Iron (Fe) is a tightly metabolically controlled mineral and growth factor for all living cells. Iron not bound in erythrocyte hemoglobin is transported by the plasma iron transport protein transferrin (Tf) and bound within cells by ferritin. Apo-Tf and apo-hemopexin are also known to be made locally in the retina. Free Fe is cytotoxic, promotes oxidation/lipid peroxidation, has been implicated as a risk factor in cardiac disease, and is itself associated with age-related macular degeneration (ARMD), the leading cause of blindness in aging western societies. The authors evaluated Fe overload serum markers and dietary intake in patients with atrophic ARMD. After obtaining informed consent, an Fe panel consisting of serum Fe, total Fe binding capacity (TIBC), and ferritin was performed on 75 veterans (70 men, five women) with an average age of 75 years with a diagnosis of atrophic ARMD by combined criteria of International Retinal Classification and psychophysical/symptom abnormalities. Tf saturation was calculated by dividing serum Fe concentration by TIBC. Dietary iron with and without supplementation and vitamin C intake were determined for 86 patients using the Harvard School of Public Health/Department of Nutrition Food Frequency Questionnaire. Statistically significant correlations (P <0.1) were found between serum and dietary Fe (r = -.26), between serum Fe and serum ferritin (r =.34), and between dietary Fe and dietary vitamin C (r =.30). The data on mostly male geriatric veterans with atrophic ARMD indicate that single time-point assessment of systemic Fe status and dietary Fe is not useful. However, serial multiple-year data, correlating Fe markers with disease, may still be important. Also, because Fe transport proteins do not cross the blood-retina barrier, the local cellular toxic effects of Fe must also be considered.