Testosterone also increases iron absorption?

[Abcdefgmo]

Apparently not only estrogen, but testosterone also inhibits hepcidin leading to too much iron absorption

So the problem isnt estrogen or testosterone, but eating iron fortified foods in the first place, and taking iron supplements, and maybe red meat ( red meat has like double zinc I think, but still people mention high iron on a carnivore diet)

thoughts?

 

[Hans]

Apparently not only estrogen, but testosterone also inhibits hepcidin leading to too much iron absorption

So the problem isnt estrogen or testosterone, but eating iron fortified foods in the first place, and taking iron supplements, and maybe red meat ( red meat has like double zinc I think, but still people mention high iron on a carnivore diet)

thoughts?

Yes when you go on trt, it's important to keep an eye on ferritin, RBC, etc. A lot of people on trt benefit from regular blood donations.

 

[golder]

Yes when you go on trt, it's important to keep an eye on ferritin, RBC, etc. A lot of people on trt benefit from regular blood donations.

Would the same apply for topical/transcrotal?

 

[Jamsey]

Whenever I see these claims of testosterone and estrogen having the same effects, I try to go looking for whether dht has the same effects to be able to conclude if this an androgen or estrogen driven effect. I haven’t found a study on direct dht administration yet, but I found this study

Testosterone alters iron metabolism and stimulates red blood cell production independently of dihydrotestosterone

Testosterone (T) stimulates erythropoiesis and regulates iron homeostasis. However, it remains unknown whether the (type II) 5α-reduction of T to dihydrotestosterone (DHT) mediates these androgenic effects, as it does in some other tissues. Our ...

www.ncbi.nlm.nih.gov

“The primary findings of this study are that finasteride (a type II 5α-reductase inhibitor) does not significantly inhibit T-induced erythropoiesis or androgen-mediated alterations in iron homeostasis. Specifically, TE administration elevated RBC and HGB production independently of finasteride, and finasteride (alone) did not significantly reduce HCT despite a >65% reduction in circulating DHT. In addition, we provide the first evidence demonstrating that type II 5α-reductase activity is not required for T-induced hepcidin suppression in elderly hypogonadal men.”

“Interestingly, we also observed that TE administration elevated circulating E2 and BioE2 and that the magnitude of change in E2was correlated to the increases in RBC count and HGB. These findings raise the possibility that estrogens may mediate several of the effects we observed. In this regard, estrogen has been shown to suppress hepcidin, and an estrogen response element is present in the promoter region of the hepcidin gene (20, 21)”

“Together, these results demonstrate that aromatase activity is not necessary for androgen-stimulated erythropoiesis, although the possibility remains that the suppression of hepcidin was at least partially influenced by the elevated E2following TE administration.”

Whether this means that estrogen or the estrogen receptor is responsible for the hepcidin suppression is up for debate. I will keep looking for dht administration studies to confirm or refute this effect.