
Ferritin
Serum Ferritin
What it is
Ferritin is the body's primary iron storage protein — a large spherical protein complex found inside cells that can sequester up to 4,500 iron atoms in a non-toxic, soluble form. A small fraction of ferritin is secreted into the blood, where its concentration provides an indirect measure of total body iron stores. Under iron-deficient conditions, cells release less ferritin; under iron excess, more ferritin is produced and more appears in serum. This makes serum ferritin the most sensitive and reliable non-invasive marker of iron status — far more informative than serum iron alone, which fluctuates significantly with meals and time of day. However, ferritin is also an acute-phase reactant. Like hsCRP and fibrinogen, ferritin production increases significantly in response to inflammation, infection, liver disease, and malignancy — independent of iron status. This means an elevated serum ferritin can reflect either iron overload or an inflammatory state, and the two causes require very different responses. Reading ferritin alongside hsCRP and IL-6 in the same Pulse draw is essential for distinguishing between them.
Why we measure it
Both ends of the ferritin spectrum carry clinical significance. Iron deficiency — even in the absence of frank anaemia — has measurable effects on cellular energy metabolism, cognitive function, immune competence, and physical performance. The brain and skeletal muscle are particularly sensitive to iron availability; iron-deficient individuals without anaemia consistently demonstrate impaired exercise capacity and cognitive performance compared to iron-replete controls. Iron deficiency is the most prevalent nutritional deficiency globally, and its non-anaemic form is substantially underdiagnosed because standard panels frequently check haemoglobin rather than ferritin. At the other extreme, iron overload drives oxidative damage through the Fenton reaction — a chemical process in which excess free iron catalyses the production of hydroxyl radicals, one of the most reactive and damaging of all reactive oxygen species. These radicals attack DNA, proteins, and lipid membranes. Hereditary haemochromatosis — caused by mutations in the HFE gene measured in the Foundation layer of the protocol — is the most common inherited cause of iron overload in populations of Northern European descent. It is largely asymptomatic until organ damage to the liver, pancreas, heart, and joints is already established. From an inflammatory standpoint, a rising ferritin in the context of elevated hsCRP and IL-6 is more likely to reflect a worsening inflammatory state than true iron loading. Conversely, an isolated ferritin elevation with normal inflammatory markers warrants investigation for iron overload. This contextual interpretation is one of the key advantages of a multi-marker protocol — no single reading exists in isolation.
Why every 3 months
Iron stores change slowly under stable dietary and metabolic conditions — typically over months rather than weeks. Quarterly measurement provides adequate resolution to track the direction of iron status without overtesting. It also provides sufficient density to identify when a rising ferritin is accompanied by rising inflammatory markers (suggesting inflammation) versus rising in isolation (suggesting iron loading). For individuals with haemochromatosis or a family history of it, quarterly monitoring of ferritin is a clinically standard part of management.
What movement means
Reference ranges for serum ferritin vary significantly by laboratory, sex, and age. The World Health Organization defines iron deficiency in adults as serum ferritin below 15 µg/L, with a higher threshold of below 30 µg/L used in some clinical contexts to account for the acute-phase reactant effect. Upper reference limits for normal vary considerably across guidelines. The ranges below reflect commonly used laboratory reference values and WHO definitions — not a single authoritative clinical diagnostic threshold.
Deficient
< 15 µg/L
The WHO threshold for iron deficiency in adults. At this level, iron stores are depleted.
World Health Organization. Serum Ferritin Concentrations for the Assessment of Iron Status. 2011
Low-normal
15 – 30 µg/L
Iron stores present but reduced. Some clinical guidelines use 30 µg/L as a conservative lower threshold, particularly in premenopausal women or where inflammatory confounding is possible.
Ganz T, Physiological Reviews, 2013; WHO Serum Ferritin Reference Values
Normal
30 – 200 µg/L (women) / 30 – 300 µg/L (men)
Within standard laboratory reference ranges for most adult populations. Wide variation between laboratories.
Standard laboratory reference ranges — vary by institution
Elevated
> 200 µg/L (women) / > 300 µg/L (men)
Above standard reference limits. Warrants contextual interpretation: if inflammatory markers are also elevated, inflammation is a likely contributor. If inflammatory markers are normal, iron overload or liver disease should be considered.
Clinical practice guidance — Adams PC et al., New England Journal of Medicine, 2005
In the protocol
References
- 1.
Ganz T. “Systemic Iron Homeostasis.” Physiological Reviews. 2013.
- 2.
World Health Organization. “Serum Ferritin Concentrations for the Assessment of Iron Status and Iron Deficiency in Populations.” WHO Vitamin and Mineral Nutrition Information System. 2011.
- 3.
Adams PC, Reboussin DM, Barton JC, et al.. “Hemochromatosis and Iron-Overload Screening in a Racially Diverse Population.” New England Journal of Medicine. 2005.
- 4.
Camaschella C. “Iron-Deficiency Anemia.” New England Journal of Medicine. 2015.
- 5.
Wish JB. “Assessing Iron Status: Beyond Serum Ferritin and Transferrin Saturation.” Clinical Journal of the American Society of Nephrology. 2006.