Despite what you’ve been told – you don’t need more iron to fix low iron. It is one enormous paradox as often, there will be an abundance of iron present locked away in tissues, yet it cannot be accessed due to a broken iron recycling system, hence the picture of iron deficiency. Iron balance is more about recycling the iron within rather than dietary intake.

The human body is an iron conservation machine.

Almost and I say almost, operated via perpetual motion requiring very little in the way of iron input. Between 90-94% of our daily iron needs are provided from within by recycling the iron contained in old red blood cells. Some 20–25 mg/day of iron is recycled by the Reticuloendothelial System leaving us with just 1.5-3mg on average needing to be obtained from diet. For men it is much less then this to account for the fact they have no way of excreting excess iron aside from Phlebotomy.

Very clearly you can see (I hope) that our focus on shoveling more iron into our body to ‘fix low iron’ is severely misguided and way off course. Our focus instead should be on why is our RES recycling system failing us and what does it need to get back up and running again.

 

 

It is only in instances of physiological blood loss or true dietary iron inadequacy that we need to take the tactic of loading more iron into the body. Lactoferrin is evidence of this. It matches or exceeds the benefits of Ferrous Iron supplementation without adding any more iron into the body pool. It also simultaneously reduces gut inflammation and improves iron recycling.

“Pregnant women with iron deficiency anemia receiving Lactoferrin of 100mg twice daily had similar or higher rises in Hb and Ferritin compared with ferrous sulfate taken at 100mg a day, with no gastrointestinal side effects.” – Paesano R.et al

Dietary iron absorption is very tightly regulated by design.

The body does not want more than it needs and there are consequences to flooding the body with more iron than it can use at any one time.

Sir Douglas B. Kell, PhD’s research – “Organisms must tightly regulate their iron levels to provide just enough for their cellular needs without developing the toxicity associated with iron excess. The body lacks a defined mechanism for active excretion of iron, so body iron levels must be regulated at the point of absorption.”

This tight regulation is also displayed in understanding that human breast milk contains very little iron. This isn’t a mistake in our design. 80% of iron storage is acquired by the fetus during the last trimester and this iron pool may be significantly enlarged by up to 500 mg iron/kg body weight by delayed umbilical cord clamping at birth to allow for complete blood transfusion from the placenta to the newborn. The newborn born at term born to iron-sufficient women has abundant iron stores for disposal during the first 4–6 months. The presence of Lactoferrin in breast milk is precisely why breastfed newborns are never iron deficient.

In healthy pregnancy there is a physiological down regulation of maternal serum hepcidin observed to enhance intestinal iron absorption and ensure its release from stores in the spleen and liver for transport to the fetus. The fetus will download approximately 300mg of iron from the mother and this demand for iron during pregnancy is again majority covered by the daily recycling of RES system. The total amount of iron used in pregnancy corresponds to about 1000–1200 mg,

Iron Storage Is a Protective Evolutionary Mechanism

Ferritin + Hemosiderin are the storage forms of iron. Ferritin gets an unfair amount of attention because iron is supposed to be in active circulation moving fluidly through the blood. Hemosiderin we have no real method of testing/ measuring for with ease but it is a veritable vault of iron locked away without a key in our tissues and it can hold a LOT, we’re talking thousands of milligrams.

Our body is programmed to put iron into storage in the presence of pathogens. Iron is a favourite food source of Parasites, Candida etc. They need it to replicate and flourish. Our immune system has been finely tuned since the beginning of life to keep that iron from them in order to protect us from becoming overrun with pathogens. This is called Nutritional Immunity. The downside of this innate protective process is that iron storage is not a good thing.

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.

Pathogenic gut infections such as H.Pylori could be driving low iron. Parasites need iron to replicate and thrive. Our body’s defence mechanism is to keep iron away from them by placing it in storage. Yeast overgrowth and leaky gut can all contribute to decreased ceruloplasmin production which impairs iron circulation. This is where Lactoferrin can be a shining light.

Iron stored in the liver = lipofuscin development (brown fat loaded with oxidised iron and the flow on is non alcoholic fatty liver. When excess iron accumulates even modestly above normal in the liver it catalyzes the Fenton reaction which just means a heck of a lot of damaging reactive oxygen species are created.

“Inflammation and iron are known extracellular stimuli for increased iron storage which causes iron to show up as low on ferritin, low on serum iron and low on saturation markers.” – Messner 2010.

Focusing on ferritin, stored iron, does not tell us what is going on with active iron metabolism. By the time ferritin shows up in the blood, after it’s filled in the liver, the spleen and the bone marrow, it’s too late – a high ferritin number is not desirable at all. On top of that, we should really consider the EMF Antennae consequence of a body with high stored tissue iron-

Jack Kruse MD:
“Too bad no one realizes that transition metals, like Iron, draw nnEMF [non-native EMF] toward them because of the D shell electrons they contain.”

Mega Doses of Iron Are Useless

Enter Hepcidin the principle iron absorption regulating hormone which inhibits intestinal iron uptake when too much is being received. Let me use the infamous FerroGrad C as a great example curiously recommended by GP’s to fix low iron…..

The active substance is Dried Ferrous Sulfate 105 mg elemental iron as the active ingredient and Vitamin C in ascorbic form. The other ingredients are acrylates copolymer, brilliant scarlet 4R (Ponceau 4R (E124), ethylcellulose, hypromellose, macrogol 400, macrogol 8000, magnesium stearate, maize starch, povidone, purified talc, titanium dioxide. Source

The ‘other ingredients’ are pure poison for a start and absolutely not pregnancy safe.

But what happens when someone takes 105mg of iron in a daily dose is that Hepcidin, a signalling protein springs into action and literally blocks ALL further iron absorbing beyond 60mg. The body literally says ‘heck no that is far too much iron and I cannot deal with more than 60mg in one sitting’. When Hepcidin is activated it blocks further iron absorption from the gut for the next 24 hours thereabouts and traps iron in organ/tissue storage sites (a self-protective mechanism to prevent overload or infection). An iron ring is now in place.

Similar findings are identified in women with iron deficiency – a 100 mg Ferrous Sulfate dose triggered strong hepcidin spikes for 24–48 hours. Stoffel et al., Haematologica, 2017

The body “sees” the excess iron as an overload event, and responds protectively by limiting further uptake. As a result, most of that 100mg iron dose never reaches systemic circulation.

The same goes for FERINJECT Intravenous Iron in which either a 100 mg, 500 mg of iron or 1000 mg of iron is received in a single dose.

Now Hepcidin is an inflammatory marker, you don’t want it to remain high as there are consequences to that. So now you have and inflamed body that refuses to absorb iron. Make that make sense.

When someone consumes iron fortified foods for decades or engages in repeat iron transfusions, iron laden supplements etc – they are essentially creating chronic iron congestion. The body adapts by converting excess iron into hemosiderin and stashes it away throughout our organs and tissues. This iron doesn’t disappear, it just becomes functionally inaccessible.

You can be simultaneously overloaded with iron and functionally iron deficient because you cannot access the iron in your tissues. Remember that you can have Anemia that is NOT caused by iron deficiency. Has your Doctor ever mentioned Anemia of Inflammation? Anemia of chronic disease, now more accurately referred to as anemia of inflammation (AI), is second only to iron deficiency as the most common type of anemia and is a situation where there is a adequate iron in the body yet the iron is ‘unavailable’ for use due to chronic inflammation and subsequent immune dysfunction.

Again, I hope you can see from the above that giving more iron doesn’t fix low iron presentation.

The Coordinated Approach to Optimize Iron Mobilization From Stores

Let’s unpack the vitamin A, copper, and lactoferrin triad and how they work together to optimize iron mobilization from stores and create a harmonious iron regulation system.

• Lactoferrin Regulates iron absorption and transport. It lowers inflammation, reduces hepcidin, and supports ferroportin expression, letting iron leave storage sites safely.
• Copper (via Ceruloplasmin) Mobilizes stored iron. If copper is low this leads to iron accumulation in tissues and low serum iron, despite “normal or high ferritin.” This is why copper deficiency can mimic iron deficiency — the iron is there, but locked away from use. Copper deficiency also increases hemosiderin.
• Vitamin A (Retinol) Signals iron release and red blood cell production. Retinol allows cells to take up circulating iron efficiently and ensures that released iron is actually used for hemoglobin and not left to oxidize. Without retinol, both copper utilization and iron transport stall.

Together, they form a closed regulatory loop that determines whether iron stays trapped in cells or moves safely into circulation and restore the body’s natural iron rhythm — absorption, release, transport, and utilization — without triggering oxidative stress.

The below plan would ideally be executed where ‘iron deficiency’ which should really be called ‘iron metabolism dysfunction’ is recognize. The same plan of attack would also be used where iron overload is determined however –

Lactoferrin

100–200 mg 1–2×/day

Empty stomach for hepcidin modulation

Copper (food form)

1–2 mg/day

Oysters, liver, cacao, bee pollen

Vitamin A (retinol form)

2,500–5,000 IU/day (dietary)

Liver, cod liver oil, pastured dairy, pastured egg yolks

 

So if this is your story, constantly being told that in order to fix low iron you simply need to up your iron intake – remember that active iron mobilization and circulation is what we are looking to achieve, and this isn’t done via simply supplying more iron. It is almost entirely counterproductive to human physiology to take that approach.

I hope there have been some golden nuggets found in here and if you did, please do keep exploring all things iron metabolism further with The Root Cause Protocol.