Vitamin A deficiency (VAD) and iron deficiency anemia coexist around the world, particularly in children and women of reproductive age in low- and middle-income countries. Within this scenario, there is a known interaction between vitamin A and iron, and it has been postulated that lack of vitamin A impairs iron metabolism, leading to vitamin A deficiency anemia (VADA). Current animal, epidemiological, and clinical studies support this notion. The objective of this study was to review the current literature on proposed metabolic mechanisms regarding how VAD modulates iron metabolism leading to anemia. To attain this objective, a literature search was conducted of research publications in the related field, without date restriction, using PubMed, Scopus, Google Scholar, and the University of Illinois’s reference system. The data support the essentiality of vitamin A for normal erythropoiesis. It indicates that, in VAD, iron mobilization is impaired, and that this mineral accumulates in the liver and spleen, making it less available for erythropoiesis. A triggering factor for the development of VADA seems to be inflammation and systemic infection, which release cytokines that upregulate the production of hepcidin by the liver. VAD may also increase hepcidin directly without the involvement of inflammation or infection. The elevated hepcidin, in turn, lowers circulating iron and sequesters iron in storage depots, downregulating erythropoietin, leading to inefficient erythropoiesis, decreased hemoglobin (Hb) production, and (subsequently) anemia. VAD may also impact the expression of iron regulatory protein 2 (IRP2), and thus affect intracellular iron metabolism gene expression. VADA is not due to iron deficiency, but to a redistribution of iron in the body. Understanding the mechanism of VADA will assist in designing more effective strategies for combating anemia worldwide.