Volume 13, Issue 1_Part_2
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645


The development of the hypothesis of the relationship of falciparum malaria to the hemoglobinopathies, thalassemia, and glucose-6-phosphate dehydrogenase (G-6-Pd) deficiency has been a stimulus to investigators in human genetics, anthropology and malariology. There are still many unanswered features of the problem, the resolution of which will add to our understanding of these genetic abnormalities of the erythrocytes and of malaria.

Although it is generally accepted that genetic traits with frequencies in racial groups higher than accountable for by mutation alone are the result of past and/or present selective factors, the substantiation of a specific selective mechanism for a genetic defect is difficult. Geographical association of certain genetic erythrocyte abnormalities with regions endemic for falciparum malaria, and the absence of the genetic traits in races never so exposed is irrefutable. On the other hand, several investigators have observed absent to very low frequency of G-6-Pd deficiency in populations exposed to falciparum malaria for centuries.


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