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)