Optimal e2 on cycle?

[Chrispy62]

I’m thinking of doing my next cycle but I’m confused on e2 management. My end of cycle blood work for my first blast showed 5620 ng/dl and e2 as 100 pg/ml. Based on pure values that e2 is high but I’ve heard that it can be more about the ratio, ideal being 20:1 or 30:1 for t/e2, but then my e2 would be considered low… going off feeling, I felt fine on that e2, I didn’t have any side effects like gyno, mood changes, oily skin, acne, nothing. I barely took any AI, maybe 6.25mg aromasin every 2 weeks.

I’m asking because I want to add in primo to my next cycle but unsure where to keep my e2 is primo will act as an ai itself

 

[Larrybagins]

numbers look scary on paper but how you feel matters a lot. if you felt good at that e2 and no sides i wouldn’t chase a lab range just to chase it. primo def pushes e2 down for a lot of guys so start low and don’t stack AI outta habit. crushed e2 feels way worse than a little high trust me. bloods mid cycle will tell you way more than guessing.

 

[riggspersonal]

E2 exerts many effects, many of which can be measured and/or felt. That is where your attention should go. If your BP and lipids are the same regardless of e2, and if you experience no change in symptoms regardless of e2, then get your e2 at the high end of the normal range and call it a day. High-normal is your best bet, but biomarkers and feels triumph 100% of the time.

Thanks for the insight here. So essentially, if you're asymptomatic (or at least perceive your state as such), and other biomarkers are in check, you would recommend not chasing the high-end of the normal reference range if you're well above it?

Or do you recommend using the high end of the normal reference range as the upper bound?

 

[HUGE McBIGLARGE]

Thanks for the insight here. So essentially, if you're asymptomatic (or at least perceive your state as such), and other biomarkers are in check, you would recommend not chasing the high-end of the normal reference range if you're well above it?

If your biomarkers and/or symptoms are better with a different e2, aim for that e2 in my opinion.

Or do you recommend using the high end of the normal reference range as the upper bound?

If you are unable to determine your ideal e2 from biomarkers and/or symptoms, I would aim for the high end of the reference range.

 

[Jaybird85uk]

Personally I feel good with it around that 30-40 (can go a little higher if running DHT derivatives) range. So high “normal” I guess.

As above I tend to look at trends rather than trying to chase a specific number.

One thing that doesn’t get mentioned much, but I’ve seen pop up a few times in both client bloodwork and my own, is how chronically high E2 can gradually compromise iron metabolism.

This doesn’t seem to be the case for everyone but estradiol appears to be a strong regulator of hepcidin.
At some point, if E2 is chronically elevated, hepcidin signalling can become dysregulated which leads to high ferritin, increased transferrin saturation…etc. More iron being trapped in storage rather than utilised efficiently.

I’ve seen this pattern most commonly in guys running supraphysiological testosterone without adequate E2 control (because they think AIs are poison) or guys chasing ratios rather than managing it directly.

Subjectively, I’ve “felt” ok with having my E2 as high as 200!! (When I was running a big dose of masteron with test). But it didn’t do me any favours for my body composition or blood work.

 

[HUGE McBIGLARGE]

At some point, if E2 is chronically elevated, hepcidin signalling can become dysregulated which leads to high ferritin, increased transferrin saturation…etc. More iron being trapped in storage rather than utilised efficiently.

I thought e2 lowered hepcidin, causing a lowering of ferritin?

Wouldn’t high ferritin and decreased serum iron be preferable for us? I figured we’re at risk of high hemoglobin and low ferritin due to increased RBC production.

 

[Jaybird85uk]

I thought e2 lowered hepcidin, causing a lowering of ferritin?

Wouldn’t high ferritin and decreased serum iron be preferable for us? I figured we’re at risk of high hemoglobin and low ferritin due to increased RBC production.

I thought e2 lowered hepcidin, causing a lowering of ferritin?

Wouldn’t high ferritin and decreased serum iron be preferable for us? I figured we’re at risk of high hemoglobin and low ferritin due to increased RBC production.

My understanding is that’s true when iron is actually being used. In high estrogen states, that often isn’t what happens.

Hepcidin is the regulator of iron movement, not iron creation. So yes, when hepicidin is suppressed, more iron is absorbed from the gut and released from storage.

Both androgens and estrogen suppress hepcidin, but the downstream effects are quite different.

Androgens strongly drive erythropoiesis. Iron gets pulled into red blood cell production, hemoglobin and hematocrit rise and ferritin often trends DOWN over time. That’s why some guys often end up needing to supplement iron…etc. or see low ferritin (exactly what you pointed out).

Estrogen also suppresses hepcidin.
However, unlike androgens, estrogen does not meaningfully upregulate erythropoietin or bone marrow drive.
As a result, iron availability increases without a proportional increase in red blood cell production.

So basically when iron influx exceeds erythropoietic demand, excess iron is restored rather than utilised, leading to rising ferritin and often elevated transferrin saturation

The idea that we are primarily at risk of low ferritin on TRT or cycles only holds true when androgen signalling dominates and estrogen is well controlled. When E2 becomes too high, iron handling often shifts toward storage rather than utilisation.

Again it seems to come down to balance….

High estrogen can skew the system toward delivery over use (high ferritin, high iron)

Excess androgens without balance can skew it toward use over delivery (low ferritin, low iron)

 

[AnabolicTacos]

There is no clinical data at all for managing asymptomatic e2 elevation on supraphysiological T. Absence of evidence is not evidence of absence.

AIs can exert side effects independent of their serum e2-lowering effects (e.g by affecting peripheral and localised aromatisation)

High androgenicity can also antagonise some but not necessarily all e2 effects. Just look at the guys running mast who experience low e2 symptoms despite high e2 in serum.

In my opinion, e2 should be managed based on: Non-E2 biomarkers > feels > e2 levels

Some people unironically suppress their e2 despite feeling worse for doing so, and despite hurting other biomarkers such as their lipids.

In my opinion, the people who believe in a ratio are nitwits, and the people who believe in absolute e2 levels are also nitwits.

E2 exerts many effects, many of which can be measured and/or felt. That is where your attention should go. If your BP and lipids are the same regardless of e2, and if you experience no change in symptoms regardless of e2, then get your e2 at the high end of the normal range and call it a day. High-normal is your best bet, but biomarkers and feels triumph 100% of the time.

SHBG levels, androgen receptor sensitivity, and estrogen receptor sensitivity can all have huge variations between individuals. So any target ratio or absolute value is completely meaningless without it being individualised to you yourself.

I appreciate that people like clean advice. “20:1 ratio bro” is clean advice. “In range bro” is clean advice. “Go at the high end of normal, then titrate your e2 up and down and assess biomarkers and symptoms and reassess periodically over the course of a few years to find what works for you” is not clean advice. It’s complicated, and it takes time, but it is the best advice.

can you please explain how shbg can influence e2 levels? and how it changes how you feel? for example i always have very low shbg

 

[HUGE McBIGLARGE]

Estrogen also suppresses hepcidin.
However, unlike androgens, estrogen does not meaningfully upregulate erythropoietin or bone marrow drive.
As a result, iron availability increases without a proportional increase in red blood cell production.

Yeah. You’re right. I was being stupid lol. It has been a while since I did or read the Vorck ferritin guide. I stopped following it because the big iron supplementation for a week every month gave me GI upset. It raised my ferritin very well, but also my hemoglobin by about 4%. I figure the GI upset and raised hemoglobin wasn’t worth it when my ferritin was only borderline low.

can you please explain how shbg can influence e2 levels?

Androgens bind more readily to SHBG than estrogens do. So SHBG will have a more pronounced effect on free androgens than free estrogens. And as androgens can antagonise some but not necessarily all estrogenic effects, this means that adhering to a ratio of T:E2 is meaningless without also considering SHBG (and any other non-testosterone androgens for that matter).

and how it changes how you feel? for example i always have very low shbg

Not sure. I have never looked into the causative effects of SHBG besides the reduction of free circulating sex hormones.