Is there data on whether heme iron, either supplement or from food, creates a different hepcedin response than elemental iron like ferrous sulfate or an iron amino acid chelate?
I don't think so, not as a human study, but I also think it has no practical utility, as none of this research above has any practical utility, so the concept of trying to biohack around hepcidin through oral dosing choices seems like a major distraction.
The hepcidin response to circulating iron is well understood. Anything that raises transferrin saturation will raise hepcidin. That is the only established way that iron status mediates hepcidin. Hepcidin also responds to inflammation, oxidative stress, and decreases in response to hypoxia, but the effect of iron status on hepcidin is mediated by transferrin saturation.
I appreciate this thread since I have been trying to maintain iron levels for years, with varying success (and failure). Today I am wondering about chromium. All my supplements include high levels of chromium and no iron. Doesn't chromium ride along on the same carrier as iron? Could a high intake of chromium (usually 250-500% daily requirement) pose a block to iron absorption? I don't know if there is a blood test to check levels of chromium in blood (don't see it on your cheat sheet) but on my hair analyses chromium is always moderately above normal, iron always low. Just trying to sort this out!
This article was really helpful. Had been wondering about this!
Is there data on whether heme iron, either supplement or from food, creates a different hepcedin response than elemental iron like ferrous sulfate or an iron amino acid chelate?
I don't think so, not as a human study, but I also think it has no practical utility, as none of this research above has any practical utility, so the concept of trying to biohack around hepcidin through oral dosing choices seems like a major distraction.
The hepcidin response to circulating iron is well understood. Anything that raises transferrin saturation will raise hepcidin. That is the only established way that iron status mediates hepcidin. Hepcidin also responds to inflammation, oxidative stress, and decreases in response to hypoxia, but the effect of iron status on hepcidin is mediated by transferrin saturation.
That simplifies things a lot - thanks!!
I appreciate this thread since I have been trying to maintain iron levels for years, with varying success (and failure). Today I am wondering about chromium. All my supplements include high levels of chromium and no iron. Doesn't chromium ride along on the same carrier as iron? Could a high intake of chromium (usually 250-500% daily requirement) pose a block to iron absorption? I don't know if there is a blood test to check levels of chromium in blood (don't see it on your cheat sheet) but on my hair analyses chromium is always moderately above normal, iron always low. Just trying to sort this out!