The Iron Paradox: Why Ferritin Alone Won't Tell You the Whole Story
Iron deficiency is the most common micronutrient deficiency in the world — yet it's still one of the most misunderstood. If you've ever been told that your ferritin (stored iron) is in your boots and you don’t know why,
Here's the paradox: too little iron causes real harm, but so does an outdated, one-dimensional approach to reading iron panels. Let's break down what's really going on.
Absolute vs Functional Iron Deficiency (They're Not the Same Thing)
Not all iron deficiency looks the same on paper, and lumping it all together leads to the wrong treatment plan.
Absolute iron deficiency is a genuine shortfall — the body's iron stores are truly depleted. This is typically driven by low dietary intake, malabsorption (think coeliac disease, SIBO, low stomach acid), pregnancy, or chronic blood loss. On a blood test, this looks like low iron, low ferritin, low transferrin saturation, and high transferrin (the body is crying out for more iron).
Functional iron deficiency is different. Here, iron stores may be normal or even elevated, but the iron simply can't be accessed or mobilised. The driver is hepcidin — the master regulator of iron — which gets switched on by inflammation and locks iron away inside cells. This shows up as low iron, normal-to-high ferritin, low transferrin saturation, and low transferrin.
When these two states overlap — someone who's genuinely low on iron and inflamed — you get a messier picture, where ferritin might be pushed artificially higher even though the person is still functionally deficient. This is why ferritin can never be read in isolation.
Put simply, you (unfortunately) can’t just look at ferritin (iron stores), and rule out iron dysfunction, because you can have “normal” or “good” levels of ferritin, but you may not being utilising it. Or it may be falsely elevated. I told you it was complicated!
The Ferritin Myth: Do We Really ALL Need It at 100?
For years, the naturopathic and nutrition world has chased a ferritin of 70-100 as the "optimal" target. But when you actually look at the evidence, this doesn't hold up for most clients.
A ferritin under 30 μg/L has high sensitivity and specificity for diagnosing iron deficiency, and levels below this are genuinely linked to poorer outcomes — neurodevelopmental issues in infants, pregnancy and birth complications, neurocognitive dysfunction, worsening thyroid disease, and cardiovascular risk.
But higher isn't automatically better. Research is increasingly showing that elevated ferritin carries its own risks:
A 2026 systematic review of over 10,000 pregnancies found ferritin levels were significantly higher in pregnancies that ended in preterm delivery, with the greatest risk when ferritin was elevated in the second trimester.
An observational study of 851 pregnancies found higher fasting blood glucose in those with ferritin above ~59 μg/L. (I have now learnt to screen clients with high ferritin for metabolic/blood sugar dysregulation, as well as previously looking at chronic viral, bacterial or parasite load, illness and inflammation)
Multiple large meta-analyses have linked higher serum ferritin to increased type 2 diabetes risk — one found risk rising by 22% with every 100 μg/L increase, with a stronger effect in women.
Large population studies (34,000+ and almost 60,000 participants) found that ferritin naturally sits in the 30-40 μg/L range for menstruating women, right up until menopause. We need to take female hormones, especially oestrogen, into account. thank goodness we are not talking about how hormones change intrepretation of bloods!
The take-home: ferritin is best thought of as a marker of adequacy, not a number to chase up up up with more supplements. Provided there's enough in the tank to draw on, more sitting in storage isn't doing anything extra for you— it's just sitting there.
"But I Have Heavy Periods…" — Not So Fast!
Menstruation gets blamed for iron deficiency constantly, but the maths often doesn't support it. A typical period (60-80mL of blood loss) - if you use a cup you can easily measure but there are other ways to assess this) only accounts for around 0.55-1mg of iron lost across the entire cycle. Someone who's menstruating absorbs roughly 1-2mg of iron per day from food — more than enough to cover that loss.
There's also a fascinating iron-oestrogen axis at play: oestrogen suppresses hepcidin, meaning higher oestrogen (as seen in the luteal phase, on the pill, and in pregnancy) actually increases iron availability, priming the body ahead of blood loss. This is part of why ferritin naturally sits lower during the reproductive years and rises after menopause — it's not necessarily pathological, it's physiological.
This doesn't mean heavy or frequent bleeding is never the cause — it absolutely can be — but a "normal" period shouldn't be the default explanation for chronic iron deficiency. If someone's cycle is genuinely moderate and they're still deficient, it's time to look elsewhere.
The Absorption Journey — and Where It Can Fail
Getting iron from a plate of food into a red blood cell is a surprisingly fragile, multi-step process, and there are several places it can break down.
In the stomach, gastric acid and enzymes need to solubilise and break down iron into an absorbable form. Low stomach acid (hypochlorhydria) — from H. pylori infection, chronic stress, PPIs, NSAIDs, or gastric sleeve surgery — means less iron even makes it to the small intestine ready to be absorbed.
In the duodenum, the microvilli need to be healthy to produce ferrireductase (which converts iron into its absorbable form) and to house the transporter that lets iron into the enterocyte. Damage from SIBO, excess alcohol, coeliac disease, or inflammation blunts this process. Notably, an estimated 1 in 30 people with iron deficiency anaemia has undiagnosed coeliac disease, and up to 70-80% of people with coeliac disease don't even they have it — so this is always worth screening for if there is no other explaination.
Inside the enterocyte, the iron only has about 72 hours before the cell dies and is shed — if the iron hasn't been released into the bloodstream by then, it's lost in the stool.
Getting into circulation requires the ferroportin "door" to be open (hepcidin's job is to shut it) and copper-dependent enzymes (ceruloplasmin and hephaestin) to convert the iron into a form that can bind to transferrin. Copper deficiency is an underrated cause of iron not "sticking" properly, even when absorption otherwise looks fine.
Hepcidin: The Gatekeeper Behind Most Chronic Cases
Hepcidin is upregulated by inflammation — regardless of whether someone's iron stores are high or low. With around 1 in 3 Australians living with a chronic inflammatory condition, and rising rates of IBD and autoimmune disease, this is one of the most common drivers seen clinically.
When hepcidin is switched on, it plugs the ferroportin door on enterocytes, macrophages, and hepatocytes — locking iron away as a (usually short-term) protective response against pathogens. The problem is the body can't tell the difference between an active infection and chronic low-grade inflammation, so if inflammation is ongoing, this "protective lockdown" becomes a long-term driver of functional iron deficiency.
This is also why iron infusions don't always work as expected. If hepcidin is elevated from inflammation, it's active throughout the whole body — not just the gut — so even iron delivered straight into the bloodstream can't be picked up by cells. This is often why ferritin spikes immediately post-infusion and then plummets again shortly after.
Gut Dysbiosis and SIBO — A Double Hit on Iron
Gut microbiome imbalance is broadly grouped into three patterns: fewer beneficial bacteria, an overgrowth of pathogens/pathobionts, or reduced overall diversity. Most patterns drive inflammation one way or another — either through more endotoxin-producing bacteria (like LPS) or less butyrate-producing beneficial bacteria.
SIBO specifically impacts iron absorption in multiple ways: it can trigger mucosal inflammation, damage the brush border, negatively affect enterocytes, and some bacteria directly consume iron for their own use. It's a genuine double whammy — inflammation driving hepcidin up, and microbes competing for the iron itself. In my own personal experience, I can vouch for having solid iron status after working on my gut (SIBO) and addressing coeliac disease, without being a red-meat eater.
The Cofactors Nobody Talks About
Iron rarely works in isolation, and several nutrients play a direct role in whether it's absorbed and used effectively:
Vitamin C — co-prescribing with iron supports absorption, increases serum haemoglobin, improves ferritin levels, and supports a higher reticulocyte percentage (a marker of active red blood cell production).
Vitamin A — improves non-heme iron absorption and, importantly, suppresses hepcidin expression, meaning it helps keep the "gates" open. We get so scared of vitamin A, especially for my pregnant friends, but it is a KEY ingredient for iron metabolism. Please don’t self prescribe or use high dose vit A in pregnancy either! but we need some :) I have seen this be a game-changer in some client’s iron status
Vitamin B12 — plays a direct role in erythropoiesis (red blood cell production) alongside iron; deficiency causes megaloblastic anaemia, which can complicate the clinical picture.
Copper — a cofactor for ceruloplasmin and hephaestin, assists absorption through enterocytes, and helps regulate hepcidin activity.
Folate — a cofactor for erythroblast proliferation and heme formation; deficiency causes erythroblast apoptosis (cell death), directly limiting red blood cell output.
If any of these are running low, iron supplementation alone may not move the needle.
Assessment Done Properly
A ferritin-only approach misses too much. A proper work-up should include:
A full iron panel — serum iron, transferrin, transferrin saturation, and ferritin, not ferritin alone.
CRP/ESR to identify coexisting inflammation that could be skewing the picture.
B12, active B12, folate, copper and ceruloplasmin, and vitamin A, given their direct role in iron metabolism.
Bloods taken rested and fasted, wherever possible, for the most accurate baseline. ** I cannot harp on about this enough!! Blood tests need to be done FASTED AND RESTED. ie no food for 10-12 hrs, and no workouts in the previous 24 hrs, as it will change your results. Also make sure you do your blood tests when you are generally WELL, ie not fighting off an infection/ cold/ virus etc.
A full blood examination (FBE) to catch anaemia patterns and other red flags.
Beyond bloods, depending on symptoms and history, it's worth investigating:
H. pylori — via GI-MAP, breath test, faecal antigen, or blood test.
SIBO — via glucose, lactulose, or fructose breath testing.
Coeliac disease — via genetic and gluten antibody testing, especially in chronic, unexplained cases.
The colonic microbiome — via DNA qPCR or metagenomic shotgun sequencing, not just a symptom picture. ie GI MAP or Microba
Blood loss pathways — via GI-MAP, Microba, faecal occult blood testing, and a proper menstrual loss assessment.
Dietary intake — especially important in children, where selective eating, food scarcity, excess dairy intake (calcium can block iron absorption) and neurodivergence-related feeding patterns can all reduce iron intake below what's needed. Children need a surprising amount of iron.
Treatment: More Than "Just Take More Iron"
Effective treatment usually needs to work on multiple levels at once:
Restore iron levels where genuinely needed — often short-term oral supplementation (iron bisglycinate is well tolerated, with fewer GI side effects and good outcomes for haemoglobin and ferritin).
Ensure adequate dietary intake, matched to age and life stage.
Support the cofactors — vitamin C, A, B12, copper, and folate — to optimise absorption and mobilisation.
Support GI function directly — including gut lining support (L-glutamine, zinc carnosine, Saccharomyces boulardii) and digestive secretion support (betaine hydrochloride, herbal bitters, pancreatic enzymes) where indicated. *again, no self-prescribing please :) I also LOVE lactoferrin and strain specific probiotics (299v) for supporting iron uptake in the gut and helping to lower inflammation in the gut if needed.
Reduce systemic inflammation — because this is often the real root cause of functional iron deficiency.
Address any genuine sources of excess blood loss. ie if it really is heavy menstrual blood loss
And critically — know when not to supplement or infuse. If your iron deficiency picture is driven primarily by inflammation (functional iron deficiency or anaemia of inflammation), pouring in more iron — orally or via infusion — often won't fix the underlying problem, and in some cases can do more harm than good. Iron infusions in particular can spike and then crash quickly if hepcidin is switched on system-wide. In these cases, the priority has to be identifying and addressing what's driving the inflammation, alongside supporting cofactors — not simply escalating the dose.
The Bottom Line
Iron deficiency isn't a "give more iron" problem. It's a multi-layered puzzle involving stomach function, gut integrity, the microbiome, systemic inflammation, and a handful of often-overlooked cofactor nutrients — and ferritin, on its own, only tells part of the story.
If you've been chasing iron that isn't responding to supplementation the way you'd expect, it's very possibly not an iron availability problem at all — it's an iron access problem.
Ready to get to the root of chronic iron deficiency?
If you have been stuck in a cycle of supplementing, retesting, and still not seeing ferritin or symptoms budge, it's time to look past the iron panel. My 12-Week Gut Health Package is designed to identify what's actually driving persistent iron deficiency — from hidden inflammation and dysbiosis to malabsorption and cofactor gaps — and build a plan that finally gets to the root cause, not just the numbers
Reach out if you would like to know more. I hope this has helped!