Blogging the Human Genome

Possible Genetic Proof That Cannibalism Was Disturbingly Common in Our Past
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July 16 2012 6:00 AM

Blogging the Human Genome

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Possible genetic proof that cannibalism was disturbingly common in our past.

Chromosome 20

Illustration by Andrew Morgan

Humans in duress eat other humans, always have. A 100-pound adult, after all, could provide his starving comrades with around 40 pounds of precious muscle protein, plus edible fat, liver, blood, and gristle. Some archaeological evidence suggests that humans have tucked into each other even when not famished. But for years, it was unclear whether most non-starvation cannibalism was religiously motivated and selective, or culinary and routine. According to some scientists, our DNA suggests routine.

We saw previously that highly conserved DNA—DNA that changes little between species—usually controls important biological processes, so nature seldom tinkers with it or allows mutations to creep in. One highly conserved gene is the prion gene on the very tip of chromosome 20, which has the vital responsibility of—well, scientists don’t quite know. But it gets pretty active inside brain tissue, and likely plays a role in day-to-day neurological functioning, perhaps by helping neurons communicate.

When the prion gene goes awry, bad things happen. One prion disorder, Creutzfeldt-Jakob disease, opens up spongy holes in neural tissues—your brain looks like tiny moths nibbled it. It can also occasionally produce gnarly protein plaques in the brain. Creutzfeldt-Jakob usually arises de novo, from a spontaneous mutation, but other prion diseases, like fatal familial insomnia, pass from parent to child. As the name suggests, fatal familial insomnia disrupts the ability to sleep so profoundly that you die. Not a fun way to go.

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Prion diseases attack the brain in an insidious way. Most victims have one functioning and one mutant version of the prion gene, and so produce some normal prion proteins and some misfolded, bad prion proteins. Unfortunately, the bad prion protein can sometimes lock onto and corrupt a good prion protein that happens to float by, preventing the good one from doing its job. And here’s the sinister part: The bad molecule corrupts the good one by twisting the good one into a clone of itself. As a result, there are now two bad copies of the protein, each of which can later float off and corrupt still more good prion proteins. It’s similar to how vampires work. They turn an innocent into a new vampire with one bite. Those two vampires can corrupt two more people in turn, making four, who then corrupt four more, and so on.

Perhaps even more insidiously, this genetic disease can spread to people who lack a bad copy of the gene; it’s like being able to catch Huntington’s disease or another destructive brain disorder. The usual route of transmission here is cannibalism.

Cannibalism per se isn’t bad for you; you can even spoon up and eat most human brains safely. But if your guest of honor happened to suffer from Creutzfeldt-Jakob or another prion disease, those misshapen proteins can slither into your own gray matter when you eat him. This exact scenario unfolded in Papua New Guinea last century, among some highland mountain tribes who consumed their relatives in ritual funeral feasts.

At its peak in the late 1950s, the PNG epidemic killed 200 tribal members per year, the proportional equivalent of 1.5 million U.S. deaths. Strangely, though, while many victims died as children, some people exposed to prions lived four decades or more before succumbing. And some people who consumed tainted brains never showed any symptoms. DNA explained the discrepancy. More than three-fourths of the long-term survivors had two different versions of the prion gene. (The difference was in the gene’s 129th DNA triplet: One version read A-T-G, one G-T-G.) Both versions produced healthy, functioning proteins, despite their slightly different shapes. The shapes made a difference only when people ate tainted brains, and faced an invasion of the infectious vampire prions. While the bad prions could latch onto one of the two shapes just fine, the other shape could shrug them off and avoid corruption. Overall, then, having two different versions of the prion gene slowed the destruction down.

If the word “prion” has been tickling the back of your brain until now, that’s probably because of the outbreak of mad-cow disease in the United Kingdom in the 1990s. Mad-cow is a prion disease that arose when humans ate cows that had been forced to cannibalize each other on factory farms. People exposed to mad-cow prions included both those who had two identical copies of the prion gene, and others who had a mixed pair. Strikingly, though, of the hundred-plus deaths from mad-cow, every victim except one had identical copies. In other words, British victims showed a similar genetic pattern to victims in Papua New Guinea: Having two different copies of the prion gene seemed to offer resistance to bad invading prions.

The funny thing is that the prion gene is highly conserved: The A-T-G version was universal among our primate ancestors. Mutations to it therefore should be rare. But the same basic mutation showed up in scads of people in both the United Kingdom and Papua New Guinea, two almost antipodal points on the globe. Follow-up work uncovered the mutation most everywhere else in the world, too.

How did GTG spread so far? Perhaps through genetic drift, a random diffusion process. Or perhaps—as a few scientists argued in a controversial paper from 2003—cannibalism was so popular in our past that all human ethnic groups had to stockpile alternative versions of the prion gene or else they’d get wiped out. What clinched the case (at least to some) was one ethnic group, mostly in Japan. This group lacked the ATG/GTG variation seen everywhere else in the 129th triplet; but they had a different mutation in the 219th triplet that, again, tweaked the protein’s shape and presumably made it harder to corrupt. The theory was that this ethnic group had somehow lost the variation at position 129 in the past, but had to acquire another defense or risk extinction.

Other scientists have since found flaws in the 2003 paper that, they say, led the original team to overestimate our ancient appetite for cannibalism. But even these critics acknowledge that the prion gene has a strange history, and that outbreaks of cannibalism like the one in Papua New Guinea could well have altered the DNA of many ethnic groups. And regardless of exactly why the exotic versions of the prion gene spread, the fact that they have means that many of us can now taste the most forbidden flesh of our fellow human beings with relative impunity. Only problem is, they can do the same to you.

Sam Kean is the best-selling author of The Disappearing Spoon and The Violinist’s Thumb. His new book, The Tale of the Dueling Neurosurgeons, comes out May 6.

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