Have you ever noticed that some patients with absolute iron deficiency, defined by a ferritin less than 10 ng/mL, never develop anemia even after years? I have been referred patients with persistently low ferritin for over four years, yet their hemoglobin has remained stable. How is that possible?
Iron is essential for many cellular processes, including mitochondrial function, myoglobin, and cytochromes. When iron is limited, the body prioritizes hemoglobin synthesis. As a result, hemoglobin levels are preserved until iron deficiency becomes severe or prolonged enough to deplete functionally available iron.
Even with ferritin <10 ng/ml, small amounts of iron may still enter the system from diet, macrophage recycling of senescent red cells, or mobilization from non–ferritin-bound pools. This minimal iron influx may be enough to support basal erythropoiesis in patients with low demand, such as postmenopausal women.
With chronic deficiency, the gut adapts by becoming more efficient at absorbing iron due to suppressed hepcidin. Meanwhile, the body continues to recycle approximately 95 percent of daily iron needs (~20-25 mg) through macrophage-mediated breakdown of aging red cells. The small dietary contribution (just 1 to 2 mg per day) covers ongoing losses through the skin, gastrointestinal tract, and menstruation.
In this way, hemoglobin becomes a late marker of iron deficiency and is fiercely defended even when iron stores are depleted. These patients are living at the edge of physiological balance, maintaining hemoglobin through a combination of increased gut absorption and efficient internal iron recycling, despite profound iron depletion.