How does iron regulates itself?
I’m sharing the musings of just one day of my efforts to research iron, and what’s posted below is only ½ of what i found. I am forever amazed at the lengths that iron researchers will go to slice and dice their findings and insights, but overlook the most important fact.
In these nine articles and there are 100’s more just like them that examine the many facets of iron metabolism and iron homeostasis, there is one word that is missing from all of these studies. Any one want to venture a guess as to what that one word might be?
Yes, that word would be copper!
They do make a point of mentioning ceruloplasmin, and on a rare occasion, will discuss the ferroxidase enzyme function, but no where do they honor or highlight that there is no such thing as iron metabolism.
There is only copper<>iron metabolism, and as I’ve noted many times, iron is, for a fact, the dummy in that metallic tango! Despite what you read on the Internet, please trust me, iron takes its cues from bioavailable copper. Solely!
And what is most important to understand is that iron is not designed to be in storage, 80% of the iron in your body is found in hemoglobin and myoglobin, which is in constant circulation. <10% is found in ferritin and that is meant to be inside the cell, not inside your serum!
The study by Vanoaica (2010, below) is unique in its recognition that ferritin-H is essential for accurate control of iron. What is ferritin-H (Heavy) chain?
It is a form of ferritin that has ferroxidase enzyme function, which is essential for proper iron egress and circulation. (They have known this since 1968!)
Before you get too excited, no, your doctor has no way to distinguish this form of ferritin from the ferritin-L (Light) chain. You would think that they would, but alas, we are left with the mushrooms, in the dark and buried in compost! In your next life you’ll want to come back as a 4-legged rat, so that you’ll know for certain what you’re ferritin fractions are, as these two tests are done all the time in the research labs.
- Chen, C., Paw, B.H. (2012). “Cellular and Mitochondrial Iron Homeostasis in Vertebrates.”
- Anderson, C.P., et al. (2012). “Mammalian iron metabolism and its control by iron regulatory proteins”
- Hentze, M.W., et al. (2010). “Two to Tango: Regulation of Mammalian Iron Metabolism”
- Kuhn, L.C. (2009). “How Iron Controls Iron” Cell Metabolism 10(6): 439-441
- Ganz T. (2008). “Iron Homeostasis: Fitting the Puzzle Pieces Together” Cell Metabolism 7(4): 288-90
- Simpson, R.J., et al. (2009). “Regulation of Intestinal Iron Absorption: The Mucosa Takes Control?” Cell Metabolism 10(2):84-87
- Andrews, N.C. (2010). “Ferrit(in)ing Out New Mechanisms in Iron Homeostasis” Cell Metabolism 12(3)-203-204
- Vanoaica, L., et al. (2010). “Intestinal Ferritin H Is Required for an Accurate Control of Iron Absorption” Cell Metabolism 12(3):272-283
- Thompson, J.W., et al. (2012). “Protein degradation and iron homeostasis” Biochimica & Biophysica Acta (BBA) – Molecular Cell Research 1823(9):1484-1490
And what these many studies are seeking to reveal is that the regulation of Iron relies on two key pathways for optimal iron circulation and R.E.cycling:
- Ferroportin<>hepcidin system, but they are silent on the fact that this system does not work without bioavailable copper in the form of ferroxidase enzyme function.
- Iron regulatory proteins (IRP1-2) and iron response elements (IREs) System, but they are silent on the fact that this system responds equally well to retinol (animal-based Vitamin-A) just as well as is does to iron supplementation. What is fascinating about that factoid is that retinol is key and foundational for the synthesis of ferroxidase enzyme need above.
C’mon now, don’t you find that just a tad bit entertaining
We are drowning in hormone-D supplements that kill retinol status in the liver!
We are drowning in iron supplements and infusions that kill our metabolism!
We are drowning in zinc supplements that cause copper to be bound up, and be not available.
We are drowning in ascorbic acid supplements that increase H2O2 (which tweaks the ceruloplasmin protein and kills the ferroxidase function) and accelerate iron storage.
Am I the only one seeing a predictable pattern here with the nutritional practices of allopathic and alternative practitioners?
I wish it weren’t this obvious, this clear and just wait until I share the other ½ of today’s research that states definitively that cancer is caused by iron. I almost fell out of my chair earlier today!
Better MAG up, and be prepared for the next iron toxicity post!
A votre sante!
Morley M. Robbins
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