.” I’ve historically believed in estrogen balance, not elimination, and recent experience alongside emerging literature, has pushed me to refine that further.

Relevant reading for context (not cherry picked, and not claiming absolutes).

Estrogen Receptor Beta as Target for Colorectal Cancer Prevention - PMC

Colorectal cancer (CRC) is a leading cause of death in the United States. Despite its slow development and the capacity for early diagnosis, current preventive approaches are not sufficient. However, a role for estrogen has been demonstrated in ...

pmc.ncbi.nlm.nih.gov

https://onlinelibrary.wiley.com/doi/full/10.1002/cam4.5242

Estrogen Receptor β Induces Antiinflammatory and Antitumorigenic Networks in Colon Cancer Cells - PMC

Combined results from gene expression and bioinformatics analyses defined ERβ regulations previously unknown and identified regulatory mechanisms with implications for colon cancer.

pmc.ncbi.nlm.nih.gov

Estrogen receptor beta reduces colon cancer metastasis through a novel miR-205 - PROX1 mechanism | Oncotarget

https://www.sciencedirect.com/science/article/pii/S0960076024000748

This post is intentionally symptom based, not lab driven, to draw out realworld consensus. Labs that correlate symptoms are welcome, I’m not dismissing labs, just not leading with them.

And to be clear, I am not claiming “estrogen prevents cancer.” I am arguing that estrogen signaling is context dependent, and that “crush E2 always” is not physiologically correct nor is extremely elevated. My historical position (and why it hasn’t changed)....Many of you have discussed this with me before. My position has long been that estrogen needs to be evaluated in the context of total androgen exposure, not as a standalone value.

In short explanation estrogen is not “high” or “low” in isolation, It is adequate or inadequate relative to androgen load. As androgens increase, they increase mechanical stress (muscle, tendon, joint, increase neural drive and sympathetic tone, increase metabolic demand, increase inflammatory signaling. Estrogen counterbalances this by supporting connective tissue integrity and joint lubrication, endothelial and vascular function, CNS modulation (sleep, mood, cognition), immune and inflammatory regulation. From this, depriving estrogen while running supraphysiologic androgens is mismatched physiology. This has held true for me across TRT, cruises, and blasts.
Where this breaks down is non aromatizing or E2 suppressive cycles. This is where the discussion often gets boring but relative.

Certain compounds functionally suppress estrogen signaling, even when aromatization itself isn’t the mechanism. Most of us acknowledge this, though there are outliers Primobolan, Equipoise, (to a degree: Masteron, DHB, high dose DHT derivatives). On these cycles, many people experience low estrogen symptoms despite, no AI use, acceptablelabs
Commonly report dry, painful joints, dull mood / anhedonia, poor sleep (early waking, light sleep), loss of libido despite high androgens, poor pump and reduced endurance, also marked cognitive dulling (feeling dumb).

In these cases, the issue is not estrogen excess, it’s estrogen insufficiency relative to androgen load. E2 supplementation corrective, not reckless (context matters)
This is where the conversation usually derails. People fear pinning E2, supplementation is not bro science, not for everyone, and not a beginner tool, but it is context dependent and deserves honest discussion. On high Primo / EQ cycles, some experienced users report benefit from low dose estradiol (injectable most commonly, oral in some cases). The goal is not supraphysiologic estrogen it’s restoring functional estrogen signaling.

Anecdotally but consistently reported improvements include...
Joint comfort returning
Libido normalizes
Sleep deepens
Mood stabilizes
Pumps improve
Overall “system tension” drops
Importantly, these improvements often occur without changing androgen dose, suggesting estrogen was the missing regulatory input. This reinforces a balance model, not an “estrogen fear".

Pretending this doesn’t work because it violates dogma isn’t honest, especially when we’re otherwise quick to acknowledge nuanced pharmacology everywhere else.

Symptom patterns (no labs)... For context as reported by many throughout my reading.

LOW ESTROGEN
(over dosed AI or functionally suppressed)
Dry, brittle, flat, disconnected
Flat mood / emotional numbness
Anhedonia
Anxiety without emotional charge
Early waking (am hours)
Dry, achy joints
Tendon stiffness
Poor pump
Libido collapse despite ↓
Mechanical erections without desire
Reduced orgasm intensity
Dry skin / dull complexion
Cold extremities
Cognitive dulling (mentally blunt)

HIGH ESTROGEN
Swollen, reactive, foggy, overwhelmed
Emotional volatility
Rumination / overthinking
Anxiety with emotional charge
Trouble falling asleep
Night sweats
Puffy joints
Water retention / edema
Facial bloating
Nipple sensitivity
ED despite desire
Head pressure

The overlap trap... Very important area.
These occur both directions, which is why estrogen is so often mismanaged on feelings.
Anxiety
Poor sleep
Libido issues
Brain fog
Fatigue

The character of the symptom matters more than the symptom itself. Why routine AI use deserves scrutiny (not dismissal).
Aromatase inhibitors don’t modulate estrogen they systemically suppress it. That means loss of ERsignaling, estrogen’s anti inflammatory effects, vascular and connective tissue support, shortterm symptom relief does not equal longterm benefit.

This doesn’t mean AIs are useless. It means chronic, routine suppression should not be the default solution.

My final thought and please I welcome all constructive input. I’m not advocating recklessness, I’m advocating physiologic consistency. Curious where the community actually lands once we move past lab screenshots and into lived experience.

Also please note for the F-ing Nancy's among us lately... Yes I used AI to defer and understand some things I did not, in medical terms. I also used it to compile this post as it was scrambled in my mind chronologically although I knew what I was trying to convey. If you have some desire to comment or drop your opinion in regards to that in this post... I humbly ask @Millard or other admin to block your privileges to this post. I'm tired of arguing with adolescence. I want constructive conversation.

 

[bananafeet]

I've been watching a LOT of videos on menopause and perimenopause. It's interesting how estrogen isn't a hormone but a group of hormones.

This complicates things. For example esterone is pro inflammatory and estrodial is anti inflammatory.

Testosterone is the safest androgen because of aromatisation into E2. This reduces ROS and protects the body and tissues (somewhat).

As for non DHT derivatives or 5a reduced steroids - they interfere with the estrogen and androgen balance. It's not as simple as a ratio but it's more like competitive signalling.

I'm not sure if we ever need estrogen out side of the reference range. It's leads to blood pressure side effects. However we need estrogen and we need gentle aromatase inhibitors that doesn't starve some tissues completely.

In a trt context you should only run as much testosterone as you can to get a good E2. Using an AI in TRT negates most of the benifits which come from the pro hormone nature of testosterone and it's downstream metabolites rather than test itself....

 

[IndividualMan]

I think the effects of 17-alpha VS 17-Beta estradiol are worth discussing.
most of the "healthy E2 effects" are equally caused by both 17-alpha and 17-beta, but the mood and gyno side are usually closer correlated with 17-beta estradiol (if you look at self proclaimed "biohackers", many of them take pretty gnarly doses of 17-alpha estradiol, and they rarely/never get the E2 sides we associate with high E2

 

[BALLISTIC]

I've been watching a LOT of videos on menopause and perimenopause. It's interesting how estrogen isn't a hormone but a group of hormones.

This complicates things. For example esterone is pro inflammatory and estrodial is anti inflammatory.

Testosterone is the safest androgen because of aromatisation into E2. This reduces ROS and protects the body and tissues (somewhat).

As for non DHT derivatives or 5a reduced steroids - they interfere with the estrogen and androgen balance. It's not as simple as a ratio but it's more like competitive signalling.

I'm not sure if we ever need estrogen out side of the reference range. It's leads to blood pressure side effects. However we need estrogen and we need gentle aromatase inhibitors that doesn't starve some tissues completely.

In a trt context you should only run as much testosterone as you can to get a good E2. Using an AI in TRT negates most of the benifits which come from the pro hormone nature of testosterone and it's downstream metabolites rather than test itself....

That’s a solid point, and I agree with a lot of it....especially the idea that this isn’t a simple ratio problem so much as competitive and dependent signaling.

You’re absolutely right that estrogen isn’t one hormone. I failed in that regard to this post so thank you. E1, E2, E3 all function differently, E1 pro inflammatory why high EQ starts to hurt badly. E2, anti inflammatory but often overly suppressed, E3 plays the modulator and middle ground absorbing some signaling and blocks excess stronger estrogens.

I also agree that testosterone is uniquely forgiving precisely because it aromatizes.

I’m not sure if we ever need estrogen outside the reference range, however with high Primo, EQ, heavy DHT stacks we’re already outside physiologic ref ranges on the androgen side, and the question becomes less normal range, and more about whether estrogen signaling is sufficient for the androgen load. Adequate estrogen signaling relative to the androgen environment in simple terms.

Anecdotal reports suggest that direct E2 add back supplementation corrects a clear low estrogen symptom cluster that doesn’t resolve otherwise, without pushing individuals into classic high E2 sides.

I strongly agree with your trt view, as it pertains to using AIs. It often conflicts with the feel good respect. If you need AI to tolerate your trt,I would suggest your trt dosing is suspect first.

I've just come to notice how often acceptable labs fail to reflect functional estrogen insufficiency, especially as androgen complexity increases.

 

[BALLISTIC]

I think the effects of 17-alpha VS 17-Beta estradiol are worth discussing.
most of the "healthy E2 effects" are equally caused by both 17-alpha and 17-beta, but the mood and gyno side are usually closer correlated with 17-beta estradiol (if you look at self proclaimed "biohackers", many of them take pretty gnarly doses of 17-alpha estradiol, and they rarely/never get the E2 sides we associate with high E2

Honestly, this just circles back to the bigger issue and you make a great point nobody considers. AIs don’t discriminate.

They nuke all estrogen signaling and let you sort out the fallout. This is exactly what gets lost when everything gets combined into keep E2 low. Good point bringing this up, as in my early years I had no understanding of this. I'm actually just learning.

17B is probably most important in regards to androgen load. But at the flip of a coin causes all the problems if you overshoot.

 

[bananafeet]

That’s a solid point, and I agree with a lot of it....especially the idea that this isn’t a simple ratio problem so much as competitive and dependent signaling.

You’re absolutely right that estrogen isn’t one hormone. I failed in that regard to this post so thank you. E1, E2, E3 all function differently, E1 pro inflammatory why high EQ starts to hurt badly. E2, anti inflammatory but often overly suppressed, E3 plays the modulator and middle ground absorbing some signaling and blocks excess stronger estrogens.

I also agree that testosterone is uniquely forgiving precisely because it aromatizes.

I’m not sure if we ever need estrogen outside the reference range, however with high Primo, EQ, heavy DHT stacks we’re already outside physiologic ref ranges on the androgen side, and the question becomes less normal range, and more about whether estrogen signaling is sufficient for the androgen load. Adequate estrogen signaling relative to the androgen environment in simple terms.

Anecdotal reports suggest that direct E2 add back supplementation corrects a clear low estrogen symptom cluster that doesn’t resolve otherwise, without pushing individuals into classic high E2 sides.

I strongly agree with your trt view, as it pertains to using AIs. It often conflicts with the feel good respect. If you need AI to tolerate your trt,I would suggest your trt dosing is suspect first.

I've just come to notice how often acceptable labs fail to reflect functional estrogen insufficiency, especially as androgen complexity increases.

I think as soon as you go past normal physiology you can sort of just throw the rule book out of the window.

So we've narrowed you key point down to this:
In the case of supra physiological doses of anabolic androgenic steroids supplemental estrodial can offset some of the downstream side effects.

So my logical question is: why not just run more testosterone?

Unless you have abnormal physiology you should be able to aromatise a sufficient amount.

Testosterone is a prohormone:
DHT - CNS and mental drive
E2 - AR upregulation, IGF1 signalling, soft tissue support (you need soft tissue remodelling to support muscle bellies), ROS and NOX, lipid regulation, SHBG signalling

Then you have the downstream metabolites of DHT which are powerful neurosteroids.

Pushing on either side of this system will cause dysregulation.

I want to trial using a dieretic to lower my blood pressure next blast on test only and see if I can get any extra anabolism out of higher E2.

Now back to the women. 25% of testosterone is made by the female ovaries. Menopause and ovarian insufficiency causes this to drop. The E2 is actually made by aromatising testosterone in the ovaries. PCOS is a combination of a lack aromatase and peripheral conversion of DHEA into testosterone. The lower estrodial reduces SHBG and increases free testosterone. This leads to hair thinning, cardiovascular disease, dyslipidemia and growing a moustache.

So this kinda applies to us men. Too many oral steroids or DHT meds or crushed E2 leads to excessive free testosterone and the negative side effects (hair, prostate, CVD).

So basically anytime you run a large amount of non testosterone steroids you encounter this problem and it can't be overcome. Maybe with exogenous E2. But then again you still have the lack of paracrine E2.

 

[bananafeet]

Where is @Ghoul @readalot and @Type-IIx when you need them.

I'm a mental midget in comparison lol

 

[BALLISTIC]

I think as soon as you go past normal physiology you can sort of just throw the rule book out of the window.

So we've narrowed you key point down to this:
In the case of supra physiological doses of anabolic androgenic steroids supplemental estrodial can offset some of the downstream side effects.

So my logical question is: why not just run more testosterone?

Unless you have abnormal physiology you should be able to aromatise a sufficient amount.

Testosterone is a prohormone:
DHT - CNS and mental drive
E2 - AR upregulation, IGF1 signalling, soft tissue support (you need soft tissue remodelling to support muscle bellies), ROS and NOX, lipid regulation, SHBG signalling

Then you have the downstream metabolites of DHT which are powerful neurosteroids.

Pushing on either side of this system will cause dysregulation.

I want to trial using a dieretic to lower my blood pressure next blast on test only and see if I can get any extra anabolism out of higher E2.

Now back to the women. 25% of testosterone is made by the female ovaries. Menopause and ovarian insufficiency causes this to drop. The E2 is actually made by aromatising testosterone in the ovaries. PCOS is a combination of a lack aromatase and peripheral conversion of DHEA into testosterone. The lower estrodial reduces SHBG and increases free testosterone. This leads to hair thinning, cardiovascular disease, dyslipidemia and growing a moustache.

So this kinda applies to us men. Too many oral steroids or DHT meds or crushed E2 leads to excessive free testosterone and the negative side effects (hair, prostate, CVD).

So basically anytime you run a large amount of non testosterone steroids you encounter this problem and it can't be overcome. Maybe with exogenous E2. But then again you still have the lack of paracrine E2.

I think we’re actually very close to saying the same thing, just from different angles. Please you know we've had discussions so if at any point I seem argumentative, that's not the case and throw rocks at me, I respond well. Haha

You’re 100 percent right that once we go past normal physiology, the rulebook starts falling to the wayside. That’s really the core of this whole discussion. I've even stated in prior discussion that once we press the super button it's anybody's guess individually.

I totally agree testosterone is the cleanest androgen we have because it selfregulates through aromatization and 5Areduction. That’s why test-only cycles tend to feel better than complex stacks, even at similar total androgen load. We can all remember what it was like for our first simplistic blast and that feeling. Then of course the bodies response and simply put no matter what you do after you're always chasing that type of response. Being a virgin if you will.

Where I think reality diverges from theory is in what happens once other androgens dominate the signaling environment. That whole system works beautifully when testosterone is the primary input. But once you start stacking, Primo, EQ, Orals, DHT derivatives, You’re no longer just adding androgen, you’re changing receptor competition, tissue level signaling, and overall dynamics.

Simply adding more testosterone doesn’t always restore balance, because DHT leaning compounds outcompetes AR signaling, estrogen signaling becomes functionally insufficient relative to total androgen pressure.

You may aromatize more, but not necessarily where or how it’s needed, and that doesn't encompass fellas like me who low aromatize. Almost void honestly.

Some guys push test higher
watch their E2 rise, yet still feel dry, flat, joint wrecked, or neurologically off. The signal is there… but it’s not landing/hitting the same.

Your point about women actually strengthens this argument, in my opinion.
Because in women the ovaries produce testosterone, estradiol is made locally via aromatization. Loss of aromatase or ovarian T equates low E2, low SHBG, high free androgens. This then leads hair thinning, dyslipidemia, CVD risk, and what they all want to avoid most...androgenic features.

So I agree large amounts of non testosterone steroids inherently create a problem that can’t be fully solved. Exogenous E2 will never perfectly replicate local production, but I don’t think it means ineffective if that makes sense. I should clarify and state I think supplementing E2 is a partial correction and restores signaling to prevent further damage.

Managing BP with a diuretic, honestly makes sense as an experiment, as long as you respect the risks. I'm interested in following up with you in this when the time comes.

So yeah... I don’t want this thread to seem about E2 supplementation is the answer. I think it’s about acknowledging that once we leave physiologic territory, balance becomes relative, and some tools exist because the system is already compromised.

In complete honesty I could be completely off, and glad you tagged those bright minds for input.

 

[bananafeet]

I agree actually with almost everything you've said.

It's more just me not being able to justify the use of large quantities of the other compounds due to their lack of tolerability long term. I think that adding back E2 is kind of redundant when you could just increase the testosterone dose instead of adding other stuff on top.

Which leads to the other argument of whether testosterone has an anabolic ceiling.... I noticed that the higher I push the test, the stronger other androgens become.

I know other steroids have special effects, but the reason why they have side effects is because of these special effects....

As for the dieretic I was just going to use that telmisartan/clinlidipine/chlorthalidone combo.

There must be a reason why guys add multiple compounds instead of a fat dose of testosterone. I think @Mac11wildcat uses this approach and stays under 2 grams total androgen load.

I'm sure he has a logical explanation for it.

Anyway I hope you don't think I'm being argumentative lol