![]() In spite of its proclivity for drama, we owe our lives to this metal. Eventually, rogue iron escapes its minders and chemical mischief ensues. However, in those who absorb more iron than average, the extra influx eventually overwhelms this transport and storage system. Under normal conditions, this meticulously coordinated system functions beautifully. As a result, all organisms dependent on iron - from primitive bacteria to mammals - go to great lengths to safely transport and store this potentially poisonous payload. Indispensable to oxygen transport and metabolism, this property may also cause disease if iron participates in unsanctioned electron exchanges that produce free radicals - an evanescent and particularly hot-blooded family of compounds that damage cells and DNA. Iron readily exchanges electrons with other elements. ![]() ![]() Essential to life, yet impulsive, promiscuous, and destructive when allowed to roam unescorted, it poses a tremendous engineering challenge to human tissues. In this search for the origin of one of the world's most common genetic diseases, emerging research in evolutionary medicine raises new questions about our history, development, and future as a species.Īs elements go, iron is a fickle and mischievous companion. Casadaban's tragic death at the hands of an infamous microbe challenges a theory that the hemochromatosis gene became common because it protected its owners from the plague. Out of this tradition of sickness rises a story of medical progress - and uncertainty - involving an atom, the wanderlust of ancient peoples, the appetite of a caveman, and a possible legacy of the Black Death. Researchers look to DNA analysis to solve a lingering biohistorical puzzle: Is the hemochromatosis gene common because it is an unintended consequence of natural selection, or because it is a relatively fresh glitch in the human genome with little time to spread to other regions? The mutation's surprising frequency and peculiar fondness for those of Irish, British, and Scandanavian heritage offers a unique opportunity for scientists and historians to study how the world of our ancestors may have shaped the landscape of modern disease. We know little about the disease's founder, but we do know that she survived long enough to pass one copy of the gene to her children, and eventually, to nearly one in ten individuals of northern European ancestry. This mutation allowed her (or him) to more readily absorb iron from food, which may have unexpectedly aided survival in lean times - possibly at the expense of iron-overload in later generations. A modern manifestation of an ancient DNA mutation, this disorder can be traced to a single unknown ancestor who lived millennia ago. Casadaban unknowingly suffered from hereditary hemochromatosis, a genetic disease leading to a toxic accumulation of iron in his organs. Michael Casadaban died at age 60 after being exposed to a weakened form of the bacterium that causes plague.
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