Abstract
No satisfactory explanation has been offered, to date, to account for the prevalence of the haemochromatosis genes in the European population and yet relative paucity of the gene in the tropics. Traditional wisdom suggests that, in antiquity, the haemochromatosis gene, which promotes iron absorption, would have protected ancient man from iron loss resulting from injury either during hunting or through war. However, such an advantage would be equally desirable for other populations where the incidence of the alleles is negligible. Others have tackled the polemic from the another view, postulating that the paucity of the haemochromatosis alleles in populations outside of Europe may be explained by the fact that iron load predisposes to infection and that iron deficiency anaemia is protective against this by limiting parasitic access to host stores of iron. This explanation alone is equally unsatisfactory as European populations are exposed to pathogens and would benefit from any protection afforded by mild anaemia. Others have mooted genetic drift as another alternative explanation. Yet this would be unexpected for a gene which is deleterious. We propose here that the driving force for the propagation of the haemochromatosis alleles was not infection per se but the nature of the parasitic fauna which sojourned with mankind. The tropics are inhabited with multicellular parasitic and highly pathogenic organisms, which consequently have a high demand for iron. The organisms have developed aggressive means of iron extraction from their hosts. Where there is iron in abundance such organisms would have a licence to multiply in an unbridled fashion at the expense of the host. Such a host, due to their increased iron load, would be able to harbour a high parasitic load which would be harmful to the population as a whole, not just the individual with the haemochromatosis allele. As man migrated from the tropics many of the larger pathogens disappeared and man had only to contend with traditional unicellular adversaries. Iron is a critical micronutrient that the host attempts to withhold for invading pathogens. We also advance the theory that the tropical anaemias including sickle cell trait, thalassaemia, glucose-6-phosphate dehydrogenase deficiency, and pyruvate kinase deficiency are an ingenious evolutionary means by the host of withholding iron from tropical pathogens while simultaneously avoiding the deleterious effects of frank iron deficiency and/or iron deficiency anaemia. The mechanism is essentially an immunological passive aggressive orchestrated by man kind.
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