Ferritin: Normal Range, What Low and High Levels Mean for Iron Stores

Most of your body's iron sits in hemoglobin. The remainder is stored — primarily in the liver, spleen, and bone marrow — bound to ferritin protein. A small amount of ferritin leaks into circulation and the level there correlates with total stored iron. Roughly 1 ng/mL of serum ferritin equals about 8–10 mg of stored iron.

Ferritin is also an acute-phase reactant — it rises with inflammation. This is the single biggest interpretive trap. A "normal" ferritin in someone with active inflammation can mask underlying iron deficiency. If ferritin and hs-CRP are both elevated, the ferritin number is misleading.

Lab reference ranges vary widely (as low as 11 to as high as 300+ ng/mL) but the clinically useful cutoffs are tighter:

• Below 15 ng/mL: definite iron deficiency, regardless of hemoglobin.
• 15–30 ng/mL: probable iron deficiency, especially with symptoms.
• 30–50 ng/mL: low normal. Increasingly recognized as suboptimal — many people are symptomatic in this range.
• 50–200 ng/mL: healthy stores for most adults.
• 200–500 ng/mL: elevated. Usually inflammation, fatty liver, or alcohol; sometimes early hemochromatosis.
• Above 500 ng/mL: high. Iron overload (hemochromatosis), severe inflammation, malignancy, or hyperferritinemia syndromes.
• Above 1000 ng/mL: warrants workup; iron overload or systemic disease likely.

For symptoms that improve with iron repletion (fatigue, restless legs, hair loss, exercise intolerance), many specialists target ferritin above 50 — sometimes above 100 in restless legs syndrome.

Most cases of high ferritin are not iron overload. The differential, in rough order of frequency:

• Inflammation — anything from a viral illness to an autoimmune flare to obesity-driven low-grade inflammation. Check hs-CRP.
• Fatty liver disease (MASLD/NASH) — extremely common; can push ferritin into the 300–800 range.
• Alcohol use — heavy alcohol raises ferritin via liver injury and direct hepatic iron loading.
• Metabolic syndrome — insulin resistance and visceral fat both elevate ferritin.
• Hemochromatosis — genetic iron overload (HFE C282Y homozygous most common). Diagnosed with transferrin saturation > 45% plus elevated ferritin, then genetic testing. Affects roughly 1 in 200–300 people of Northern European descent.
• Cancer — particularly hematologic malignancies and liver cancer.
• Recurrent transfusions — each unit of blood adds about 200 mg of iron.

If ferritin is elevated, also order transferrin saturation (TSAT). High ferritin + high TSAT (above 45%) suggests iron overload. High ferritin + normal TSAT usually means inflammation or fatty liver.

Low ferritin always means low iron stores, even when other tests look normal. There is no false-low ferritin — only false-normal in inflammation. Common causes:

• Heavy menstrual bleeding — the leading cause in pre-menopausal women.
• Pregnancy — physiologic depletion in the second and third trimesters.
• Inadequate dietary iron — vegetarian/vegan diets without attention to iron, restrictive eating, post-bariatric surgery.
• Gastrointestinal blood loss — colorectal cancer, peptic ulcer, celiac disease, chronic NSAID use. In any adult man or postmenopausal woman with iron deficiency, GI workup is mandatory until proven otherwise.
• Malabsorption — celiac disease, atrophic gastritis, H. pylori, post-gastric surgery.
• Chronic illness, kidney disease, dialysis.

Symptoms of iron deficiency without anemia (often missed): fatigue, exercise intolerance, hair loss, brittle nails, restless legs at night, brain fog, cold intolerance, frequent infections, pica (craving ice or non-food items).

How to correct:

• Oral iron — ferrous sulfate, ferrous bisglycinate (chelated form is better tolerated), or polysaccharide-iron complex. Take with vitamin C; avoid taking with calcium, coffee, or tea.
• Every-other-day dosing is often more effective than daily — recent studies show daily iron raises hepcidin and blocks the next dose.
• IV iron — for severe deficiency, malabsorption, intolerance to oral iron, or pregnancy where rapid repletion matters. Modern formulations (iron carboxymaltose, iron isomaltoside) require fewer infusions and have an excellent safety profile.
• Recheck ferritin in 6–8 weeks. Hemoglobin recovers in 4–6 weeks; ferritin takes longer. Continue treatment for 3–6 months after ferritin normalizes to fully refill stores.

Three patterns to recognize:

• Low ferritin, normal hemoglobin — iron deficiency without anemia. Symptoms may be substantial. Treat.
• Low ferritin, low hemoglobin — iron deficiency anemia. Treat and look for the cause of blood loss.
• Normal ferritin, low hemoglobin, elevated hs-CRP — likely "anemia of inflammation." The ferritin can be falsely reassuring. Check transferrin saturation; if it is low, iron deficiency may still be present.

For tracking response to treatment, a serial ferritin every 6–12 weeks tells you whether stores are refilling. Stable ferritin above 50 ng/mL with adequate dietary intake is the goal for most patients.

• Ferritin below 30 in any adult — treat. In men or postmenopausal women, also investigate for GI blood loss.
• Ferritin above 500 — workup for cause. Order transferrin saturation, hs-CRP, ALT, AST, and consider HFE genotyping.
• Ferritin above 1000 — urgent workup. Hemochromatosis, malignancy, hemophagocytic lymphohistiocytosis, and other serious causes need to be excluded.
• Iron deficiency that recurs after treatment — find the source. Persistent unexplained iron deficiency is a colorectal cancer flag.

• Hemoglobin and complete blood count — anemia detection and red cell indices (low MCV in iron deficiency).
• Transferrin saturation (TSAT) — calculated from serum iron and TIBC. Low in iron deficiency, high in iron overload.
• Serum iron and total iron binding capacity (TIBC) — components of TSAT.
• hs-CRP — interpret ferritin cautiously when CRP is elevated.
• Reticulocyte hemoglobin content (CHr) — detects iron-restricted erythropoiesis early.
• HFE genetic testing — for suspected hereditary hemochromatosis.