- • Primary status marker: serum ferritin (target >50 ng/mL for most indications)
- • Preferred form: iron bisglycinate (better tolerability, equivalent absorption)
- • Inhibitors: tea, coffee, calcium within 2 hours of dose
- • Enhancers: vitamin C 100mg with dose
- • Populations at risk: menstruating women, vegetarians, postpartum
Iron is an essential mineral required for hemoglobin synthesis, oxygen transport, mitochondrial electron transport, and dopamine synthesis. Iron deficiency progresses through stages: depleted stores (low ferritin with normal hemoglobin), iron-deficient erythropoiesis, and finally iron deficiency anemia. Functional effects on fatigue, cognition, and mood can occur at ferritin levels well above the hematologic threshold for anemia, which is why target ferritin above 50 ng/mL is used clinically for symptomatic indications rather than the WHO anemia threshold of 15 ng/mL.
Iron deficiency predicts multiple conditions. In ADHD children, 84% have ferritin below 30 ng/mL versus 44 ng/mL in controls, with ferritin inversely correlating with symptom severity (Konofal et al., 2004). Postpartum ferritin below 50 ng/mL predicts approximately 4-fold higher postpartum depression risk (Albacar et al., 2011). Iron deficiency contributes to restless legs syndrome, hair loss, and reduced exercise capacity before overt anemia develops. Menstruating women, vegetarians, endurance athletes, blood donors, and postpartum women represent elevated-risk populations warranting screening.
Supplementation with iron bisglycinate (25-65mg elemental) offers improved gastrointestinal tolerability compared to traditional ferrous sulfate at equivalent absorption. Take with 100mg vitamin C to enhance non-heme iron absorption and separate from calcium, tea, coffee, and antacids by at least 2 hours. Alternate-day dosing reduces hepcidin-mediated absorption blockade and may be more efficient than daily dosing. Target ferritin above 50 ng/mL typically requires 8-12 weeks of consistent supplementation. Chronic iron supplementation without confirmed deficiency risks iron overload, especially in individuals with hereditary hemochromatosis variants.