Ferritin

Blood

Iron Studies

Ferritin is the protein that stores iron in your body, so its level reflects how much iron you have in reserve. It also acts as an acute-phase reactant, meaning it rises with inflammation independent of iron status. A preventive practice tracks ferritin as both a gauge of iron stores and a clue to underlying inflammation.

What It Measures

Iron storage protein; also acute-phase reactant (rises with inflammation)

Optimal vs. Lab Range

Longevity Optimal

40–100 ng/mL (M), 40–80 (F)

Target range for optimal health and longevity based on research.

Standard Lab

12–300 ng/mL (M), 12–150 (F)

Population-based reference range from standard labs.

Why It Matters

Low ferritin is the clearest sign of depleted iron stores and iron deficiency, the most common nutrient deficiency worldwide, and can drive fatigue, restless legs, and hair loss even before anemia appears. High ferritin is more complex: it may indicate genuine iron overload such as hemochromatosis, but it can also be falsely elevated by inflammation, liver disease, or infection. Because of this dual nature, an elevated ferritin should not be assumed to mean too much iron without considering inflammatory context. Interpreting it alongside serum iron, TIBC, transferrin saturation, and hs-CRP is essential to distinguish iron status from inflammation.

When Low

Iron deficiency (most common nutrient deficiency globally), fatigue, restless legs, hair loss

When High

Iron overload (hemochromatosis), inflammation (false elevation), liver disease, infection

How to Optimize

The right direction depends entirely on the cause. If ferritin is low from deficiency, physician-guided iron supplementation and attention to dietary iron are appropriate, ideally after confirming the underlying reason. If it is genuinely elevated from iron overload, physician-directed phlebotomy may be indicated, whereas an inflammation-driven elevation calls for a workup of the underlying cause rather than iron removal. Because misreading the direction can cause harm, changes should follow a full iron-studies interpretation. Targets and treatment are individualized with your physician; this content is educational and not a substitute for medical advice.

Key Interventions & Linked Compounds

Strong evidence

Key Interventions

Iron supplementation (if deficient)

phlebotomy (if overloaded)

inflammation workup

Linked Compounds & Supplements

Iron bisglycinate

Vitamin C (absorption)

Lactoferrin

Curated from clinical literature. Individual results vary; consult a qualified clinician before changing a protocol.

Ordering Notes

Specimen

Serum or plasma (venous draw)

Patient prep

No fasting required. Maintain usual diet and medications unless advised.

Recommended cadence

Semi-annual

Reporting unit

Confirm with the performing lab — units vary by region.

Pre-analytic notes

Standardize draw time of day, hydration, and recent exercise. Note any acute illness, supplements, or hormonal therapies on the requisition.

Recommended Follow-Up Actions

1
Confirm the result is reliable
Repeat abnormal values before acting — preferably from the same lab, same time of day, and under consistent prep. Rule out acute illness, recent intense exercise, or medication effects that can shift Ferritin.
2
Compare against optimal, not just lab range
Use the optimal window above as the target. Lab "normal" is built from the general population and often misses early dysfunction.
3
Pair with related markers
Order a complementary panel covering metabolic, inflammatory, and hormonal context to interpret this marker properly.
4
Discuss interventions with a clinician
Use the interpretation guidance above to frame the conversation. Bring trends, not just one datapoint, to your visit.
5
Re-test on a defined cadence
If a change is implemented, re-measure in 8–12 weeks for fast-moving markers, or 3–6 months for slower ones, to confirm response before escalating.