Over the past 3 decades, increasing incidence of hepatic iron storage disease has been documented in captive birds, particularly associated with frugivorous species of the families Paradiseadae (birds of paradise), Ramphastidae (toucans), and Sturnidae (starlings). Hematology and serum biochemical analyses are of little diagnostic value for assessment of iron storage disease in birds. A liver biopsy is needed to confirm the condition antemortem; enlargement of the liver, heart, or spleen is often seen radiographically. Both a genetic predisposition for altered regulation of intestinal iron uptake in sensitive species, as well as dietary factors influencing iron metabolism, are considered important in understanding the development and management of this condition. Physiological mechanisms that may have evolved to compensate for a low bioavailability of dietary iron in situ appear to contribute to iron storage disease in managed feeding programs. Although dietary iron requirements of frugivorous species remain unknown, many practical diets contain higher iron concentrations of greater bioavailability compared with domestic poultry recommendations (50–120 mg/kg) due to specific ingredients and/or nutrient interactions in mixed diets=mthe latter including effects of other minerals, ascorbic acid, polyphenols, and specific sugars. Treatment of the disease includes phlebotomy, targeted iron chelation therapy, and diet alteration. Current recommendations for managing this multifactorial issue include: analysis of dietary iron and vitamin C concentrations, particularly those of iron-sensitive species; formulation of low iron diets; minimization or elimination of animal proteins in diets of frugivorous birds; ascorbic acid levels < 100 mg/kg and/or the feeding of vitamin C-containing foods separately. Further study of possible interactions among dietary sugars, minerals, natural chelators (for example tannins, fiber, phytates) and iron metabolism in avian species is encouraged.