Aiello and Wheeler noted that this dramatic increase in brain size would seem to have required a dramatic increase in metabolism—the same way that adding an air-conditioning system to a house would increase the electricity bill. Yet humans burn the same number of calories, scaled to size, as other primates. Somehow, Aiello and Wheeler argued, our ancestors found a way to balance their energy budget. As they expanded their brains, perhaps they slimmed down other organs.
The scientists compared the sizes of organs in humans and other primates. Relatively speaking, our liver is about the same size as a baboon’s. Our heart is on par with a gorilla’s. But our guts have shriveled. They weigh only 60 percent of what you’d expect in a primate of our size. Intestinal cells also need a lot of energy, because they are highly innervated. Losing such a big portion of their guts could have allowed our ancestors to compensate for much of the brain’s extra energy demand.
Aiello and Wheeler christened their idea “the expensive tissue hypothesis.” To test it, they compared the size of brains and guts in a range of primate species (pdf). They found that the bigger a primate’s brain relative to the species’s overall body size, the smaller the guts tend to be. This consistent trade-off suggested that trimming our guts was essential to supersizing our brains.
Then William Leonard, a biological anthropologist at Northwestern University, put the expensive tissue hypothesis to a new test. Instead of correlating brain and gut size across primate species, Leonard decided to look at mammal species overall. Beyond the primates, he found, there existed no correlation whatsoever between brain size and gut size.
This suggested that the gut-shrinking phenomenon within the primate groups was probably too subtle to explain our increase in brain size completely. Something else had to be going on as well. That something, Leonard says, is diet. After studying the diets of primate species and tallying the quantity and quality of food consumed, Leonard found a switch from lower-energy diets of bark and leaves to higher-energy cuisines of seeds, tubers, and meat in the brainier species. As brain-to-body ratio increases, presumably, the denser calories supply the additional needed fuel.
Greg Wray, an evolutionary
biologist at Duke University, is finding secrets to big brains in an entirely different place: the human genome. One of the genes involved in feeding the big brain, called SLC2A1, builds a protein for transporting glucose from blood vessels into cells. It is vital to the brain’s well-being. Mutations that reduce the number of transporter proteins in the brain lead to disorders such as epilepsy and learning disabilities. If one copy of the SLC2A1 gene is completely dysfunctional, the results are devastating: The brain develops to only a portion of its normal size. If neither copy of the gene works, a fetus simply dies.
Wray and his colleagues compared SLC2A1 in humans and other animals. They discovered that our ancestors acquired an unusually high number of mutations in the gene. The best explanation for that accumulation of mutations is that SLC2A1 experienced natural selection in our own lineage, and the new mutations boosted our reproductive success. Intriguingly, the Duke team discovered that the mutations didn’t alter the shape of the glucose transporters. Rather, they changed stretches of DNA that toggled the SLC2A1 gene on and off.
Wray guessed that these mutations changed the total number of glucose transporters built in the human brain. To test his theory, he looked at slices of human brain tissue. In order to make glucose transporters, the cells must first make copies of the SLC2A1 gene to serve as a template. Wray discovered that in human brains there were 2.5 to 3 times as many copies of SLC2A1 as there were in chimpanzee brains, suggesting the presence of more glucose transporters as well.
Then he looked at glucose transporters that deliver the sugar to muscles. The gene for these muscle transporters, called SLC2A4, also underwent natural selection in humans, but in the opposite direction. Our muscles contain fewer glucose transporters than in chimps’ muscles. Wray’s results support the notion that our ancestors evolved extra molecular pumps to funnel sugar into the brain, while starving muscles by giving them fewer transporters.
Becoming Homo megalencephalus was hardly a simple process. It was not enough for evolution to shrink our gut and shift our diet. It had to do some genetic engineering, too.
Carl Zimmer is an award-winning biology writer and author of The Tangled Bank: An Introduction to
Evolution, among other books. His blog, The Loom, runs at blogs.discover