Published 18 August 2026 · HodieLabs Clinical Governance Lead · From the HodieLabs Evidence-Based Clinical Library
Ferritin is the protein your body stores iron inside, and serum ferritin is the closest thing medicine has to a fuel gauge for total body iron. It is also an acute phase reactant, which means it climbs during infection, inflammation, liver disease and metabolic dysfunction whether or not your iron stores are full. That single fact breaks the way most people read the result. A ferritin of 55 µg/L can mean healthy stores in one person and an empty tank in another, and the number alone will never tell you which.
Iron is one of the few nutrients the human body cannot actively excrete. Absorption is regulated at the gut and everything that gets in stays in, distributed between haemoglobin, muscle myoglobin, enzymes and storage. Both ends of the range cause damage. Too little and oxygen delivery, exercise capacity and cognition suffer before the haemoglobin ever drops. Too much and free iron catalyses oxidative reactions in the liver, pancreas, heart and joints.
The WHO published a dedicated guideline on ferritin thresholds in 2020, and its central recommendation is the one most often ignored in Australian general practice. In healthy adults, a ferritin below 15 µg/L defines iron deficiency. In the presence of infection or inflammation, that cut-off moves up to 70 µg/L. Same patient, same iron stores, different threshold, because ferritin is measuring two things at once and only one of them is iron.
So the practical consequence is that a ferritin result reported without an inflammatory marker beside it is close to uninterpretable in anyone who is unwell, carrying excess visceral fat, or training hard. Endurance athletes are a good illustration. Heavy training raises inflammation and hepcidin, which pushes ferritin up, while foot-strike haemolysis and sweat losses quietly drain the stores underneath. The number goes up as the tank goes down.
Australian laboratory reference intervals sit at roughly 30–300 µg/L for men and 15–200 µg/L for women. Those intervals describe the spread of a reference population, not the level at which a person functions well, and the female lower bound of 15 µg/L is famously permissive. A menstruating woman reported as "normal" at 18 µg/L has stores that will not survive a heavy cycle, a pregnancy or a blood donation.
Read ferritin with transferrin saturation, hs-CRP and the red cell indices, or do not bother reading it at all.
Elevated ferritin is one of the most common abnormal results in Australian pathology, and it is misattributed constantly. The reflex assumption is iron overload. The reality, in the large majority of cases, is metabolic. Fatty liver, high alcohol intake, obesity and chronic low-grade inflammation account for most raised ferritin results, which is why an elevated ferritin so often travels with a raised GGT and the picture described in our piece on metabolic fatty liver disease.
Transferrin saturation separates the two. It measures the percentage of circulating transferrin actually carrying iron, so it reflects iron delivery rather than the inflammatory state. Above 45% on two separate fasting morning samples is the accepted screening threshold for hereditary haemochromatosis and the trigger for HFE genotyping. Below 20% alongside a low ferritin confirms deficiency. Both thresholds are in the Australian pathology standards and neither can be inferred from ferritin.
Timing matters more here than most people expect. Serum iron has a strong diurnal rhythm and responds to meals, so transferrin saturation calculated from an afternoon non-fasting sample is unreliable. Morning, fasting, and at least 48 hours clear of any iron supplement.
Hereditary haemochromatosis is the most common inherited genetic disorder in Australians of northern European ancestry, and the numbers around it are widely misquoted in both directions.
The clinical logic follows from those two numbers. Because penetrance is low, screening the whole population with genetic testing makes little sense. Because the treatment is venesection, which costs almost nothing and works completely when started before organ damage, missing the people who are loading is unforgivable. Transferrin saturation is the test that sorts them out, and it costs almost nothing to add.
Iron is the most casually self-prescribed supplement in the country, and the trial evidence is more mixed than the marketing suggests.
The best evidence for treating deficiency without anaemia comes from Verdon and colleagues in the BMJ in 2003. They randomised 144 non-anaemic women aged 18 to 55 with unexplained fatigue to 80 mg of elemental iron daily or placebo for four weeks. Fatigue fell further on iron than on placebo, and the benefit was concentrated in the women who started with a ferritin below 50 µg/L. That is a real effect in a properly blinded trial, and it is also a modest one over a short period in a selected group.
Against that, PREVENTT, published in the Lancet in 2020, gave intravenous iron or placebo to anaemic patients 10 to 42 days before major open abdominal surgery across 46 UK centres. The co-primary endpoint of death or blood transfusion by 30 days was 29% with iron and 28% with placebo. Correcting a number on a lab report is not the same as changing what happens to the patient.
IRONMAN, in the Lancet in 2022, sits between the two. It randomised 1,137 UK patients with heart failure, ejection fraction of 45% or lower and iron deficiency defined by transferrin saturation under 20% or ferritin under 100 µg/L, to intravenous ferric derisomaltose or usual care over a median 2.7 years. Heart failure hospitalisations and cardiovascular death trended lower with iron, but the primary endpoint did not reach conventional statistical significance. Supportive, not definitive, and honest reporting should say so.
Taken together the trials point the same direction. Iron helps people who are genuinely iron deficient and symptomatic. It does very little for people whose ferritin is merely lower than they would like, and it carries real downside in anyone with unrecognised HFE homozygosity, in whom routine supplementation accelerates exactly the loading that causes the damage.
Ferritin, serum iron, transferrin and transferrin saturation are measured together in every Health Blueprint at our Melbourne Preventative Health & Longevity Clinic, alongside hs-CRP, haemoglobin, MCV and liver markers, from a morning fasting sample. Every result is interpreted against published clinical authority standards rather than invented optimal ranges, which is the governing rule across The HodieLabs Evidence-Based Clinical Library. Where transferrin saturation is persistently above 45%, the pathway is HFE genotyping rather than watchful waiting, and where ferritin is high with a normal saturation, the investigation moves to the liver and metabolic panel.
If you have had a ferritin done in the last year, go and look at the report. If there is no transferrin saturation next to it and no inflammatory marker anywhere on the page, you did not have your iron measured. You had one number taken, and nobody knows what it meant.
1. World Health Organization. WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations. Geneva: WHO; 2020.
2. Allen KJ, Gurrin LC, Constantine CC, et al. Iron-overload-related disease in HFE hereditary hemochromatosis. N Engl J Med. 2008;358(3):221–230.
3. Adams PC, Reboussin DM, Barton JC, et al. Hemochromatosis and iron-overload screening in a racially diverse population. N Engl J Med. 2005;352(17):1769–1778.
4. Verdon F, Burnand B, Stubi CL, et al. Iron supplementation for unexplained fatigue in non-anaemic women: double blind randomised placebo controlled trial. BMJ. 2003;326(7399):1124.
5. Richards T, Baikady RR, Clevenger B, et al. Preoperative intravenous iron to treat anaemia before major abdominal surgery (PREVENTT): a randomised, double-blind, controlled trial. Lancet. 2020;396(10259):1353–1361.
6. Kalra PR, Cleland JGF, Petrie MC, et al. Intravenous ferric derisomaltose in patients with heart failure and iron deficiency in the UK (IRONMAN): an investigator-initiated, prospective, randomised, open-label, blinded-endpoint trial. Lancet. 2022;400(10369):2199–2209.
7. Royal College of Pathologists of Australasia. RCPA Manual: iron studies and common reference intervals.
This article is general information, not medical advice. Speak with your GP about what testing and care is appropriate for you.
Australian laboratory reference intervals run roughly 30–300 µg/L for men and 15–200 µg/L for women. The WHO 2020 guideline defines iron deficiency in healthy adults below 15 µg/L, and raises that cut-off to 70 µg/L when infection or inflammation is present.
Yes. Ferritin is an acute phase reactant, so infection, obesity, liver disease and hard training all push it up. A ferritin of 60 µg/L with a raised hs-CRP can still sit on top of empty stores. Read it with transferrin saturation and an inflammatory marker.
Usually not iron overload. Fatty liver, alcohol, obesity and inflammation explain most raised results. True overload shows up as a raised transferrin saturation, and above 45% on two fasting morning samples is the trigger for HFE gene testing.
About 1 in 200 Australians of Anglo-Celtic ancestry carry two copies of HFE C282Y. In the Melbourne HealthIron study (NEJM 2008), documented iron-overload-related disease appeared in 28.4% of male homozygotes and 1.2% of female homozygotes.
Ferritin, serum iron, transferrin and transferrin saturation, read with haemoglobin, MCV and hs-CRP. Take the sample fasting in the morning, at least 48 hours after any iron supplement, because serum iron swings with meals and time of day.
Sometimes, modestly. Verdon et al. (BMJ 2003) randomised 144 non-anaemic women with unexplained fatigue to 80 mg elemental iron or placebo. Iron won, with the benefit concentrated below a ferritin of 50 µg/L. Do not supplement speculatively, since excess iron cannot be excreted.
Full iron studies with transferrin saturation and doctor-led interpretation are included in every Health Blueprint at our Melbourne Preventative Health and Longevity Clinic.