Iron Toxicity Post #39: excess unbound iron is very bad! Get properly tested.
Posted on June 14, 2016 by Morley Robbins
Please share this “oldie, but goodie” with your favorite practitioner:
Williams, D.M., Lee, G.R., Cartwright, G.E. (1976). “Role of Copper in Mitochondrial Iron Metabolism.”
I am also quoting from another article that I was just reading:
Griffith, D.P., et al. (2009). “Acquired Copper Deficiency: A Potentially Serious & Preventable Complication Following Gastric Bypass Surgery”
…Mitochondrial cytochrome c oxidase, which plays a critical role in the transfer of Iron to the cytosol for incorporation into heme . Ceruloplasmin ferroxidase is also thought to contributes to anemia, as it is essential [emphasis added] in the loading of transferrin with iron in the liver and is markedly diminished in parallel with copper (ceruloplasmin) .” (Please note, the former linked article is citation  noted above)
It is well known in iron research circles that low hemoglobin is a clinical sign of copper deficiency (i.e. low bioavailable copper). I will now go out on a limb and assert that low ferritin, low serum iron, and low % saturation are indicative of copper deficiency, as well.
What is clearly emerging from the literature is that these 3 markers noted are highly correlated and highly indicative of what is called Anemia of Chronic Illness, or Anemia of Inflammation.
They are not indications of iron deficiency. They are signs of iron dysregulation that is fueled by low bioavailable copper as best expressed by low ceruloplasmin.
For those that want to see it in “red,” please order this test:
What I am finding is that you cannot properly interpret a set of iron markers without knowing magnesium RBC, plasma zinc, serum copper and serum ceruloplasmin.
It is essential to have an understanding of the minerals that regulate iron, in addition to iron itself.
A votre sante!
MORLEY M. ROBBINS
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