Presence of porotic hyperostosis has been frequently used in the anthropologic literature as evidence of iron deficiency anemia. This perspective appears to represent a hypothesis that may not have been adequately tested. Any process which increases marrow activity (evidenced by porotic hyperostosis) increases consumption of basic nutrients. Iron stores, often low to begin with, are typically the most rapidly depleted. Thus, individuals with hemoglobinopathies or hemolytic anemia develop the "hair on end" phenomenon and only subsequently become deficient of iron. Even those clinical reports (which claim occurrence of diploic skull changes in patients with iron deficiency) report a very low frequency of the phenomenon. The only identified study of the frequency of skull changes in iron deficiency (Agarwal et al. 1970) revealed a frequency of only 0.68%! This certainly does not support iron deficiency as the explanation for the high frequency of porotic hyperostosis noted (approximating 50%) in some populations. There is also no relationship of degree of anemia or of iron deficiency to occurrence of the "hair on end" phenomenon of porotic hyperostosis. What then is the significance of porotic hyperostosis?. Ascribing high population frequency occurrence of porotic hyperostosis to iron deficiency anemia no longer seems tenable. Perhaps further exploration of presence of genetic hemolytic anemias, parasite exposure, hemoglobinopathies, and nutritional bases will prove enlightening