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THE GENETICS OF VULNERABILITY

In August 1967 a missionary’s two-year-old daughter came down with measles in a village on the Toototobi River in Brazil, near the border with Venezuela. She and her family had just returned from the Amazonian city of Manaus and had been checked and cleared by Brazilian doctors before departure. Nonetheless the distinctive spots of measles emerged a few days after the family’s arrival on the Toototobi. The village, like many others in the region, was populated mainly by Yanomami Indians, a forest society on the Brazil-Venezuela border that is among the least Westernized on earth. They had never before encountered the measles virus. More than 150 Yanomami were in the village at the time. Most or all caught the disease. Seventeen died despite the horrified missionaries’ best efforts. And the virus escaped and spread throughout the Yanomami heartland, carried by people who did not know they had been exposed.

Partly by happenstance, the U.S. geneticist James Neel and the U.S. anthropologist Napoleon Chagnon flew into Yanomami country in the midst of the epidemic. Neel, who had long been worried about measles, was carrying several thousand doses of vaccine. Alas, the disease had preceded them. They frantically tried to create an epidemiological “firebreak” by vaccinating ahead of the disease. Despite their efforts, the affected villages had a mean death rate of 8.8 percent. Almost one out of ten people died from a sickness that in Western societies was just a childhood annoyance.

Later Neel concluded that the high death rate was in part due to grief and despair, rather than the virus itself. Still, the huge toll was historically unprecedented. The implication, implausible at first glance, was that Indians in their virgin-soil state were more vulnerable to European diseases than virgin-soil Europeans would have been. Perhaps surprisingly, there is some scientific evidence that Native Americans were for genetic reasons unusually susceptible to foreign microbes and viruses—one reason that researchers believe that pandemics of Dobynsian scale and lethality could have occurred.

Here I must make a distinction between two types of susceptibility. The first is the lack of acquired immunity—immunity gained from a previous exposure to a pathogen. People who have never had chicken pox are readily infected by the virus. After they come down with the disease, their immune system trains itself, so to speak, to fight off the virus, and they never catch it again, no matter how often they are exposed. Most Europeans of the day had been exposed to smallpox as children, and those who didn’t die were immune. Smallpox and other European diseases didn’t exist in the Americas, and so every Indian was susceptible to them in this way.

In addition to having no acquired immunity (the first kind of vulnerability), the inhabitants of the Americas had immune systems that some researchers believe were much more restricted than European immune systems. If these scientists are correct, Indians as a group had less innate ability to defend themselves against epidemic disease (the second kind of vulnerability). The combination was devastating.

The second type of vulnerability stems from a quirk of history. Archaeologists dispute the timing and manner of Indians’ arrival in the Americas, but almost all researchers believe that the initial number of newcomers must have been small. Their gene pool was correspondingly restricted, which meant that Indian biochemistry was and is unusually homogeneous. More than nine out of ten Native Americans—and almost all South American Indians—have type O blood, for example, whereas Europeans are more evenly split between types O and A.

Evolutionarily speaking, genetic homogeneity by itself is neither good nor bad. It can be beneficial if it means that a population lacks deleterious genes. In 1491, the Americas were apparently free or almost free of cystic fibrosis, Huntington’s chorea, newborn anemia, schizophrenia, asthma, and (possibly) juvenile