Anemia

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.

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, Cinrently 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).

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.