In archeological skeletal remains, evidence of two types of anemia, although not common, are well known and of considerable biological consequence. Genetic anemias, the less common of the two, are restricted to a few geographic areas of the world. Anemia resulting from malnutrition can occur anywhere. Because of the pitfalls in diagnosing anemia in skeletal material, an understanding of the biological processes involved in this condition is helpful.

In anemia there is an abnormal increase in the need for blood formation. This may be the result of several conditions, including excessive blood loss through chronic bleeding from intestinal parasites. In the genetic anemias, the hemoglobin in red blood cells is defective. This reduces the normal life span of the cells, which in turn creates an increased demand for new blood formation. Dietary iron deficiency can also result in abnormal hemoglobin with results similar to those that exist in the genetic anemias.

Because of the increased demand for blood formation, tissues that create blood occupy more space. The bone marrow spaces that in an infant or young child are normally required for blood formation are now inadequate, and hematopoietic marrow tends to expand at the expense of cortical bone. In the postcranial skeleton the marrow volume of the long bones increases at the expense of that of the cortex, which decreases in thickness (Ortner and Putschar 1981). In the skull the diploe enlarges primarily at the expense of the outer table; the skull becomes thicker, and the external appearance of the skull becomes porous. Although many descriptive terms have been applied to this condition in the skull, currently the most commonly accepted one is porotic hyperostosis, introduced by Angel (1966).

Unfortunately, there are other conditions that may be associated with porous lesions of the skull, including infection and metabolic diseases such as scurvy and rickets (Ortner and Putschar 1981; Ortner 1984, 1986). Thus, unless there is unambiguous evidence of an expansion of marrow space in at least some of the cases in the skeletal sample exhibiting porous lesions of the skull, a diagnosis of anemia should be offered with caution.

Angel (1966, 1972, 1977) proposed an intriguing connection between falciparum malaria and porotic hyperostosis in the eastern Mediterranean. He hypothesized that this condition in the skeletal remains of the region is indicative of thalassemia, one of the genetic anemias that may provide some immunity against malaria, and further proposed an association between the incidence of porotic hyperostosis and the cycles of malarial severity throughout the past 10,000 years. Malaria, he argues, did not become endemic until the population settlement and increase of the Neolithic period, when the frequency of porotic hyperostosis reached 50 percent (Angel 1972). After the Neolithic, porotic hyperostosis declined to 12 percent in the Bronze Age and 2 percent in the City State period (650-300 B.C.; Angel 1972). Angel attributes this decline in anemia, and presumably malaria, to changes in environment, including lowered sea levels and drained marshes. In a book of readings edited by M. Cohen and G. Armelagos (1984b), Cohen concludes, while reviewing data presented during a symposium, that porous lesions of the skull vault and eye orbit either appeared or increased in frequency with the advent of agriculture. He cautiously argues that this trend is indicative of an increase in anemia at that time.

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