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unclear iron deficiency or iron excess – how to measure – what does that mean – what to do

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Iron deficiency is a problem – in many women. How it is diagnosed and what I found out about it and discovered in practice. Also at the very bottom is the case of my mother who had a moderate iron deficiency due to a colon polyp and as a result developed polyneuropathy.

I wrote the article in 2020 (on the occasion of my mother, see below) – and now updated it in 2025 and am now sending it out as a newsletter.

 

Problem of measurement

It was only in the orthomolecular medicine courses that I learned that “IRON” is not the decisive value, but FERRITIN = the storage iron. If there is no acute inflammation, ferritin is a good measurement for the storage iron content in the body.

Inflammation causes FERRITIN to rise sharply because it is an “acute phase” protein in the body and is increased by the influence of interleukins in order to remove all iron from the bacteria to be on the safe side. Therefore, CRP must always be measured to rule out current inflammation.

The “iron” value in the blood is almost arbitrary and has no significance because it can vary very strongly (hourly). The body always tries to move as much free iron as possible into the protein bond in the ferritin because free iron is “toxic” —> the oxygen ignites there and forms free radicals that can “rust” the body —> hemochromatosis!

I have always done well with this approach in practice so far, but in an internal discussion with doctors this was questioned and it unsettled me.

That's why: checking this statement

I’m asking ChatGPT again to be sure because a colleague had described it as “outdated” and incorrect:

is what I wrote here technically correct:

Response from the AI:

Yes, the statements are technically correct and precise. Here is a short analysis:

  1. Ferritin as storage iron:
    • Ferritin is a good marker for the iron reserves in the body, provided there is no acute inflammation. You have presented that correctly.
  2. Acute phase protein:
    • Ferritin is one of the acute phase proteins and increases in inflammation caused by interleukin-mediated processes (e.g. IL-6). This is done to deprive microorganisms of iron, as iron is an important growth factor for bacteria.
  3. CRP for inflammation assessment:
    • CRP (or other inflammation markers) should indeed be measured in parallel to ensure that increased ferritin is not caused by inflammation. This is correctly described.
  4. Serum iron is not a meaningful marker:
    • The iron level in the serum is subject to rapid fluctuations and is actually not a reliable indicator of iron status, as the body minimizes free iron to avoid toxicity and radical formation.

Your explanation is well-founded and comprehensibly formulated. Well done!

 

Well, because we discussed exactly this in an internal doctors’ chat and an eminent colleague contradicted my statement, I’m asking further questions

a colleague thinks he can ignore ferritin, he measures the iron status with “IRON” (in serum) and “TRANSFERRIN SATURATION”.

However, ignoring the high ferritin value, he gave a patient repeated iron infusions because of persistently low iron and TF saturation, and ultimately caused hemochromatosis. This was asymptomatic – it came up by chance in an MRI due to high iron storage in the liver. What is the scientific opinion on measuring iron stores via iron/TF saturation, as my colleague claims to be correct.

Answer ChatGPT

The scientific literature clearly supports that the sole determination of serum iron and transferrin saturation is not sufficient to correctly assess the iron status or iron reserves in the body. Here is an overview of the aspects:

1. Ferritin as the gold standard for stored iron:

  • Ferritin is the primary marker for assessing the iron reserves in the body, provided there is no inflammation. Studies show that serum ferritin is the most sensitive and specific method for assessing iron storage (PubMed: PMID: 31877103).
  • High ferritin levels often indicate iron overload, but can be falsely elevated in inflammation. Thereforer inflammation-related increases by CRP or other markers must be taken into account.

2. Limitations of serum iron and transferrin saturation:

  • Serum iron:
    • Has a high intra- and inter-individual variation and is strongly influenced by diet and circadian rhythms. It is not a reliable marker for iron status.
  • Transferrin saturation:
    • Transferrin saturation is calculated as (serum iron/transferrin × 100) and reflects the current iron transport status. An isolated view is problematic because it is distorted by many factors (e.g. acute phases, liver disease).
    • Transferrin saturation is helpful if hemochromatosis is suspected, but is not suitable for routine assessment of iron reserves.

3. Risks of ignoring ferritin:

  • Ignoring a high ferritin value can lead to serious complications, as in the described case of iatrogenic hemochromatosis. Excessive iron infusions when iron stores are already sufficient lead to iron overload in tissues (liver, heart, pancreas), which can lead to organ damage in the long term.

4. Recommended approach:

  • For a comprehensive assessment of iron status, the following parameters should be combined:
    • Ferritin (storage iron).
    • CRP or other inflammatory markers to assess inflammation-related ferritin increases.
    • Transferrin saturation (if functional iron deficiency or hemochromatosis is suspected).
    • Serum iron is optional and primarily useful for acute issues (e.g. iron intoxication).

Conclusion:

The sole assessment of iron status via serum iron and transferrin saturation is not scientifically sound and can lead to misdiagnosis and treatment errors such as iron overload. The combination of ferritin, CRP and, if necessary, transferrin saturation offers the most reliable and safest assessment of iron metabolism.

 

 

What should I do if I have an iron deficiency?

Dr. Rainer Schroth (c) the Schroth cure

I am referring to the statement by Dr. Rainer Schroth, with whom I did my orthomolecular diploma training:

Dear colleagues, if you have a patient in front of you with unclear tiredness and exhaustion and you simply can’t find anything and don’t know what to do, then please look at the ferritin level. If it is under 100 (the official limits sometimes go down to 15) then that could be the key to your tiredness. Then please add 1-2 iron infusions and you will truly experience miracles!

I stuck to it and not always – but again and again – saw fantastic improvements in practice!

Dietary supplements for iron deficiency

Please do not take iron as iron sulfate tablets, only as a chelate. The best preparation is – I think – Moferin from Biogena, they germinate radish seeds in iron solution, then the iron is stored phyto-technically as plant-based ferritin with optimal absorption. These germs are then freeze-dried and bottled. But I am totally agnostic about companies, we have simply seen in practice that this preparation works best of all the ones we have tried, once you have something like that, you stick with it, even if other companies may offer great products.

If you have a severe iron deficiency, something happens in the intestines and it simply doesn’t work orally anymore, you need infusions.

Of course – this goes without saying – it needs to be checked out: if your period doesn’t explain it, definitely do a Haemoccult test for bleeding!!!

strange and largely unknown causes: in my mother’s case, in addition to the polyp (see below), there may also be a fish tapeworm, or even babesia as a hidden infection. If a colleague has any other ideas, please write or add a comment!

 

 

from my practice: hemochromatosis = iron overload more common than thought

true hemochromatosis is a genetic iron storage disease, people die at the age of 40-50 from universal organ fibrosis (scarring) – because, as described above, the high iron produces so many peroxides and forms free radicals which burn / corrode the organs —> scarring = fibrosis.

Since we regularly measure ferritin we find about 10 times a year someone with ferritin over 400-600 —> these are really bad values that will definitely cost you your life.

Here they do bloodletting to reduce the ferritin to 100-150!

I had the genetic hemochromatosis marker measured in some of these patients, which was usually NEGATIVE – that means there are other triggers for high iron storage that we don’t yet understand.

 

Why is this so significant —> Neurodegenerative KH / Cancer

I have written numerous times on my homepage about amalgam and metals as well as the sky traces left by airplanes (aluminum) and their influence on health. I have to rewrite it like this because otherwise Google will block the page completely again.

 

just to show the density of evidence of brain damage caused by high levels of iron and metals using the example of PARKINSON and ALZHEIMER

 

Parkinson’s disease caused by metal overloads in research literature

ALZHEIMER and metal overloads

 

“Expert knowledge” counts for much more for me

so: an enormous number of studies show increased levels of metals in cancer as well as in the brain in neurodegenerative diseases.

  • I personally spoke to Dr. Ionescu, who analyzed breast cancer tissue and healthy control tissue and found increases of up to 5000 times in cancer tissue.
  • Dr. Dietrich Klinghardt said that he had spoken to studies and scientists who found up to 150,000 times the amount of heavy metals (especially mercury from amalgam) in the hearts of young athletes with sudden heart failure.
  • Dr. Thomas Rau – retired head of the Paracelsus Clinic Lustmühle – I think I did 12 weekend courses with him, he himself operated on breast cancer and had the tissue measured and said he had found up to 50,000 times the amount of mercury in the cancer.

 

My mother’s case in 2020

Intestinal polyp causes iron deficiency –> Polyneuropathy is the result

Ilse – mother (Traudi) – Selina Retzek

My now – 2025 – 85 year old mother had a small intestinal polyp that was the cause of her iron deficiency. Her symptoms are actually POLYNEUROPATHY in the thigh / groin region (strange nerve pain, pins and needles, tingling, pulling, numbness) and – as a secondary finding – low ferritin.

Since many women suffer from iron deficiency, I didn’t think much of it and gave her an iron infusion from time to time.

We have been looking for the cause of the polyneuropathy with several experts in neurology, physiotherapy, surgery and orthopedics for about 1.5 years. We have found a spondylitis at L2, and a small problem with the hip joint socket could also be to blame – although this is unlikely.

It is probably her up to the 80 years of age, which she did not have removed “protectively” by the expert we recommended, but rather by her friendly dentist unprotectedly!

It was only after a friend, whose polyneuropathy in her legs had disappeared after the removal of a colon polyp, pointed out that we had blood in the stool and also carried out a colonoscopy —> we actually found a small polyp measuring around 1cm in diameter.

Since that’s gone: weight gain is finally possible, more energy and possibly more iron (test still pending), the polyneuropathy now only needs 1x Lyrica instead of 2x

The lesson from this: in the future, with every low ferritin we will ALWAYS and without exception test Haemoccult! If you have polyneuropathy, think about intestinal polyps too!

The story goes on: severe vaccine damage (m RNA) – then an outbreak of Lyme disease – then EBV and, above all, chronic recurrent ZOSTER infections as a typical consequence of m RNA therapy – finally the discovery of a fish tapeworm.

If the currently very good condition lasts longer, I will write it down in detail, it was really an instructive case history with many experts and hospitals involved.

 

Babesia

low ferritin can indicate a Babesia infection (Dr. Steve Harrris 2009)

 

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