Mark Changizi is an evolutionary neurobiologist and director of human cognition at 2AI Labs. He is the author of The Brain from 25000 Feet, The Vision Revolution, and his newest book, Harnessed: How Language and Music Mimicked Nature and Transformed Ape to Man.”
What do ironing and hang-gliding have in common? Not much really, except that we weren’t designed to do either of them. And that goes for a million other modern-civilization things we regularly do but are not “supposed” to do. We’re fish out of water, living in radically unnatural environments and behaving ridiculously for a great ape. So, if one were interested in figuring out which things are fundamentally part of what it is to be human, then those million crazy things we do these days would not be on the list.
But what would be on the list?
At the top of the list of things we do that we’re supposed to be doing, and that are at the core of what it is to be human rather than some other sort of animal, are language and music. Language is the pinnacle of usefulness, and was key to our domination of the Earth (and the Moon). And music is arguably the pinnacle of the arts. Language and music are fantastically complex, and we’re brilliantly capable at absorbing them, and from a young age. That’s how we know we’re meant to be doing them, i.e., how we know we evolved brains for engaging in language and music.
But what if this gets language and music all wrong? What if we’re not, in fact, meant to have language and music? What if our endless yapping and music-filled hours each day are deeply unnatural behaviors for our species? (What if the parents in Footloose* were right?!)
I believe that language and music are, indeed, not part of our core—that we never evolved by natural selection to engage in them. The reason we have such a head for language and music is not that we evolved for them, but, rather, that language and music evolved—culturally evolved over millennia—for us. Our brains aren’t shaped for these pinnacles of humankind. Rather, these pinnacles of humankind are shaped to be good for our brains.
by Richard Wrangham, as told to Discover’s Veronique Greenwood. Wrangham is the chair of biological anthropology at Harvard University, where he studies the cultural similarities between humans and chimpanzees—including our unique tendencies to form murderous alliances and engage in recreational sexual activity. He is the author of Catching Fire: How Cooking Made Us Human.
When I was studying the feeding behavior of wild chimpanzees in the early 1970s, I tried surviving on chimpanzee foods for a day at a time. I learned that nothing that chimpanzees ate (at Gombe, in Tanzania, at least) was so poisonous that it would make you ill, but nothing was so palatable that one could easily fill one’s stomach. Having eaten nothing but chimpanzee foods all day, I fell upon regular cooked food in the evenings with relief and delight.
About 25 years later, it occurred to me that my experience in Gombe of being unable to thrive on wild foods likely reflected a general problem for humans that was somehow overcome at some point, possibly through the development of cooking. (Various of our ancestors would have eaten more roots and meat than chimpanzees do, but I had plenty of experience of seeing chimpanzees working very hard to chew their way through tough raw meat—and had even myself tried chewing monkeys killed and discarded by chimpanzees.) In 1999, I published a paper [pdf] with colleagues that argued that the advent of cooking would have marked a turning point in how much energy our ancestors were able to reap from food.
To my surprise, some of the peer commentaries were dismissive of the idea that cooked food provides more energy than raw. The amazing fact is that no experiments had been published directly testing the effects of cooking on net energy gained. It was remarkable, given the abiding interest in calories, that there was a pronounced lack of studies of the effects of cooking on energy gain, even though there were thousands of studies on the effects of cooking on vitamin concentration, and a fair number on its effects on the physical properties of food such as tenderness. But more than a decade later, thanks particularly to the work of Rachel Carmody, a grad student in my lab, we now have a series of experiments that provide a solid base of evidence showing that the skeptics were wrong.
Whether we are talking about plants or meat, eating cooked food provides more calories than eating the same food raw. And that means that the calorie counts we’ve grown so used to consulting are routinely wrong. Read More
One of the strangest aspects of our understanding of evolutionary biology is the tendency to conflate a sprawling protean dynamic into a sliver of a phenomenon. Most prominently, evolution is often reduced to a process driven by natural selection, with an emphasis on the natural. When people think of populations evolving they imagine them being buffeted by inclement weather, meteors, or smooth geological shifts. These are all natural, physical phenomena, and they all apply potential selection pressures. But this is not the same as evolution; it’s just one part. A more subtle aspect of evolution is that much of the selection is due to competition between living organisms, not their relationship to exterior environmental conditions.
The question of what drives evolution is a longstanding one. Stephen Jay Gould famously emphasized of the role of randomness, while Richard Dawkins and others prioritize the shaping power of natural selection. More finely still, there is the distinction between those which emphasize competition across the species versus within species. And then there are the physical, non-biological forces.
Evolution as selection. Evolution as drift. Evolution as selection due to competition between individuals of the same species. Evolution as selection due to competition between individuals of different species. And so forth. There are numerous models, theories, and conjectures about what’s the prime engine of evolution. The evolutionary biologist Richard Lewontin famously observed that in the 20th century population geneticists constructed massively powerful analytic machines, but had very little data which they could throw into those machines. And so it is with theories of evolution. Until now.
Over the past 10 years in the domain of human genetics and evolution there has been a swell of information due to genomics. In many ways humans are now the “trial run” for our understanding of evolutionary process. Using theoretical models and vague inferences from difficult-to-interpret signals, our confidence in the assertions about the importance of any given dynamic have always been shaky at best. But now with genomics, researchers are testing the data against the models.
A recent paper is a case in point of the methodology. Using 500,000 markers, ~50 populations, and ~1,500 people, the authors tested a range of factors against their genomic data. The method is conceptually simple, though the technical details are rather abstruse. The ~1,500 individuals are from all around the globe, so the authors could construct a model where the markers varied as a function of space. As expected, most of the genetic variation across populations was predicted by the variation across space, which correlates with population demographic history; those populations adjacent to each other are likely to have common recent ancestors. But the authors also had some other variables in their system which varied as a function of space in a less gradual fashion: climate, diet, and pathogen loads. The key is to look for those genetic markers and populations where the expectation of differences being driven as a function of geography do not hold. Neighbors should be genetically like, but what if they’re not? Once you find a particular variant you can then see how it varies with the factors listed above.
Consider two pandemics: the white-nose syndrome now devastating North American bats and the Black Death that killed a third or more of Europeans in the 14th century. Lethality aside, they may not seem to have much in common. But recent studies suggest they both offer important lessons about understanding that the deadliness of disease organisms is very much a product of the circumstances in which they appear.
Two weeks ago in Nature, a multi-institutional team of U.S. Geological Survey scientists presented conclusive evidence the parasitic fungus that lends white-nose syndrome its name is indeed the cause of the mysterious bat epidemic. The illness came to light in New York in 2006, when cave explorers started finding thousands of little brown bats (and later, other species) dead together in the caves where they spent the winter months, their bodies covered with a white fungus, Geomyces destructans. It has since spread throughout the northeastern U.S., where bat populations have declined on average by 73 percent—which may make it one of the most rapid declines in wildlife populations ever observed. Worse, white-nose syndrome is still on the move, with documented cases in four Canadian provinces and states as far south and west as Tennessee, Missouri, and Oklahoma.
This post was originally published at Ed Yong’s Discover blog, Not Exactly Rocket Science.
Two people are dancing a waltz, and it is not going well. One is tall and the other short; one is graceful, the other flat-footed; and both are stepping to completely different rhythms. The result is chaos, and the dance falls apart. Their situation mirrors a problem faced by all complex life on Earth. Whether we’re animal or plant, fungus or alga, we all need two very different partners to dance in step with one another. A mismatch can be disastrous.
Virtually all organisms with complex cells—better known as eukaryotes—have at least two separate genomes. The main one sits in the central nucleus. There’s also a smaller one in tiny bean-shaped structures called mitochondria, little batteries that provide the cell with energy. Both sets of genes must work together. Neither functions properly without the other.
Mitochondria came from a free-living bacterium that was engulfed by a larger cell a few billion years ago. The two eventually became one. Their fateful partnership revolutionised life on this planet, giving it a surge of power that allowed it to become complex and big (see here for the full story). But the alliance between mitochondria and their host cells is a delicate one.
Both genomes evolve in very different ways. Mitochondrial genes are only passed down from mother to child, whereas the nuclear genome is a fusion of both mum’s and dad’s genes. This means that mitochondria genes evolve much faster than nuclear ones—around 10 to 30 times faster in animals and up to a hundred thousand times faster in some fungi. These dance partners are naturally drawn to different rhythms.
This is a big and underappreciated problem because the nuclear and mitochondrial genomes cannot afford to clash. In a new paper, Nick Lane, a biochemist at University College London, argues that some of the most fundamental aspects of eukaryotic life are driven by the need to keep these two genomes dancing in time. The pressure to maintain this “mitonuclear match” influences why species stay separate, why we typically have two sexes, how many offspring we produce, and how we age.