Category Archives: Evolution

Huddled mice could change the way we think about evolution

Stuart P Wilson, University of Sheffield and James V Stone, University of Sheffield

Adapt or die. That’s the reality for an animal species when it is faced with a harsh environment. Until now, many scientists have assumed that the more challenging an animal’s environment, the greater the pressure to adapt and the faster its genes evolve. But we have just published new research in Royal Society Open Science that shows that genes might actually evolve faster when the pressure to adapt is reduced.

We built a simple computer model of how evolution may be affected by the way animals interact with each other when they’re in groups. Specifically, we looked at what happens to animals that huddle together to keep warm.

We found that when animals huddle in larger groups, their genes for regulating temperature evolve faster, even though there is less pressure to adapt to the cold environment because of the warmth of the huddle. This shows that an organism’s evolution doesn’t just depend on its environment but also on how it behaves.

When animals such as rats and mice huddle together in groups, they can maintain a high body temperature without using as much energy as they would on their own. We wanted to understand how this kind of group behaviour would affect a species’ evolution.

To do this, we built a computer model simulating how the species’ genes changed and were passed on over multiple generations. When the effects of huddling were built into the computer model, the reduced pressure to adapt was actually found to accelerate evolution of the genes controlling heat production and heat loss.

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A unified theory of evolution requires input from Darwin and Lamarck

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Michael Skinner writes: The unifying theme for much of modern biology is based on Charles Darwin’s theory of evolution, the process of natural selection by which nature selects the fittest, best-adapted organisms to reproduce, multiply and survive. The process is also called adaptation, and traits most likely to help an individual survive are considered adaptive. As organisms change and new variants thrive, species emerge and evolve. In the 1850s, when Darwin described this engine of natural selection, the underlying molecular mechanisms were unknown. But over the past century, advances in genetics and molecular biology have outlined a modern, neo-Darwinian theory of how evolution works: DNA sequences randomly mutate, and organisms with the specific sequences best adapted to the environment multiply and prevail. Those are the species that dominate a niche, until the environment changes and the engine of evolution fires up again.

But this explanation for evolution turns out to be incomplete, suggesting that other molecular mechanisms also play a role in how species evolve. One problem with Darwin’s theory is that, while species do evolve more adaptive traits (called phenotypes by biologists), the rate of random DNA sequence mutation turns out to be too slow to explain many of the changes observed. Scientists, well-aware of the issue, have proposed a variety of genetic mechanisms to compensate: genetic drift, in which small groups of individuals undergo dramatic genetic change; or epistasis, in which one set of genes suppress another, to name just two.

Yet even with such mechanisms in play, genetic mutation rates for complex organisms such as humans are dramatically lower than the frequency of change for a host of traits, from adjustments in metabolism to resistance to disease. The rapid emergence of trait variety is difficult to explain just through classic genetics and neo-Darwinian theory. To quote the prominent evolutionary biologist Jonathan B L Bard, who was paraphrasing T S Eliot: ‘Between the phenotype and genotype falls the shadow.’

And the problems with Darwin’s theory extend out of evolutionary science into other areas of biology and biomedicine. For instance, if genetic inheritance determines our traits, then why do identical twins with the same genes generally have different types of diseases? And why do just a low percentage (often less than 1 per cent) of those with many specific diseases share a common genetic mutation? If the rate of mutation is random and steady, then why have many diseases increased more than 10-fold in frequency in only a couple decades? How is it that hundreds of environmental contaminants can alter disease onset, but not DNA sequences? In evolution and biomedicine, the rates of phenotypic trait divergence is far more rapid than the rate of genetic variation and mutation – but why?

Part of the explanation can be found in some concepts that Jean-Baptiste Lamarck proposed 50 years before Darwin published his work. Lamarck’s theory, long relegated to the dustbin of science, held, among other things, ‘that the environment can directly alter traits, which are then inherited by generations to come’. [Continue reading…]

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Watching evolution happen in two lifetimes

Emily Singer writes: When Rosemary and Peter Grant first set foot on Daphne Major, a tiny island in the Galápagos archipelago, in 1973, they had no idea it would become a second home. The husband and wife team, now emeritus biology professors at Princeton University, were looking for a pristine environment in which to study evolution. They hoped that the various species of finches on the island would provide the perfect means for uncovering the factors that drive the formation of new species.

The diminutive island wasn’t a particularly hospitable place for the Grants to spend their winters. At less than one-hundredth the size of Manhattan, Daphne resembles the tip of a volcano rising from the sea. Visitors must leap off the boat onto the edge of a steep ring of land that surrounds a central crater. The island’s vegetation is sparse. Herbs, cactus bushes and low trees provide food for finches — small, medium and large ground finches, as well as cactus finches — and other birds. The Grants brought with them all the food and water they would need and cooked meals in a shallow cave sheltered by a tarp from the baking sun. They camped on Daphne’s one tiny flat spot, barely larger than a picnic table.

Though lacking in creature comforts, Daphne proved to be a fruitful choice. The Galápagos’ extreme climate — swinging between periods of severe drought and bountiful rain — furnished ample natural selection. Rainfall varied from a meter of rain in 1983 to none in 1985. A severe drought in 1977 killed off many of Daphne’s finches, setting the stage for the Grants’ first major discovery. During the dry spell, large seeds became more plentiful than small ones. Birds with bigger beaks were more successful at cracking the large seeds. As a result, large finches and their offspring triumphed during the drought, triggering a lasting increase in the birds’ average size. The Grants had observed evolution in action.

That striking finding launched a prolific career for the pair. They visited Daphne for several months each year from 1973 to 2012, sometimes bringing their daughters. Over the course of their four-decade tenure, the couple tagged roughly 20,000 birds spanning at least eight generations. (The longest-lived bird on the Grants’ watch survived a whopping 17 years.) They tracked almost every mating and its offspring, creating large, multigenerational pedigrees for different finch species. They took blood samples and recorded the finches’ songs, which allowed them to track genetics and other factors long after the birds themselves died. They have confirmed some of Darwin’s most basic predictions and have earned a variety of prestigious science awards, including the Kyoto Prize in 2009.

Now nearly 80, the couple have slowed their visits to the Galápagos. These days, they are most excited about applying genomic tools to the data they collected. They are collaborating with other scientists to find the genetic variants that drove the changes in beak size and shape that they tracked over the past 40 years. Quanta Magazine spoke with the Grants about their time on Daphne; an edited and condensed version of the conversation follows. [Continue reading…]

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Tardigrades: The most fascinating animals known to science

 

Brian Resnick writes: Paul Bartels gets a rush every time he discovers a new species of tardigrade, the phylum of microscopic animals best known for being both strangely cute and able to survive the vacuum of space.

“The first paper I wrote describing a new species, there was a maternal-paternal feeling — like I just gave birth to this new thing,” he tells me on a phone call.

The rush comes, in part, because tardigrades are the most fascinating animals known to science, able to survive in just about every environment imaginable. “There are some ecosystems in the Antarctic called nunataks where the wind blows away snow and ice, exposing outcroppings of rocks, and the only things that live on them are lichens and tardigrades,” says Bartels, an invertebrate zoologist at Warren Wilson College in North Carolina.

Pick up a piece of moss, and you’ll find tardigrades. In the soil: tardigrades. The ocean: You get it. They live on every continent, in every climate, and in every latitude. Their extreme resilience has allowed them to conquer the entire planet.

And though biologists have known about tardigrades since the dawn of the microscope, they’re only just beginning to understand how these remarkable organisms are able to survive anywhere. [Continue reading…]

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Your gut bacteria predates appearance of humans, genetic study finds

The Guardian reports: The evolutionary history of the bacteria in your guts predates the appearance of humans, and mirrors that of our great ape relatives, according to a genetic study.

The research suggests that microbes in our ancestors’ intestines split into new evolutionary lineages in parallel with splits in the ape family tree.

This came as a surprise to scientists, who had thought that most of our gut bacteria came from our surroundings – what we eat, where we live, even what kind of medicine we take. The new research suggests that evolutionary history is much more important than previously thought.

“When there were no humans or gorillas, just ancestral African apes, they harboured gut bacteria. Then the apes split into different branches, and there was also a parallel divergence of different gut bacteria,” said Prof Andrew Moeller of the University of California, Berkeley who led the study, published in Science. This happened when gorillas separated somewhere between 10-15 million years ago, and again when humans split from chimps and bonobos 5 million years ago. [Continue reading…]

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‘Gene drives’ that tinker with evolution are an unknown risk, researchers say

MIT Technology Review reports: With great power — in this case, a technology that can alter the rules of evolution — comes great responsibility. And since there are “considerable gaps in knowledge” about the possible consequences of releasing this technology, called a gene drive, into natural environments, it is not yet responsible to do so. That’s the major conclusion of a report published today by the National Academies of Science, Engineering, and Medicine.

Gene drives hold immense promise for controlling or eradicating vector-borne diseases like Zika virus and malaria, or in managing agricultural pests or invasive species. But the 200-page report, written by a committee of 16 experts, highlights how ill-equipped we are to assess the environmental and ecological risks of using gene drives. And it provides a glimpse at the challenges they will create for policymakers.

The technology is inspired by natural phenomena through which particular “selfish” genes are passed to offspring at higher rate than is normally allowed by nature in sexually reproducing organisms. There are multiple ways to make gene drives in the lab, but scientists are now using the gene-editing tool known as CRISPR to very rapidly and effectively do the trick. Evidence in mosquitoes, fruit flies, and yeast suggests that this could be used to spread a gene through nearly 100 percent of a population.

The possible ecological effects, intended or not, are far from clear, though. How long will gene drives persist in the environment? What is the chance that an engineered organism could pass the gene drive to an unintended recipient? How might these things affect the whole ecosystem? How much does all this vary depending on the particular organism and ecosystem?

Research on the molecular biology of gene drives has outpaced ecological research on how genes move through populations and between species, the report says, making it impossible to adequately answer these and other thorny questions. Substantially more laboratory research and confined field testing is needed to better grasp the risks. [Continue reading…]

Jim Thomas writes: If there is a prize for the fastest emerging tech controversy of the century the ‘gene drive’ may have just won it. In under eighteen months the sci-fi concept of a ‘mutagenic chain reaction’ that can drive a genetic trait through an entire species (and maybe eradicate that species too) has gone from theory to published proof of principle to massively-shared TED talk (apparently an important step these days) to the subject of a US National Academy of Sciences high profile study – complete with committees, hearings, public inputs and a glossy 216 page report release. Previous technology controversies have taken anywhere from a decade to over a century to reach that level of policy attention. So why were Gene Drives put on the turbo track to science academy report status? One word: leverage.

What a gene drive does is simple: it ensures that a chosen genetic trait will reliably be passed on to the next generation and every generation thereafter. This overcomes normal Mendelian genetics where a trait may be diluted or lost through the generations. The effect is that the engineered trait is driven through an entire population, re-engineering not just single organisms but enforcing the change in every descendant – re-shaping entire species and ecosystems at will.

It’s a perfect case of a very high-leverage technology. Archimedes famously said “Give me a lever long enough and a fulcrum on which to place it, and I shall move the world. ” Gene drive developers are in effect saying “Give me a gene drive and an organism to put it in and I can wipe out species, alter ecosystems and cause large-scale modifications.” Gene drive pioneer Kevin Esvelt calls gene drives “an experiment where if you screw up, it affects the whole world”. [Continue reading…]

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Earliest evidence of fire making by prehumans in Europe found

Science News reports: Prehumans living around 800,000 years ago in what’s now southeastern Spain were, literally, trailblazers. They lit small, controlled blazes in a cave, a new study finds.

Discoveries in the cave provide the oldest evidence of fire making in Europe and support proposals that members of the human genus, Homo, regularly ignited fires starting at least 1 million years ago, say paleontologist Michael Walker of the University of Murcia in Spain and his colleagues. Fire making started in Africa (SN: 5/5/12, p. 18) and then moved north to the Middle East (SN: 5/1/04, p. 276) and Europe, the researchers conclude in the June Antiquity.

If the age estimate for the Spain find holds up, the new report adds to a “surprising number” of sites from deep in the Stone Age that retain evidence of small, intentionally lit fires, says archaeologist John Gowlett of the University of Liverpool in England.

Excavations conducted since 2011 at the Spanish cave, Cueva Negra del Estrecho del Río Quípar, have uncovered more than 165 stones and stone artifacts that had been heated, as well as about 2,300 animal-bone fragments displaying signs of heating and charring. Microscopic and chemical analyses indicate that these finds had been heated to between 400° and 600° Celsius, consistent with having been burned in a fire. [Continue reading…]

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How the event that killed off the dinosaurs wiped out life in Antarctica

By James Witts, University of Leeds

The Cretaceous–Paleogene mass extinction 66m years ago was the most recent of five similar crises to have devastated life on Earth over the last 540m years. It rapidly killed off an estimated 76% of species around the globe, including, most famously, the dinosaurs.

But exactly how this event affected different areas of the globe has not been entirely understood. Some scientists have suggested that creatures living at high latitudes could have been sheltered from the worst effects of the mass extinction. Now our new research, published in the journal Nature Communications, reveals that this wasn’t the case – even marine molluscs in Antarctica were affected.

Scientists are still debating what caused the extinction. Many researchers believe it was a sudden crisis, triggered by a catastrophic asteroid impact. This formed the 200km Chicxulub crater, today buried off Mexico’s Yucatan Peninsula. It also produced a thin layer of rock found all over the world known as the “K–Pg boundary”. This “fallout” layer is rich in debris from the asteroid impact and an element called Iridium, rare on Earth but common in space rocks. It coincides with many of the extinctions in the fossil record to within 32,000 years – a geological blink of an eye.

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How Neanderthal DNA helps humanity

Emily Singer writes: Early human history was a promiscuous affair. As modern humans began to spread out of Africa roughly 50,000 years ago, they encountered other species that looked remarkably like them — the Neanderthals and Denisovans, two groups of archaic humans that shared an ancestor with us roughly 600,000 years earlier. This motley mix of humans coexisted in Europe for at least 2,500 years, and we now know that they interbred, leaving a lasting legacy in our DNA. The DNA of non-Africans is made up of roughly 1 to 2 percent Neanderthal DNA, and some Asian and Oceanic island populations have as much as 6 percent Denisovan DNA.

Over the last few years, scientists have dug deeper into the Neanderthal and Denisovan sections of our genomes and come to a surprising conclusion. Certain Neanderthal and Denisovan genes seem to have swept through the modern human population — one variant, for example, is present in 70 percent of Europeans — suggesting that these genes brought great advantage to their bearers and spread rapidly.

“In some spots of our genome, we are more Neanderthal than human,” said Joshua Akey, a geneticist at the University of Washington. “It seems pretty clear that at least some of the sequences we inherited from archaic hominins were adaptive, that they helped us survive and reproduce.”

But what, exactly, do these fragments of Neanderthal and Denisovan DNA do? What survival advantage did they confer on our ancestors? Scientists are starting to pick up hints. Some of these genes are tied to our immune system, to our skin and hair, and perhaps to our metabolism and tolerance for cold weather, all of which might have helped emigrating humans survive in new lands.

“What allowed us to survive came from other species,” said Rasmus Nielsen, an evolutionary biologist at the University of California, Berkeley. “It’s not just noise, it’s a very important substantial part of who we are.” [Continue reading…]

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Genes are overrated

Nathaniel Comfort writes: In the Darwinian struggle of scientific ideas, the gene is surely among the select. It has become the foundation of medicine and the basis of vigorous biotechnology and pharmaceutical industries. Media coverage of recent studies touts genes for crime, obesity, intelligence — even the love of bacon. We treat our genes as our identity. Order a home genetic-testing kit from the company 23andMe, and the box arrives proclaiming, “Welcome to you.” Cheerleaders for crispr, the new, revolutionarily simple method of editing genes, foretell designer babies, the end of disease, and perhaps even the transformation of humanity into a new and better species. When we control the gene, its champions promise, we will be the masters of our own destiny.

The gene has now found a fittingly high-profile chronicler in Siddhartha Mukherjee, the oncologist-author of the Pulitzer Prize–winning The Emperor of All Maladies, a history of cancer. The Gene’s dominant traits are historical breadth, clinical compassion, and Mukherjee’s characteristic graceful style. He calls it “an intimate history” because he shares with us his own dawning awareness of heredity and his quest to make meaning of it. The curtain rises on Kolkata, where he has gone to visit Moni, his paternal cousin, who has been diagnosed with schizophrenia. In addition to Moni, two of the author’s uncles were afflicted with “various unravelings of the mind.” Asked for a Bengali term for such inherited illness, Mukherjee’s father replies, “Abheder dosh” — a flaw in identity. Schizophrenia becomes a troubling touchstone throughout the book. But the Indian interludes are tacked onto an otherwise conventional triumphalist account of European-American genetics, written from the winners’ point of view: a history of the emperor of all molecules. [Continue reading…]

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Missing mitochondria show life doesn’t relentlessly pursue complexity

Sarah Kaplan writes: Life on Earth used to be simple.

Once upon a time, every organism on the planet was a single, simple cell. Scientists call them prokaryotes. They are about as basic as a living thing can be — just little balloons of DNA and protein, with no grander goals in life than to swim around, eat and occasionally duplicate themselves to produce more swimmers and eaters.

Then, about 1.5 billion years ago, something strange and spectacular happened. One prokaryote engulfed another, and instead of digesting it, he put the little guy to work. They established an endosymbiotic relationship: The smaller internal cell performed lots of helpful tasks — such as making energy and building proteins — and in exchange, the bigger cell kept it safe and well-fed. This lucky bit of teamwork gave rise to the complex (a.k.a. eukaryotic) cell that exists today, from curious single-celled protists to the cells that make up all plants, fungi and animals — including us.

The eukaryotes are a weird and diverse lot, but at the cellular level we’ve all got the same basic components: a nucleus to store our DNA, and mitochondria — the descendants of that ancient swallowed organism — to make energy and perform other essential functions. Other internal structures, called organelles, may vary, but those two are so universal that biologists assumed we couldn’t exist without them.

“They’re part of the definition of eukaryotic cell,” said Anna Karnkowska, an evolutionary biologist at the University of British Columbia. “If you open a biology textbook to a picture of a eukaryotic cell, that’s what you’ll see.”

Which is why she was so shocked to find a eukaryote that didn’t have any mitochondria at all: a single-celled relative of the giardia parasite called Monocercomonoides.

The discovery, which Karnkowska made with other biologists when she was a post-doctoral fellow at Charles University in Prague, seems to rip up that textbook illustration. One of her co-authors compared it to finding a city with no utilities or public works department.

“This is the first example of a eukaryote lacking any form of a mitochondrion,” the researchers write in their study, which was published Thursday in the journal Current Biology, “demonstrating that this organelle is not absolutely essential for the viability of a eukaryotic cell.” [Continue reading…]

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Brainless intelligence observed in slime

Phys.org reports: What is intelligence? The definitions vary, but all infer the use of grey matter, whether in a cat or a human, to learn from experience.

On Wednesday, scientists announced a discovery that turns this basic assumption on its head.
A slime made up of independent, single cells, they found, can “learn” to avoid irritants despite having no central nervous system.

“Tantalizing results suggest that the hallmarks for learning can occur at the level of single cells,” the team wrote in a paper published in the journal Proceedings of the Royal Society B. [Continue reading…]

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Humans paid for bigger brains with energy-hungry bodies

Ed Yong writes: Evolution works on a strict energy budget. Each adaptation burns through a certain number of calories, and each individual can only acquire so many calories in the course of a day. You can’t have flapping wings and a huge body and venom and fast legs and a big brain. If you want to expand some departments, you need to make cuts in others. That’s why, for example, animals that reproduce faster tend to die earlier. They divert energy towards making new bodies, and away from maintaining their own.

But humans, on the face of it, are exceptional. Compared to other apes, we reproduce more often (or, at least, those of us in traditional societies do) and our babies are bigger when they’re born and we live longer. And, as if to show off, our brains are much larger, and these huge organs sap some 20 percent of our total energy.

“We tend to have our cake and eat it too,” says Herman Pontzer from Hunter College. “These traits that make us human are all energetically costly. And until now, we didn’t really understand how we were fueling them.” [Continue reading…]

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One gene can produce many different proteins

Veronique Greenwood writes: The millimeter-long roundworm Caenorhabditis elegans has about 20,000 genes — and so do you. Of course, only the human in this comparison is capable of creating either a circulatory system or a sonnet, a state of affairs that made this genetic equivalence one of the most confusing insights to come out of the Human Genome Project. But there are ways of accounting for some of our complexity beyond the level of genes, and as one new study shows, they may matter far more than people have assumed.

For a long time, one thing seemed fairly solid in biologists’ minds: Each gene in the genome made one protein. The gene’s code was the recipe for one molecule that would go forth into the cell and do the work that needed doing, whether that was generating energy, disposing of waste, or any other necessary task. The idea, which dates to a 1941 paper by two geneticists who later won the Nobel Prize in medicine for their work, even has a pithy name: “one gene, one protein.”

Over the years, biologists realized that the rules weren’t quite that simple. Some genes, it turned out, were being used to make multiple products. In the process of going from gene to protein, the recipe was not always interpreted the same way. Some of the resulting proteins looked a little different from others. And sometimes those changes mattered a great deal. There is one gene, famous in certain biologists’ circles, whose two proteins do completely opposite things. One will force a cell to commit suicide, while the other will stop the process. And in one of the most extreme examples known to science, a single fruit fly gene provides the recipe for more than 38,000 different proteins.

But these are dramatic cases. It was never clear just how common it is for genes to make multiple proteins and how much those differences matter to the daily functioning of the cell. Many researchers have assumed that the proteins made by a given gene probably do not differ greatly in their duties. It’s a reasonable assumption — many small-scale tests of sibling proteins haven’t suggested that they should be wildly different.

It is still an assumption, however, and testing it is quite an endeavor. Researchers would have to take a technically tricky inventory of the proteins in a cell and run numerous tests to see what each one does. In a recent paper in Cell, however, researchers at the Dana-Farber Cancer Institute in Boston and their collaborators reveal the results of just such an effort. They found that in many cases, proteins made by a single gene are no more alike in their behavior than proteins made by completely different genes. Sibling proteins often act like strangers. It’s an insight that opens up an interesting new set of possibilities for thinking about how the cell — and the human body — functions. [Continue reading…]

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Why are your gut microbes different from mine?

Ed Yong writes: There are tens of trillions of bacteria in my gut and they are different from those in yours. Why?

This is a really basic question about the human microbiome and, rather vexingly, we still don’t have a good answer. Sure, we know some of the things that influence the roll call of species — diet and antibiotics, to name a few — but their relative importance is unclear and the list is far from complete. That bodes poorly for any attempt to work out whether these microbes are involved in diseases, and whether they can be tweaked to improve our health.

Two new studies have tried to address the problem. They’re the largest microbiome studies thus far published, looking at 1,135 Dutch adults and 1,106 Belgians respectively. Both looked at how hundreds of factors affect the microbiome, including age, height, weight, sleep, medical history, smoking, allergies, blood levels of various molecules, and a long list of foods. Both found dozens of factors that affect either the overall diversity of microbial species, or the abundance of particular ones. And encouragingly, their respective lists overlap considerably.

But here’s the important thing: Collectively, the factors they identified explain a tiny proportion of the variation between people’s microbiomes — 19 percent in the Dutch study, and just 8 percent in the Belgian. Which means we’re still largely in the dark about what makes my microbiome different from yours, let alone whether one is healthier than the other. [Continue reading…]

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Your lungs are full of microorganisms … and that’s a good thing

By Ian Hall, University of Nottingham

When we’re born, our lungs are thought to be sterile. But from the moment we take our first breath, our pristine lungs are exposed to all the bugs that are in the air. It has become clear in the last 10 years that the lungs rapidly acquire a population of many different microorganisms (mostly bacteria and viruses) that colonise the lungs and remain with us for the rest of our lives. This population of bugs is called the lung microbiome.

We now know more about the lung microbiome thanks to genetics. In the past, identifying the types of bugs present in the lungs depended on being able to grow them in a laboratory, and for many types of bug this was difficult. The big change that happened recently is our ability to recognise both the different bug species, and their relative abundance, by using DNA sequencing. This can be done either from a sample taken from the lungs or from sputum (the mucus we cough up when we have an infection).

Is the lung microbiome a good or a bad thing?

We all know that bacteria in the lungs can be harmful. When harmful bacteria multiply, they cause pneumonia which, despite the existence of antibiotics, can still be deadly. However, it seems that the lung microbiome usually exists in a balanced state, such that harmful types of bugs do not increase in number sufficiently to cause pneumonia. In fact, it’s possible that the very presence of such a diverse range of bugs in the lungs is one of the reasons it’s quite difficult for harmful bugs to multiply and cause disease.

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In order for our minds to go beyond syntax to semantics, we need feelings

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Stephen T Asma writes: After you spend time with wild animals in the primal ecosystem where our big brains first grew, you have to chuckle a bit at the reigning view of the mind as a computer. Most cognitive scientists, from the logician Alan Turing to the psychologist James Lloyd McClelland, have been narrowly focused on linguistic thought, ignoring the whole embodied organism. They see the mind as a Boolean algebra binary system of 1 or 0, ‘on’ or ‘off’. This has been methodologically useful, and certainly productive for the artifical intelligence we use in our digital technology, but it merely mimics the biological mind. Computer ‘intelligence’ might be impressive, but it is an impersonation of biological intelligence. The ‘wet’ biological mind is embodied in the squishy, organic machinery of our emotional systems — where action-patterns are triggered when chemical cascades cross volumetric tipping points.

Neuroscience has begun to correct the computational model by showing how our rational, linguistic mind depends on the ancient limbic brain, where emotions hold sway and social skills dominate. In fact, the cognitive mind works only when emotions preferentially tilt our deliberations. The neuroscientist Antonio Damasio worked with patients who had damage in the communication system between the cognitive and emotional brain. The subjects could compute all the informational aspects of a decision in detail, but they couldn’t actually commit to anything. Without clear limbic values (that is, feelings), Damasio’s patients couldn’t decide their own social calendars, prioritise jobs at work, or even make decisions in their own best interest. Our rational mind is truly embodied, and without this emotional embodiment we have no preferences. In order for our minds to go beyond syntax to semantics, we need feelings. And our ancestral minds were rich in feelings before they were adept in computations.

Our neo-cortex mushroomed to its current size less than one million years ago. That’s a very recent development when we remember that the human clade or group broke off from the great apes in Africa 7 million years ago. That future-looking, tool-wielding, symbol-juggling cortex grew on top of the limbic system. Older still is the reptile brain — the storehouse of innate motivational instincts such as pain-avoidance, exploration, hunger, lust, aggression and so on. Walking around (very carefully) on the Serengeti is like visiting the nursery of our own mind. [Continue reading…]

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Why ‘natural selection’ became Darwin’s fittest metaphor

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Kensy Cooperrider writes: ome metaphors end up forgotten by all but the most dedicated historians, while others lead long, productive lives. It’s only a select few, though, that become so entwined with how we understand the world that we barely even recognize them as metaphors, seeing them instead as something real. Of course, why some fizzle and others flourish can be tricky to account for, but their career in science provides some clues.

Metaphors, as we all by now know, aren’t just ornamental linguistic flourishes — they’re basic building blocks of everyday reasoning. And they’re at their most potent when they recast a difficult-to-understand phenomenon as something familiar: The brain becomes a computer; the atom, a tiny solar system; space-time, a fabric. Metaphors that tap into something familiar are the ones that generally gain traction.

Charles Darwin gave us both kinds, big winners and total flops. Natural selection, his best-known metaphor, is still a fixture of evolutionary biology. Though it’s not always recognized as a metaphor today, that’s exactly what it was to Darwin and his contemporaries. After all, evolution was a foreign and unwieldy concept. So Darwin set out to make it accessible by comparing it to a method employed in farmyards around the world.

For years, Darwin — a fancy pigeon breeder — obsessed over what he called artificial selection, what cattle-breeders, gardeners, and crop-growers did to create new varieties of plant and animal: allowing just the ones with desirable traits to reproduce. Darwin’s first-hand experience with breeding set the stage for his now-famous metaphoric leap. [Continue reading…]

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