Ferritin in the serum is a sign of tissue pathophysiology. Without the ceruloplasmin ferroxidase enzyme, iron doesn’t load properly into ferritin. So it gets damaged and takes on the properties of hemosiderin where iron is stored and doesn’t come out.
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Your iron isn’t low, it’s non-functional: Make it functional by raising ceruloplasmin.
You are not anemic! You have ‘anemia’ of chronic inflammation, which means you are iron toxic, and it’s being stored in your tissues.
Iron Toxicity Post #47: The truth about the cause of mitochondrial dysfunction (as least as I see it)
How the key (copper) and the fuel (cardiolipin) prevents mitochondrial dysfunction in the lipids getting rusty. The cause of mitochondrial dysfunction.
Low hemoglobin, ferritin, serum iron and saturation are all indications of iron dysregulation caused by low bioavailable copper which is expressed as low ceruloplasmin.
The objective of iron metabolism is mobilization, and ceruloplasmin is the metabolic agent to guarantee that functional requirement is met.
Morley shares a master thesis on ceruloplasmin and the importance on neurological diseases and the molecular linker between the copper and iron metabolism.
Endometriosis and iron overload.