Implications of Reappraising the Iron‐Deficiency Anemia Hypothesis

Abstract In 2009, Walker and colleagues questioned the validity of the iron‐deficiency anemia hypothesis as an explanatory mechanism for the presence of porotic hyperostosis (PH) and cribra orbitalia. They presented evidence demonstrating that iron deficiency inhibits, rather than promotes, marrow hypertrophy and argued a link between both PH and hemolytic or megaloblasic anemias (including vitamin B 12 deficiency). This paper suggests that dismissing the iron‐deficiency anemia hypothesis may be premature, but, if dismissed, may result in unforeseen consequences. Vitamin B 12 deficiency and iron deficiency often result from similar proximate causes, i.e. lack of animal protein in the diet and sanitation problems that lead to parasitic or diarrheal diseases, thereby promoting nutrient losses. As a result, vitamin B 12 deficiency and iron deficiency commonly co‐occur. In individuals with a co‐occurrence of iron deficiency and vitamin B 12 deficiency, a possible inhibition of marrow hypertrophy caused by iron deficiency may prevent the development of PH, despite the presence of (vitamin B 12 ) nutritional deficiency. The implications of dismissing the iron‐deficiency anemia hypothesis are that many skeletal populations may exhibit hidden heterogeneity, i.e. individuals who are the most nutritionally stressed, with multiple nutrient deficiencies, would mimic the non‐stressed individuals and neither would show evidence of PH. However, the inclusion of multiple stress indicators and greater understanding of biocultural context in bioarchaeological analyses may mitigate the potential impacts of hidden heterogeneity in the expression of PH. Copyright © 2013 John Wiley & Sons, Ltd.