In fairness, even if the diet hypothesis crumbles in light of future evidence, one can still wonder if iron deficiency anemia sufficiently threatened human
development, productivity, and survival at earlier periods in history that the C282Y mutation might still have been useful before the Neolithic. However,
it may well be the case that this allele is indeed evolutionary useless -- a new and random mutation with insufficient time for it to spread to Asia and
Africa. Or, maybe, its value lies elsewhere.
Perhaps C282Y protected against disease. The hypothesis is not outrageous; malaria was, and still is, such a decimating force in Africa and Asia that
certain protective traits also responsible for sickle-cell disease, thalassemia, and glucose-6-phosphatase deficiency are still commonplace in these
endemic regions. In another example, one mutation seen in cystic fibrosis may protect heterozygotes from cholera, typhoid fever, and other diarrheal
diseases. These examples of the "heterozygote advantage" illustrate how certain mutations may be advantageous alone, but detrimental when inherited in
duplicate. Recall that it takes roughly one million years for a neutral mutation to spread through our population. These disease-causing mutations are less
than ten thousand years old, yet they appear across the world; this can be no accident. Infectious diseases must be "among the strongest selective
pressures in human history."
As we domesticated cereal grains, we so domesticated animals; in the process, our population grew, and we altered our environment. We developed unsavory
new habits: Standing water from crop irrigation spread mosquitoes, domesticated animals spewed new germs into the barns adjoining herders' homes, and trade
routes promoted exchange of new goods -- and new microbes. Amid this tinderbox emerged the familiar epidemic killers of the modern world: measles,
smallpox, tuberculosis, influenza, pertussis, malaria, and bubonic plague. Like toddlers in one large, runny-nosed, ancient daycare, our ancestors
inevitably fell ill.
, a stowaway bacterium in the gut of a stowaway flea feasting off a stowaway black rat in the cargo hold of an Egyptian trading ship, arrived in the port
of Constantinople in 541 AD. Taking foothold in Emperor Justinian's capital city, the bubonic plague infiltrated outward through a preoccupied and
vulnerable Roman empire. Drained by years of conflict with Goths, Huns, and Persians, Rome festered with opportunities for disease spread though trade and
war. The bodies stacked by the thousands.
From Constantinople and Alexandria, the firestorm reached Rome within the year. It subsequently spread west and north to modern-day Germany, France, and
the United Kingdom before smoldering to embers. The plague no sooner returned to Ireland and Britain, in the 660's AD, as the mouldboard plow and
three-field crop-rotation system boosted production of wheat, rye, oats, and barley, and stimulated trade with hungry, battered, and sporadically
plague-infested Mediterranean port cities.
The Plague of Justinian, spanning 541 to 767 AD, was only the first plague pandemic of the recorded era. At least 25 million people died. The second
outbreak, the infamous Black Death of the 14th century, killed up to one in three persons living in mainland Europe, Asia, and Africa, leaving behind a
much lonelier world. It was, according to Sylvia Thrupp, "a golden age of bacteria."