“Am I really anemic” Playbook or said another way: “Not known because not looked for”
When last we met during Iron Toxicity Post #59:
https://www.facebook.com/groups/MagnesiumAdvocacy/permalink/1366914676709931/
I developed what I believe (& hope that you agree with) is a compelling set of facts to seriously question the validity and the clinical relevance of ferritin-only blood tests as a stand-alone indicator of true metabolic iron status in the human body.
In that post, I noted that there were two more posts coming, one on key questions to ask, and an additional post on suggested tests to broaden our understanding and assessment of the other factors involved in iron metabolism. In the spirit of keep it simple seeker (K.I.S.S.), I have elected to simplify this process. I am going to blend the two pending posts, which is the focus of this set of comments and insights in this current post #60.
Before proceeding, let me amplify the second half of the title: “Not known because not looked for.”
We are led to believe that the medical system is exhaustive in its blood-testing search for clues to what’s not right with our metabolism. What I have come to discover is that much of the laboratory testing, that is commercially available around the world, is based far more on availability, not so much on clinical accuracy or applicability.
An obvious case in point: No one tests for Magnesium RBC, despite its obvious importance in all 100 trillion cells, as well as some 3, 751 proteins known as the magnesome.
Another more obvious point: No one tests for ferroxidase enzyme function, the master anti-oxidant enzyme in the human body that no one seems to know about.
These are but two key tests, among scores of “missing” tests from the typical arsenal that doctors are trained to provide, and allowed to order. Though this group of available tests does little to meaningfully pull back the curtain on the true mineral dysregulation that is driving the cellular dynamics of metabolic dysfunction.
At the end of the day, all we can do is the best that’s currently available, but that should not deter us from pointing out the glaring shortages and inadequacies of current laboratory testing for iron status, that drive inconclusive, and at times, faulty clinical conclusions.
What now follows is my best recommendations for a 10-point plan for “Questions to ask,” and where appropriate, “Tests to demand,” when confronted with the oft-repeated phrase: “You’re anemic!” I strongly advise you all to stand your ground and get the truth of what’s really driving your iron markers. I trust that you will find the following information, both useful and life-changing:
Q. 1) Doctor, given that ferritin is not synthesized in the blood, exactly how does a serum measurement of ferritin (i.e. an extracellular marker, and akin to “kitchen temperature”) relate to, or have any relevance to, the intracellular ferritin protein level (i.e. the storage protein synthesized Inside the cells, and is more akin to “oven temperature”)?
Recommended test: There is no known measure of intracellular ferritin.
Q. 2) Given that there are two forms of ferritin, what form(s) of ferritin are present in this serum measurement: ferritin-h (heavy, with ferroxidase enzyme function) and/or ferritin-l (light, without the key ferroxidase enzyme function)?
Recommended test: Distinction of ferritin-h or ferritin-l (this is a standard test in research studies, but I’m not certain that this test is even available commercially. the intent here is to drive home the point that a ferritin-only test is spurious, and misleading, at best).
Q. 3) Doctor, what’s the status of my hemoglobin, given that ~80% of my body’s iron is complexed in that key oxygen transport protein — as opposed to ferritin that has ~10% of the body’s iron?
Recommended test: Hemoglobin
requestatest.com/hemoglobin-testing
Q. 4) What is the status of my mineral and vitamin co-factors that regulate iron metabolism: i.e. magnesium, bioavailable copper, zinc, ceruloplasmin (ferroxidase enzyme), and several select iron markers?
Recommended test:
requestatest.com/mag-zinc-copper-panel-with-iron-panel-testing
https://requestatest.com/mag-zinc-copper-panel-with-iron-panel-plus-vitamin-a-and-vitamin-d-test
Q. 5) I realize that all you’re seeing in this “low ferritin” is “anemia of iron deficiency” (AID), but is there a chance that I could, in fact, be dealing with “anemia of chronic inflammation” (ACI)? (It is a well-established fact that inflammation causes “hypoferremia,” i.e. low iron in the blood)
Recommended test: Markers of inflammation: bun/creatinine ratio; hs-CRP; IL-6, blood glucose; Hgb A1-c; etc.
Q. 6) Exactly how would you know about this distinction between AID and ACI if you haven’t done these additional tests that assess inflammation? In an inflammatory process, wouldn’t we expect to see an elevated IL-6, but that if there were a true iron deficiency, IL-6 would not be elevated? Wouldn’t that be a decisive indicator of true iron status?
Recommended test: Interleukin-6; Interleukin-1; TNF-a; and NF-kB (These markers are routinely assessed in research studies, but I’m not sure about their availability with the commercial labs)
Q. 7) Is it possible that my low level of bioavailable copper, as expressed by low ceruloplasmin (Cp, as known as ferroxidase), or suspiciously high Cp, could be causing “iron retention” in the macrophages, thus impairing proper iron egress from the cells in my body?
Recommended test: Stress the importance of the serum ceruloplasmin test as a sign of bioavailable copper.
Q. 8) Doctor, is it possible that my hepcidin level, the iron peptide hormone, could be elevated which would then prevent iron from being released from:
- Enterocytes in the digestive tract?
- Hepatocytes in the liver (key to blocking iron recycling)
- Macrophages in the iron R.E.cycling system, how would we know if we don’t test the status of this key iron hormone?
Recommended test: This is routinely done in research studies, but it is not available, to my knowledge, in a commercial lab.
Q. 9) Given that hepcidin is a “Janus (2-faced) peptide”, serving as both an iron regulatory, as well as anti-microbial agent, wouldn’t it be critical to our understanding hepcidin status before assuming “iron deficiency,” and especially before “iron supplementation,” given that:
- Hepcidin increases with iron supplementation, as well as with the conditions of both infections and/or inflammation (Note: increased hepcidin expression causes “hypoferremia”)
- Hepcidin expression decreases with increased need for iron in the body. Therefore, we expect low hepcidin expression if there were a true need of iron.
Recommended test: This is routinely done in research studies, but it is not available, to my knowledge, in a commercial lab.
Q. 10) Doctor, given my long-standing litany of symptoms and issues, how many of them are, for a fact, caused by iron-induced oxidative stress? I’m curious if you’ve had a chance to read any of the 59 Posts on Iron Toxicity that I shared with you recently?
Recommended link:
https://therootcauseprotocol.com/category/research/iron-toxicity/
I think you all get my point that assessing true iron status is a far cry from measuring your height or your weight. It is a Rubik’s Cube of interlocking factors that do not lend themselves to “one and done” testing.
Furthermore, as you can see, even the most sophisticated commercial labs are a veritable “swiss cheese” of blood tests, many of which are not available. As noted at the outset: “Not known because not looked for” That does not mean that if they are not available, that they are not relevant to your situation, especially given the importance of knowing your true iron status. In fact, I would contend that it is just the opposite.
This testing “patch-work” is a classic case of designed & selective awareness. Given that most of these tests are routinely done in research studies, around the globe, underscores their clinical importance, as well as their significance. In my humble opinion, it raises countless red flags why they are not available to your practicing physician(s) and to us as a group of individuals seeking to know the truth. I’ve got some theories on why this is the case, but I’ll let you draw your own conclusions.
I am also aware of the inherent “discomfort” that this series of questions raises for each of you in terms of your ongoing relationship with your healthcare practitioner.
My intention is to put a spotlight on the set of variables and clinical factors that are essential for properly assessing and concluding that you are dealing with “iron deficiency,” and not “chronic inflammation!” And if your practitioner is resistant to your well-informed questions, you may want to consider seeking out a more open-minded healthcare provider.
This raises serious questions about what they know, and what they want you to know. So, I do hope you find this set of questions helpful, and that it reinforces the points that I’ve made in my many, many posts on Iron Toxicity
A votre sante!
Morley M Robbins
For Facebook Discussion:
https://www.facebook.com/groups/MagnesiumAdvocacy/permalink/1385659851502080/