Anemia: Why everything you've learned about iron deficiency may be wrong.


Here's an interesting article on's long, but Chris Kresser and Morley Robbins have both provided more concise summaries.

Basically, the gist of it all is that supplementing iron to get ferritin levels up over 50, as advocated by many thyroid groups, may really be creating a toxic iron overload state and a deficiency of magnesium and bioavailable copper due to low ceruloplasmin. Taking iron supplements will only worsen this situation and won't actually improve health or vitality.

Longevity studies have apparently consistently found that ferritin levels over 50 are associated with higher mortality. Cardiologists may regularly prescribe blood donation, especially to men or post-menopausal women, because having lower iron levels is better for heart function.

Interestingly enough, Morley Robbins also suggests that gluten isn't actually the problem for many people with non-celiac gluten may actually be the iron that is added to the wheat flour that is causing issues for people. Did you know that you can pick up cereal with a magnet due to the added iron fillings? Yuck. You can see the iron fillings in a typical supplement capsule too.

So toxic iron levels are also associated with many conditions related to MECFS including infections, metabolic disease like diabetes/metabolic syndrome, and even histamine overload because bioavailable copper is required for DAO, MAO and NHMT (the enzymes that metabolizes histamine) to work properly. Morley Robbins also links excess toxic iron to MTHFR mutations and estrogen dominance.

Personally, I don't think many people at all should or need to be taking iron supplements. I think iron deficiency is often misdiagnosed and is either the anemia of chronic disease (for which taking iron supplements can actually prove fatal) or is actually in toxic overload in the liver for the reasons stated above.

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular 'reactive oxygen species' (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation.

We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation).
The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible.

This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, since in some circumstances (especially the presence of poorly liganded iron) molecules that are nominally antioxidants can actually act as pro-oxidants. The reduction of redox stress thus requires suitable levels of both antioxidants and effective iron chelators. Some polyphenolic antioxidants may serve both roles.
Understanding the exact speciation and liganding of iron in all its states is thus crucial to separating its various pro- and anti-inflammatory activities. Redox stress, innate immunity and pro- (and some anti-)inflammatory cytokines are linked in particular via signalling pathways involving NF-kappaB and p38, with the oxidative roles of iron here seemingly involved upstream of the IkappaB kinase (IKK) reaction. In a number of cases it is possible to identify mechanisms by which ROSs and poorly liganded iron act synergistically and autocatalytically, leading to 'runaway' reactions that are hard to control unless one tackles multiple sites of action simultaneously. Some molecules such as statins and erythropoietin, not traditionally associated with anti-inflammatory activity, do indeed have 'pleiotropic' anti-inflammatory effects that may be of benefit here.

Overall we argue, by synthesising a widely dispersed literature, that the role of poorly liganded iron has been rather underappreciated in the past, and that in combination with peroxide and superoxide its activity underpins the behaviour of a great many physiological processes that degrade over time. Understanding these requires an integrative, systems-level approach that may lead to novel therapeutic targets.



I have hemolytic anemia, mild, all nutrients concerned b12, iron/ferritin and folate all tested high. Medication can be a cause but more likely chronic infections.

I'm on a high protein/meat diet as well as take dessicated liver tablets which are high in blood building nutrientd. I dont think trying to increase all these is really going to help when the cause is probably infection related
Rest avs and abx for me.

I thought of you when I read this, in particular. If there ever was a textbook case of iron overload and copper deficiency, it sounds like you have it!

This condition allows infections to flourish too so they may be a result and not a cause.

Something to consider anyway. Blood donation is easy and cheap. I'd for sure skip the iron supplements if I were you though.


I dont take iron. My nutrient levels were within the high normal range, unless thats an issue?

Im not game to donate blood, id probably give some poor bugger who is immune suppressed vzv or cmv. Maybe leeches haha
Yes, leeches then. ;)

Would your doctor just prescribe a therapeutic phlebotomy?

It might be worth stopping any high iron supps, like liver, for the meanwhile.

I'd probably try high fat/moderate protein too rather than high protein. Then you have ammonia to deal with as well.

You could try some bio available copper. It's called MitoSynergy.


My protein intake is around 1gram per kg. I use yucca for ammonia, this initially seem to help sleep.
Copper i will look into. Whats an average dose and foods high in copper.

How does the phlebotomy help low hb or neutropenia ?

I will dig out my blood work with ferritin levels?
Protein levels are tricky. For every person saying one thing, there are 12 more saying 12 other things. For me, I try to stick with between 0.5-1g/kg of LEAN body weight. Another formula I like is 1 g/kg -10%. The important thing is to make sure to get at least 30g of protein at a don't dribble it in through the day in lesser amounts. This makes leucine most available to the muscles for building strength. So I try to have two 30 gram servings of protein a day which is less than you might think.

The only bioavailable copper that I know of is MitoSynergy. It's expensive but I definitely think it helps. It's one of my favorite supplements this year.

I'll have to quote Morley Robbins on how phlebotomy helps with low hemoglobin...but basically it is because it helps to remove the high iron. Quercetin is another supplement that can chelate iron and is also very useful in mast cell issues. This is from a podcast interview recently:

But it was also well understood from 1860 to about 1870 that when someone was anemic that that meant that they had low bioavailable copper because every facet of red blood cell metabolism is copper-dependent.

Let me give you an example.

So the signal to produce a red blood cell originates in the adrenal gland and it’s the hormone erythropoietin that gets made there and signals the bone marrow to make more red blood cells. You can’t make that hormone without bioavailable copper.

Then once that signal is received in the bone marrow, it starts to make heme, the heme protein. You can’t make heme protein unless you have bioavailable copper.
And the origin of hemoglobin is the protoporphyrin ring. We can’t put four heme together unless you have bioavailable copper. Then the rate-limiting step of making hemoglobin is called ferrochelatase enzyme. And that’s the enzyme that actually serves as a crane to drop the iron into the protoporphyrin ring to create hemoglobin. And ferrochelatase doesn’t work unless you have available copper.

And then you monitor the viability of this process and the red blood cell is monitored by heme oxygenase. Guess what? You got to have copper to do that too.
So, every facet of red blood cell metabolism is dependent on copper. And that’s what they know from 1860 to about 1970, that hemoglobin is off the copper zone. And that was considered the engine of red blood cell metabolism because that’s where the action is. That makes the hemoglobin to provide oxygen so that the cell can make some ATP. It’s really important to have oxygen to do that.

In 1972, a British team published some research about the ferritin protein. And ferritin is supposed to be in the spleen. It is in the bone marrow and it’s in the liver. But it also shows up in the blood.

And what they did is they put the spotlight on ferritin in the blood. And it made it very clear in this early literature that it was supposed to just be a small amount. And suddenly, it began to get twisted and distorted and now we got people trying to get their ferritin up into the low 100s, which is utter insanity.

And that’s what it was for about 40 years until a physiologist from University of Manchester—his name is Douglas B. Kell. He’s PhD physiologist in England who is recently knighted for his work. And he has been putting the spotlight on ferritin and just how toxic it is inside the body.

In fact, one of his signature articles is called Iron Misbehaving Badly. And so when someone publishes an article of some substance, you would expect it to be about 10 or 12 pages long and have maybe 100 citations. His article, his particular article is about 14 pages long, but it has 2400 citations.

Wendy Myers: A little OCD. We want that in our researchers.

Morley Robbins: Exactly, absolutely, we want OCD. And what’s interesting about it is he is making a very clear statement that not only does medicine have it wrong, they have it dead wrong and that ferritin is a storage protein and when it shows up in the blood, it’s a sign of damaged tissue.

And what most people probably don’t know is that each molecule of ferritin can hold up to 4500 atoms of iron. That’s a lot of iron. And I don’t know how much ferritin is in a unit of measurement, but when people start to get up into the hundreds, it gets to be a really serious problem. And the body doesn’t work right when it gets too high.

And so the analogy that I use is that many of us drive cars, many of us have had engine trouble with our cars. And when we have that happen, we take it to a mechanic. We expect the mechanic to open up the hood and look at the engine—not run around to the trunk and start measuring the size of the trunk.

And that’s what happened to medicine today around this whole issue of iron. They are completely ignoring the engine, which is called hemoglobin. They are completely ignoring the oil, which I call ceruloplasmin. And all they are doing is obsessing about how big is your trunk. And I think it’s painfully absurd. And it is causing a lot of misery around the world.




Well-Known Member
Maybe not relevant here...Bacteria will also eat your iron, leaving you deficient. This was happening to me for the year before I had any understanding. Kept supplementing, high quality Fe, and still levels always tested low.

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