Ferritin Interpreter.

Ferritin is the body's iron storage protein. Its serum concentration reflects total-body iron stores: ~1 ng/mL of serum ferritin corresponds to roughly 8–10 mg of stored iron. Unlike serum iron (which fluctuates hourly), transferrin saturation (which can be normal even in deficiency), or hemoglobin (which only drops once iron deficiency has progressed to anemia), ferritin tells you whether the bank account is full, empty, or overflowing.

The trade-off: ferritin is an acute-phase reactant. It rises with inflammation, infection, liver disease, and active autoimmune flare. A "normal" ferritin in the presence of high hs-CRP may actually be masking real iron deficiency, while a high ferritin without inflammation suggests true iron overload.

Pre-menopausal women lose ~30 mg of iron per menstrual cycle and have lower normal ferritin ranges than men or post-menopausal women. The WHO 2020 deficiency threshold (<15 ng/mL) is the same for all adults — but the *normal* range diverges sharply: ~30–150 ng/mL for pre-menopausal women, ~50–300 ng/mL for men and post-menopausal women.

Many "functional medicine" practitioners argue that the standard reference range is too permissive on the low end — symptomatic iron deficiency (fatigue, restless legs, hair loss, exercise intolerance) often appears at ferritin 30–50 ng/mL even with normal CBC. Recent reviews (Camaschella NEJM 2015, Pasricha Lancet 2021) support treating low-end "normal" values in symptomatic patients.

In adult men or post-menopausal women, low ferritin (<30 ng/mL) is GI blood loss until proven otherwise. Screening colonoscopy, H. pylori testing, and celiac panel are the standard workup. Iron deficiency in this population is a *symptom* — supplementation without finding the source can delay diagnosis of colon cancer.

In pre-menopausal women, the usual cause is heavy menstrual bleeding — but pregnancy losses, dietary inadequacy (especially in vegetarians and vegans), poor absorption (celiac, IBD, gastric bypass, PPI use), and athletic foot-strike hemolysis (runners) are also common.

Recent trials (Stoffel et al., Lancet Haematol 2017, 2020) have flipped the standard advice: daily iron dosing downregulates absorption via hepcidin, so *every-other-day* dosing actually moves ferritin faster and produces fewer GI side effects. Standard protocol: 60–120 mg elemental iron (e.g. 325 mg ferrous sulfate = 65 mg elemental) every other day with vitamin C, on an empty stomach if tolerated.

Coffee, tea, calcium, dairy, antacids, PPIs, and phytate-rich foods all block non-heme iron absorption — separate by 2+ hours. Heme iron (red meat, liver, oysters, dark poultry) is absorbed 15–35% regardless of these blockers. Re-check ferritin in 8–12 weeks.

Persistently elevated ferritin (>300 ng/mL women / >400 ng/mL men, with normal hs-CRP) raises concern for iron overload — most commonly hereditary hemochromatosis, which is the most common autosomal recessive disorder in people of Northern European descent (1 in 200–300 carriers in some populations).

Workup: transferrin saturation (TSAT > 45% women / 50% men is suspicious), HFE gene testing (C282Y, H63D), liver enzymes (chronic iron overload damages liver and pancreas). Confirmed hereditary hemochromatosis is treated with scheduled therapeutic phlebotomy — donating blood every few months — which lowers iron stores effectively and prevents long-term organ damage.