Iron Toxicity Post #51: The Deceit of ‘Anemia’
Posted on January 26, 2017 by Morley Robbins
This is dedicated to members and other clients, as well as the millions of women/moms around the globe who are being misguided by their practitioners about the misinformation of iron metabolism.
This post, the gloves are coming off while I addressed the common iron anemia thing.
If any of the following conditions apply, I would sincerely ask that you read this post and the accompanying articles, very slowly and carefully:
- “I’m anemic…”
- “My iron is low…”
- “My ferritin is too low…”
- “I’m tired and I need more iron…”
- “I need to raise my ferritin more…”
- “I’m taking iron supplements/infusions…”
- Or any variation on these Iron themes.
You are not “anemic!
The only “anemia” that you may suffer from is your practitioner’s in the dark about how to understand iron metabolism. The ability or the know how to measure it properly in the human body, thereby realized that every facet of iron activity is ruled and regulated by bioavailable copper.
If you are at all curious about my stance and wonder why I believe that your practitioner got iron metabolism all wrong, please read this important article below:
Messner, D.J., Kowdley, K.V. (2010). “Biting the Iron Bullet t: Endoplasmic Reticulum Stress Adds the Pain of Hepcidin to Chronic Liver Disease.” Hepatology; 51(2):705-707
What this article is trying to tell us is:
“Inflammation and iron are known [emphasis added] extracellular stimuli for hepcidin expression.”
What does that mean?
Well, hepcidin (Hpn), which has 25 amino acids, is mainstream medicine’s popular focus and is supposedly the regulatory hormone for iron metabolism. But when you compared Hpn to ceruloplasmin, which has 1,046 amino acids, you can begin to understand how it dissociates in the teaching.
This article really highlights what is really going on with getting iron out of the cell and back into circulation:
Musci, G., et al. (2014). “Ceruloplamsin-ferroportin system of iron traffic in vertebrates.”
The failure not to understand the pivotal dynamics between Ceruloplasmin <> Ferroportin <> Hepcidin is where conventional practitioners create chaos in the bodies of their all clients!
Iron metabolism is meant to be a sophisticated recycling program. Iron is meant to be in constant circulation, literally, and ceruloplasmin & ferroportin guarantees that process. What happens is increased expression of hepcidin disrupting this process therefore more hepcidin is not what you want rather you want more ceruloplasmin to get the iron moving.
So, when iron is showing low on the blood work, it is not unreasonable to assume that a pathogenic infection has triggered our immune system to do what it has been designed to do. It pulls all of the iron out of the blood and put it into storage. Why does it do that?
All critters (bacteria, virus, fungus and parasites) must have iron to live, to replicate and to thrive. Our immune system is finely tuned since life to keep that iron from them. This system has worked for a long time, until changing our food and giving Rx meds began around 75yrs ago. What happened is that it has changed the foundational understanding of copper, as well as the critical interplay between Copper <> Iron in regulating these metals. This has an impact on our metabolic functions, especially in our liver.
Ok, I get that, so then what’s the problem?
Well, as laid out in this Messner (2010) article, we now are learning that inflammation and iron increases the production and expression of hepcidin! Remember that we know that iron causes inflammation.
So what does that mean?
Increased Hepcidin =>
Increased Iron Storage =>
Decreased iron appearance in blood work
To translate that key phrase, noted earlier, from this Messner (2010) article to:
“Inflammation and iron are known extracellular stimuli for increased iron storage [emphasis added] which causes iron to show up low on ferritin, show up low on serum iron, and show up low on % saturation markers.”
This is where it gets really interesting when you realized when was the last time your favorite practitioner measured your hepcidin level? They never do because you cannot order it from commercial labs.
The article is also silent on our buddy, ceruloplasmin (Cp)! So what is that research from Dr. Musci trying to teach us?
- When ceruloplasmin is strong, as the ferroxidase enzyme, hepcidin is low.
- When ceruloplasmin is weak, as the ferroxidase enzyme, hepcidin is high.
So, excess, unbound iron from your anemia-inspired confusion is causing:
- Hepcidin to rise
- Inflammation to rise (hepcidin triggers inflammation)
- Iron to get stored in tissue (that does not show up on a blood test)
- Cp’s ferroxidase-form of the enzyme to fall
- Copper metabolism to then be compromised
- Iron metabolism to then become chaotic, at best
Then what happens is your overall health start to suffer across a wide spectrum of symptoms that form your Ferrous Wheel.
If you are taking iron supplements, or getting iron infusions or taking any daily multi-vitamins that have iron in them, you are changing how our body metabolise iron.
It is more likely you have Anemia of Chronic Inflammation rather than Anemia of Iron Deficiency, which regularly appears on my client’s blood work via these five blood markers:
1) Low magnesium RBC
2) Low or suspiciously high ceruloplasmin (high Cp is a clinical sign of Inflammation)
3) Low serum iron
4) Low % saturation (serum iron/serum TIBC)
5) Low or high ferritin (high ferritin is routinely flagged as a marker for inflammation)
Those wanting to better understand this Anemia of Chronic Inflammation might enjoy reading this:
Weinstein, D.A., et al. (2002). “Inappropriate expression of hepcidin is associated with iron refractory anemia: Implications for the anemia of chronic disease.”
Are you not sure what to do now?
- Please do the following:
Get the Full Monty Iron Panel
- Get that blood test properly interpreted by a RCP Consultant that is trained to understand the truth of copper<>iron metabolism, and how often this “anemia of chronic inflammation” appears.
- Get these articles cited above into the hands of your favorite practitioner(s).
- See if you can get their commitment to read them and have an open and honest dialogue about what these studies really mean, and how they will change the course of your treatment.
- Understand what is your about your true iron status.
- Reconsider having iron supplements/infusions and know that you are not anemic, but you need more bioavailable copper to move the iron into the blood.
- Get onto the Root Cause Protocol, and watch your symptoms disappear.
I have endured the slings and arrows over the abject ignorance and insanity i.e. hormone-D, and this anemic issue, in my humble opinion, is 10 times more important and 10 times more destructive to your overall health! I am becoming numb as the number of clients grows that have been misdiagnosed and are now suffering mightily for their body’s inability to cope with the assault of the excess, unbound iron.
Those that have taken the precious time to get this far, I encourage you to share it with your circles of family/friends, and to educate their health practitioners about this key reality.
A votre sante!
Morley M. Robbins
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