Ferritin is the body’s primary storage protein for iron, housing it within cells and releasing it as needed. Measuring serum ferritin provides a direct look into these iron reserves and is a highly sensitive indicator of overall iron status. A drop in ferritin is often the first sign of iron depletion, occurring long before iron deficiency anemia develops. This allows healthcare providers to identify and address low iron stores early, preventing progression to anemia.
Understanding the Role of Ferritin
The clinical value of measuring ferritin is its ability to delineate the stages of iron deficiency. A low ferritin level indicates depleted iron stores, often termed non-anemic iron deficiency when hemoglobin levels remain normal. Iron deficiency anemia, the final stage, occurs when stores are so low that the body cannot produce enough functional red blood cells, causing hemoglobin to drop. Reference ranges for serum ferritin vary, but levels below 15 to 30 nanograms per milliliter (ng/mL) generally indicate depleted stores. A low ferritin reading is the most reliable marker of true iron deficiency.
Causes Related to Blood Loss
Chronic blood loss represents the most frequent cause of iron depletion in adults, continuously draining iron reserves that diet alone often cannot replenish. This loss can be visible or hidden. In pre-menopausal women, heavy menstrual bleeding (HMB) is the most common single cause. Blood loss exceeding 80 milliliters per cycle significantly depletes iron stores over time, requiring substantially higher iron intake compared to men or post-menopausal women.
Hidden or occult blood loss often originates in the gastrointestinal (GI) tract, resulting in a steady ferritin drop without noticeable external bleeding. Conditions such as peptic ulcers, inflammatory bowel disease (IBD), polyps, or GI cancers can cause this chronic, low-grade iron loss. For any adult male or post-menopausal female with unexplained low ferritin, searching for a GI bleeding source is a standard diagnostic step.
Medications like chronic low-dose aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) contribute to occult blood loss by irritating the GI lining. Even a low daily dose of aspirin can lead to a decline in ferritin levels and increased iron deficiency. This effect is primarily due to minor, non-clinically apparent bleeding, resulting in a slow but consistent depletion of stored iron.
Causes Related to Intake and Absorption Issues
A second major category of causes relates to the body’s inability to acquire or properly process iron from food. Inadequate dietary intake is a common factor, particularly in individuals following strict plant-based diets. Iron exists in two forms: highly bioavailable heme iron found in animal products, and non-heme iron found in plants. Non-heme iron absorption is inhibited by compounds like phytates in grains and legumes, meaning that a vegetarian or vegan diet may require up to 1.8 times the iron intake to compensate for lower absorption.
Malabsorption syndromes represent a severe barrier to maintaining iron stores, interfering with iron uptake in the gut. Celiac disease damages the villi of the small intestine, specifically the duodenum, the primary site for iron absorption. This damage reduces the surface area available for uptake, leading to iron deficiency even with adequate dietary intake. Inflammatory bowel diseases like Crohn’s disease and ulcerative colitis also impair absorption due to chronic inflammation and damage to the intestinal lining.
Surgical alterations to the digestive tract, most notably gastric bypass and other bariatric procedures, drastically reduce iron absorption. These surgeries often bypass the duodenum, the segment of the small intestine where the majority of iron is absorbed. Furthermore, the reduction in stomach acid following surgery hinders the conversion of ferric iron into the more absorbable ferrous form. Iron deficiency and subsequent ferritin drops are a common, long-term complication.
Causes Related to Increased Physiological Demand
Situations that place a high demand on the body’s iron resources can quickly deplete ferritin stores. Pregnancy is a prime example, as the total iron requirement increases by approximately 1000 milligrams to support the expanding maternal red cell mass, fetal growth, and compensate for delivery blood loss. This demand is highest in the second and third trimesters, often leading to iron deficiency if supplemental iron is not used.
Periods of rapid growth, such as infancy and adolescence, also accelerate the depletion of iron stores. The pubertal growth spurt requires significant iron to support the rapid expansion of muscle mass and total blood volume. For adolescent girls, this growth demand is compounded by the onset of menstrual blood loss, making them a vulnerable group.
Intense physical activity in endurance athletes can create an imbalance between iron supply and demand. This deficiency results from factors like chronic GI bleeding and the mechanical destruction of red blood cells in the feet (foot-strike hemolysis). Exercise-induced inflammation also elevates the hormone hepcidin, which blocks the release of stored iron and inhibits its absorption, causing ferritin stores to drop.