Ferritin is a protein that stores iron within cells, acting as the body’s primary iron reservoir. Measuring the concentration of ferritin in the serum or plasma provides the most effective means for clinicians to gauge the body’s total iron reserves. This simple blood test offers a reliable, indirect assessment of the iron stores held within various organs and tissues.
The Role of Ferritin in Iron Homeostasis
Ferritin manages iron balance by keeping the mineral in a soluble, non-toxic form, preventing the formation of damaging free radicals. The majority of the body’s iron stores are housed within ferritin molecules primarily located in the liver, spleen, and bone marrow. This intracellular storage mechanism ensures iron is readily available when the body requires it for processes like red blood cell production.
While ferritin is predominantly an intracellular protein, a small amount is secreted into the bloodstream. The concentration of this circulating serum ferritin reliably reflects the amount of iron stored inside the cells. For healthy adults, typical reference ranges for serum ferritin are 30 to 300 nanograms per milliliter (ng/mL) for men and 10 to 200 ng/mL for women. Measuring this small fraction in the blood allows for a non-invasive estimate of overall iron status.
Interpreting Low Ferritin Levels and Iron Deficiency
A low serum ferritin concentration directly indicates that the body’s iron stores are depleted. The progression of iron depletion occurs in distinct stages, beginning with the exhaustion of storage iron before affecting functional iron. In the first stage, storage iron depletion, ferritin levels drop below the standard threshold, often below 30 ng/mL, even while hemoglobin (Hb) and mean corpuscular volume (MCV) remain within normal limits.
If the negative iron balance continues, the condition progresses to iron-deficient erythropoiesis, where there is not enough iron to support normal red blood cell production. The body attempts to compensate by increasing the amount of transferrin, the iron transport protein, but the percentage of iron bound to it (transferrin saturation) drops significantly. Only in the final stage, iron deficiency anemia, do the hemoglobin and MCV levels fall, indicating a reduced capacity to carry oxygen.
Common causes for this depletion include chronic blood loss, such as heavy menstrual bleeding or occult bleeding from the gastrointestinal tract. Dietary iron insufficiency, particularly in vegetarian or vegan diets where iron is less bioavailable, is another frequent contributor. Conditions that impair nutrient absorption, like celiac disease or inflammatory bowel disease, can also prevent the body from obtaining sufficient iron.
Individuals with low ferritin may experience nonspecific indications that precede full-blown anemia, such as fatigue and weakness. Other specific findings include pallor, a strong desire to eat non-food items like ice or dirt (pica), and restless leg syndrome. Because ferritin is the first parameter to fall, identifying a low level allows for intervention before the onset of anemia.
Understanding Elevated Ferritin Levels
Elevated ferritin levels are complex to interpret because ferritin serves a dual role as both an iron storage marker and an acute phase reactant. When ferritin is elevated due to true iron overload, it reflects an excess of stored iron that can accumulate and damage organs. Hereditary Hemochromatosis (HH) is the most common genetic disorder resulting in this condition, typically caused by a mutation in the HFE gene.
In HH, the body absorbs a high percentage of dietary iron, leading to its deposition in organs like the liver, heart, and pancreas. Early signs of true iron overload include an elevated transferrin saturation (TSAT), often above 45 percent, which indicates that the circulating iron transport proteins are oversaturated. This pattern of high ferritin and high TSAT is highly suggestive of iron overload.
The second, non-iron-related cause of high ferritin is its function as an acute phase reactant, meaning its levels rise in response to inflammation. Conditions such as chronic kidney disease, autoimmune disorders like rheumatoid arthritis, infections, and liver diseases can all trigger a ferritin increase independent of total iron stores. The mechanism involves inflammatory signals, such as the cytokine Interleukin-6 (IL-6), which stimulate the production of the hormone hepcidin.
Hepcidin traps iron inside storage cells, preventing its release into the circulation and reducing its availability for red blood cell production. This process can lead to the anemia of inflammation, where ferritin is high while circulating iron is low. To distinguish between true iron overload and inflammation-driven elevation, clinicians examine the full iron panel: in inflammation, high ferritin is usually accompanied by a low or normal TSAT, unlike the high TSAT seen in iron overload states.