The short version
Ferritin measures your iron stores and is the best single first test for deficiency — with one important catch: it is an acute-phase reactant, so infection, inflammation, liver disease and obesity all push it up and can mask a genuine deficiency. Serum iron measures the iron circulating right now, which changes hour to hour and jumps sharply after an iron tablet, so it means very little alone. TIBC (and transferrin) measures carrying capacity, which rises when stores are low. Transferrin saturation is the ratio — low in deficiency, high in overload. Your clinician reads the pattern, not any one number.
Ferritin: your iron savings account (and its blind spot)
Ferritin is the protein that stores iron inside cells. A small amount leaks into the bloodstream in proportion to how much iron is banked, which makes serum ferritin a reasonable proxy for total body stores. In a systematic review of diagnostic tests for iron deficiency anaemia, ferritin outperformed mean cell volume and transferrin saturation as a predictor — which is why most clinicians order it first.
Thresholds are where it gets genuinely messy, and it is worth knowing that experts disagree. The World Health Organization's 2020 guideline uses ferritin below 15 µg/L to define iron deficiency in apparently healthy adults. Many haematology and gastroenterology sources use a more liberal cutoff: the American Gastroenterological Association's 2020 guideline explicitly advises a ferritin cutoff of 45 ng/mL rather than 15 ng/mL when diagnosing iron deficiency in a patient who is already anaemic, because the lower number misses too many people. A ferritin under 30 µg/L has been reported with around 92% sensitivity for iron deficiency anaemia. Meanwhile, several laboratories still report a "normal" range starting at 10 or 12 µg/L — a range built largely from unselected populations that included plenty of iron-depleted women. That mismatch is a live debate in haematology, not settled science, and it is the single most common reason a woman is told her iron is "fine" when it isn't. If your result sits in that 15–50 zone with symptoms, it is a reasonable thing to raise with your clinician rather than accept as normal. Our guide to a low ferritin result goes deeper on what happens next.
The blind spot: ferritin is an acute-phase reactant. Interleukin-6 and other inflammatory signals tell the liver to make more of it. So a recent infection, a flare of rheumatoid arthritis or inflammatory bowel disease, chronic kidney disease, heart failure, fatty liver disease, heavy alcohol use, hyperthyroidism and obesity can all lift ferritin into the "normal" band while your stores are actually empty. This is why WHO makes a conditional recommendation (low certainty of evidence) to use a higher ferritin threshold — 70 µg/L in adults — when inflammation is present, and why a CRP is often drawn alongside. In chronic inflammatory conditions, many specialists treat ferritin under 100 µg/L, or 100–300 µg/L with a transferrin saturation under 20%, as consistent with iron deficiency.
Why is serum iron nearly useless on its own?
Serum iron is a snapshot of the iron bound to transferrin in your blood at the moment of the draw. It is genuinely volatile:
- Time of day. Serum iron tends to peak in the morning and fall through the day toward a low point near midnight — though studies show the pattern is not consistent in everyone. Day-to-day variation within the same person runs roughly 25–30%.
- Recent iron intake. Blood drawn about three hours after an oral iron dose can show serum iron three to five times higher. Even a multivitamin containing 18 mg of elemental iron can do it. This is why labs commonly ask you not to take an iron supplement in the 24 hours before the draw, and why testing is often scheduled for the morning after an overnight fast. Do not stop a prescribed supplement on your own to game a test — ask the ordering clinician how they want it timed. (See timing iron supplements and our overview of iron supplements.)
A single normal serum iron does not rule out deficiency, and a single low one does not confirm it. Its real job is to feed the transferrin saturation calculation.
TIBC and transferrin: the delivery fleet
Transferrin is the protein that ferries iron through the blood. TIBC (total iron-binding capacity) estimates how much iron all that transferrin could carry if fully loaded. The counterintuitive part: when stores fall, the body makes more transferrin, so TIBC goes up. High TIBC with low serum iron is a classic deficiency signature. In iron overload, TIBC tends to be low or low-normal. TIBC also falls in chronic inflammation, malnutrition and liver disease, because transferrin is a negative acute-phase protein — which is exactly what separates anaemia of inflammation from straightforward deficiency.
Transferrin saturation: the most practical single ratio
Transferrin saturation (TSAT) is serum iron divided by TIBC, expressed as a percentage — how full the delivery fleet is. Roughly 20–45% is a common reference band, though this varies by laboratory.
Below about 20% points toward insufficient iron reaching the bone marrow, and TSAT is especially useful when ferritin is unreliable because of inflammation. Above 45% points the other way: the American Association for the Study of Liver Diseases uses a fasting transferrin saturation of 45% as the screening threshold for haemochromatosis, a level that identifies close to all C282Y homozygotes, with higher values increasing specificity. Because TSAT inherits serum iron's volatility, it is usually confirmed on a repeat fasting sample before anyone acts on it.
Where the CBC fits: haemoglobin, MCV and reticulocytes
The iron panel tells you about supply. The complete blood count tells you what the bone marrow managed to build with it.
- Haemoglobin defines anaemia. Crucially, iron deficiency happens before anaemia — you can have an empty tank and a normal haemoglobin, which is why "your haemoglobin is normal" doesn't close the question.
- MCV (average red cell size) falls late in iron deficiency, producing small, pale cells. A normal MCV is common in early deficiency, and can also be a mixed picture if B12 or folate deficiency (which enlarges cells) is present at the same time.
- Reticulocytes are newly released red cells. A low reticulocyte count suggests the marrow isn't producing; a rising count after iron is started is an early sign of response. Some labs also report reticulocyte haemoglobin content, which reflects iron availability within days rather than weeks.
| Pattern | Ferritin | Serum iron | TIBC | TSAT | Typical picture |
|---|---|---|---|---|---|
| Iron deficiency | Low | Low | High | Low (<20%) | Depleted stores; marrow starved of iron. Cause still needs finding. |
| Anaemia of inflammation | Normal or high | Low | Low or normal | Low | Iron is present but locked in storage by hepcidin. CRP often raised. |
| Mixed (deficiency + inflammation) | Normal-ish (falsely reassuring) | Low | Low or normal | Low | The hardest pattern; higher ferritin thresholds or extra tests may be used. |
| Iron overload / haemochromatosis | High | High | Low | High (>45% fasting) | Prompts repeat fasting testing and, often, genetic evaluation. |
| High ferritin, normal TSAT | High | Normal | Normal | Normal | Usually inflammation, liver disease, alcohol or metabolic causes — not overload. |
What if the panel is ambiguous?
When inflammation muddies ferritin, clinicians sometimes add soluble transferrin receptor (sTfR) or the sTfR–ferritin index, which are less affected by inflammation. These are not universally available, assays are not well standardised between laboratories, and cutoffs vary — so treat them as useful extras rather than a clean tiebreaker. In some cases the honest answer is a supervised trial of iron with repeat testing, or a bone marrow assessment in rare unclear situations.
Practical things that change your numbers
- Ask whether to fast and whether to hold supplements the day before — then follow whatever the ordering clinician says.
- Recent illness, vaccination, surgery or a flare can raise ferritin for days to weeks. Retesting when you're well often gives a truer reading.
- Reference ranges differ by laboratory, assay and units (µg/L and ng/mL are numerically equivalent for ferritin). Compare results to the range printed on your own report.
- A single reading is a data point, not a verdict. Trends over time are far more informative.
- Recent blood donation, pregnancy, endurance training and heavy periods all shift iron status in ways worth mentioning at the appointment.
If you want help organising what your report says before that appointment, our lab results explainer tool walks through common values, and the iron and anaemia hub collects the rest.
When to see a doctor
Interpretation and any treatment decision belongs to a clinician who knows your history. Book an appointment if:
- You have symptoms of iron deficiency — persistent fatigue, breathlessness on stairs, hair shedding, restless legs, cravings for ice — whether or not your haemoglobin is normal.
- Your ferritin is low, or your ferritin is normal but transferrin saturation is under about 20%.
- Your transferrin saturation is above 45%, or ferritin is persistently high. This warrants proper evaluation, not self-treatment.
Seek prompt medical care if you are postmenopausal and anaemic, or have any bleeding after menopause. Iron deficiency anaemia in a postmenopausal woman or in a man is treated as occult gastrointestinal blood loss until proven otherwise — the American Gastroenterological Association strongly recommends bidirectional endoscopy (upper endoscopy plus colonoscopy) in this group. This is not a wait-and-see finding. More in anaemia after menopause.
Go to urgent or emergency care for chest pain, fainting, severe breathlessness at rest, a racing heart that won't settle, black or tarry stools, visible blood in stool or vomit, or bleeding heavy enough to soak through a pad an hour. Severe anaemia and active bleeding are emergencies, and their symptoms overlap with cardiac ones.
Nothing here is a dose, a diagnosis, or a reason to start, stop or change any supplement or medication — those are prescriber decisions.



