We’ve all had that annoying feeling when we fail to find a word that’s just at the tip of our tongues. Usually, these moments are passing nuisances, but they are a more severe impediment for a British family known as JR. Eight of them suffer from an unusual problem with “semantic cognition” – the ability to bind words to their meanings during thought or communication.
They can’t remember words, names, or topics of conversation – all of us get this, but the JR family experiences a more extreme version. They make errors in everyday conversations when they use words with related meanings in the wrong places. Their comprehension falters to the extent that reading books or following films is hard work.
These difficulties have caused them much social anxiety, and hampered their ability to cope with school and work. But for scientists, they are undeniably exciting because they seem to stem from a single errant gene. If that’s the case, the gene apparently affects the intertwining of concepts and language, but not any other mental abilities – the affected family members are otherwise intelligent and articulate. The JR family could lead us to new insights about language, thought and memory, just as similar families have done in the past.
Countries around the world have tried many tactics to encourage people to vote, from easier access to polling stations to mandatory registration. But Christopher Bryan from Stanford University has found a startlingly simple weapon for increasing voter turnout – the noun. Through a simple linguistic tweak, he managed to increase the proportion of voters in two groups of Americans by at least 10 percentage points.
During the 2008 presidential election, Bryan recruited 34 Californians who were eligible to vote but hadn’t registered yet. They all completed a survey which, among other questions, asked them either “How important is it to you to be a voter in the upcoming election?” or “How important is it to you to vote in the upcoming election?”
It was the tiniest of tweaks – the noun-focused “voter” versus the verb-focused “vote” – but it was a significant one. Around 88% of the noun group said they were very or extremely interested in registering to vote, compared to just 56% of the verb group.
Just as petrified fossils tell us about the evolution of life on earth, the words written in books narrate the history of humanity. They words tell a story, not just through the sentences they form, but in how often they occur. Uncovering those tales isn’t easy – you’d need to convert books into a digital format so that their text can be analysed and compared. And you’d need to do that for millions of books.
Fortunately, that’s exactly what Google have been doing since 2004. Together with over 40 university libraries, the internet titan has thus far scanned over 15 million books, creating a massive electronic library that represents 12% of all the books ever published. All the while, a team from Harvard University, led by Jean-Baptiste Michel and Erez Lieberman Aiden have been analysing the flood of data.
Their first report is available today. Although it barely scratches the surface, it’s already a tantalising glimpse into the power of the Google Books corpus. It’s a record of human culture, spanning six centuries and seven languages. It shows vocabularies expanding and grammar evolving. It contains stories about our adoption of technology, our quest for fame, and our battle for equality. And it hides the traces of tragedy, including traces of political suppression, records of past plagues, and a fading connection with our own history.
This is an old article, reposted from the original WordPress incarnation of Not Exactly Rocket Science. I’m on holiday for the moment, but you can expect a few new pieces here and there (as well as some exciting news…)
The birth of new languages is accompanied by a burst of rapid evolution consisting of large changes in vocabulary that are followed by long periods of relatively slower change.
Languages are often compared to living species because of the way in which they diverge into new tongues over time in an ever-growing linguistic tree. Some critics have claimed that this comparison is a superficial one, a nice metaphor but nothing more.
But the new study by Quentin Atkinson, now at the University of Oxford, suggests that languages evolve at a similar stop-and-start pace, which uncannily echoes a long-standing theory in biology, known as ‘punctuated equilibrium’. The theory’s followers claim that life on Earth also evolved at an uneven pace, full of rapid bursts and slow periods.
In the 1970s, a group of deaf Nicaraguan schoolchildren invented a new language. The kids were the first to enrol in Nicaragua’s new wave of special education schools. At first, they struggled with the schools’ focus on Spanish and lip-reading, but they found companionship in each other. It was the first time that deaf people from all over the country could gather in large numbers and through their interactions – in the schoolyard and the bus – Nicaraguan Sign Language (NSL) spontaneously came into being.
NSL is not a direct translation of Spanish – it is a language in its own right, complete with its own grammar and vocabulary. Its child inventors created it naturally by combining and adding to gestures that they had used at home. Gradually, the language became more regular, more complex and faster. Ever since, NSL has been a goldmine for scientists, providing an unparalleled opportunity to study the emergence of a new language. And in a new study led by Jennie Pyers from Wellesley College, it even tells us how language shapes our thought.
By studying children who learned NSL at various stages of its development, Pyers has shown that the vocabulary they pick up affects the way they think. Specifically, those who learned NSL before it developed specific gestures for left and right perform more poorly on a spatial awareness test than children who grew up knowing how to sign those terms.
We like to be in control of our own lives, and some of us have an automatic rebellious streak when we’re told what to do. We’re less likely to do a task if we’re ordered to do it than if we make the choice of our own volition. It seems that this effect is so strong that it even happens when the people giving the orders are… us.
In a set of three experiments, Ibrahim Senay from the University of Illinois has shown that people do better at a simple task if ask themselves whether they’ll do it than if they simply tell themselves to do so. Even a simple reversal of words – “Will I” compared to “I will” – can boost motivation and performance.
Therapists and managers alike are taught to ask people open questions that prompt them to think about problems for themselves, rather than having solutions imposed upon them. Senay’s work suggests that this approach would work even if we’re counselling or managing ourselves. When we question ourselves about our deeds and choices, we’re more likely to consider our motivations for doing something and feel like we’re in control of our actions. The effect is small but significant.
Many human languages achieve great diversity by combining basic words into compound ones – German is a classic example of this. We’re not the only species that does this. Campbell’s monkeys have just six basic types of calls but they have combined them into one of the richest and most sophisticated of animal vocabularies.
By chaining calls together in ways that drastically alter their meaning, they can communicate to each other about other falling trees, rival groups, harmless animals and potential threats. They can signal the presence of an unspecified threat, a leopard or an eagle, and even how imminent the danger is. It’s a front-runner for the most complex example of animal “proto-grammar” so far discovered.
Many studies have shown that the chirps and shrieks of monkeys are rich in information, ever since Dorothy Cheney and Robert Seyfarth’s seminal research on vervet monkeys. They showed that vervets have specific calls for different predators – eagles, leopards and snakes – and they’ll take specific evasive manoeuvres when they hear each alarm.
Campbell’s monkeys have been equally well-studied. Scientists used to think that they made two basic calls – booms and hacks – and that the latter were predator alarms. Others then discovered that the order of the calls matters, so adding a boom before a hack cancels out the predator message. It also turned out that there were five distinct types of hack, including some that were modified with an -oo suffix. So Campbell’s monkeys not only have a wider repertoire of calls than previously thought, but they can also combine them in meaningful ways.
Now, we know that the males make six different types of calls, comically described as boom (B), krak (K), krak-oo (K+), hok (H), hok-oo (H+) and wak-oo (W+). To decipher their meaning, Karim Ouattara spent 20 months in the Ivory Coast’s Tai National Park studying the wild Campbell’s monkeys from six different groups. Each consists of a single adult male together with several females and youngsters. And it’s the males he focused on.
With no danger in sight, males make three call sequences. The first – a pair of booms – is made when the monkey is far away from the group and can’t see them. It’s a summons that draws the rest of the group towards him. Adding a krak-oo to the end of the boom pair changes its meaning. Rather than “Come here”, the signal now means “Watch out for that branch”. Whenever the males cried “Boom-boom-krak-oo”, other monkeys knew that there were falling trees or branches around (or fighting monkeys overhead that could easily lead to falling vegetation).
Interspersing the booms and krak-oos with some hok-oos changes the meaning yet again. This call means “Prepare for battle”, and it’s used when rival groups or strange males have showed up. In line with this translation, the hok-oo calls are used far more often towards the edge of the monkeys’ territories than they are in the centre. The most important thing about this is that hok-oo is essentially meaningless. The monkeys never say it in isolation – they only use it to change the meaning of another call.
But the most complex calls are reserved for threats. When males know that danger is afoot but don’t have a visual sighting (usually because they’ve heard a suspicious growl or an alarm from other monkeys), they make a few krak-oos.
If they know it’s a crowned eagle that endangers the group, they combine krak-oo and wak-oo calls. And if they can actually see the bird, they add hoks and hok-oos into the mix – these extra components tell other monkeys that the peril is real and very urgent. Leopard alarms were always composed of kraks, and sometimes krak-oos. Here, it’s the proportion of kraks that signals the imminence of danger – the males don’t make any if they’ve just heard leopard noises, but they krak away if they actually see the cat.
The most important part of these results is the fact that calls are ordered in very specific ways. So boom-boom-krak-oo means a falling branch, but boom-krak-oo-boom means nothing. Some sequences act as units that can be chained together to more complicated ones – just as humans use words, clauses and sentences. They can change meaning by adding meaningless calls onto meaningful ones (BBK+ for falling wood but BBK+H+ for neighbours) or by chaining meaningful sequences together (K+K+ means leopard but W+K+ means eagle).
It’s tempting to think that monkeys have hidden linguistic depths to rival those of humans but as Ouattara says, “This system pales in contrast to the communicative power of grammar.” They monkeys’ repertoire may be rich, but it’s still relatively limited and they don’t take full advantage of their vocabulary. They can create new meanings by chaining calls together, but never by inverting their order (e.g. KB rather than BK). Our language is also symbolic. I can tell you about monkeys even though none are currently scampering about my living room, but Ouattara only found that Campbell’s monkeys “talk” about things that they actually see.
Nonetheless, you have to start somewhere, and the complexities of human syntax probably have their evolutionary origins in these sorts of call combinations. So far, the vocabulary of Campbell’s monkeys far outstrips those of other species, but this may simply reflect differences in research efforts. Other studies have started to find complex vocabularies in other forest-dwellers like Diana monkeys and putty-nosed monkeys. Ouattara thinks that forest life, with many predators and low visibility, may have provided strong evolutionary pressures for monkeys to develop particularly sophisticated vocal skills.
And there are probably hidden depths to the sequences of monkey calls that we haven’t even begun to peer into yet. For instance, what calls do female Campbell’s monkeys make? Even for the males, the meanings in this study only become apparent after months of intensive field work and detailed statistical analysis. The variations that happen on a call-by-call basis still remain a mystery to us. The effect would be like looking at Jane Austen’s oeuvre and concluding, “It appears that these sentences signify the presence of posh people”.
Reference: PNAS doi:10.1073/pnas.0908118106
More on monkey business (clearly, I need more headline variation):
Today, a new paper published in Nature adds another chapter to the story of FOXP2, a gene with important roles in speech and language. The FOXP2 story is a fascinating tale that I covered in New Scientist last year. It’s one of the pieces I’m proudest of so I’m reprinting it here with kind permission from Roger Highfield, and with edits incorporating new discoveries since the time of writing.
The FOXP2 Story (2009 edition)
Imagine an orchestra full of eager musicians which, thanks to an incompetent conductor, produces nothing more than an unrelieved cacophony. You’re starting to appreciate the problem faced by a British family known as KE. About half of its members have severe difficulties with language. They have trouble with grammar, writing and comprehension, but above all they find it hard to coordinate the complex sequences of face and mouth movements necessary for fluid speech.
Thanks to a single genetic mutation, the conductor cannot conduct, and the result is linguistic chaos. In 2001, geneticists looking for the root of the problem tracked it down to a mutation in a gene they named FOXP2. Normally, FOXP2 coordinates the expression of other genes, but in affected members of the KE family, it was broken.
It had long been suspected that language has some basis in genetics, but this was the first time that a specific gene had been implicated in a speech and language disorder. Overeager journalists quickly dubbed FOXP2 “the language gene” or the “grammar gene”. Noting that complex language is a characteristically human trait, some even speculated that FOXP2 might account for our unique position in the animal kingdom. Scientists were less gushing but equally excited – the discovery sparked a frenzy of research aiming to uncover the gene’s role.
Several years on, and it is clear that talk of a “language gene” was premature and simplistic. Nevertheless, FOXP2 tells an intriguing story. “When we were first looking for the gene, people were saying that it would be specific to humans since it was involved in language,” recalls Simon Fisher at the University of Oxford, who was part of the team that identified FOXP2 in the KE family. In fact, the gene evolved before the dinosaurs and is still found in many animals today: species from birds to bats to bees have their own versions, many of which are remarkably similar to ours. “It gives us a really important lesson,” says Fisher. “Speech and language didn’t just pop up out of nowhere. They’re built on very highly conserved and evolutionarily ancient pathways.”
Two amino acids, two hundred thousand years
The first team to compare FOXP2 in different species was led by Wolfgang Enard from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. In 2001, they looked at the protein that FOXP2 codes for, called FOXP2, and found that our version differs from those of chimpanzees, gorillas and rhesus macaques by two amino acids out of a total of 715, and from that of mice by three. This means that the human version of FOXP2 evolved recently and rapidly: only one amino acid changed in the 130 million years since the mouse lineage split from that of primates, but we have picked up two further differences since we diverged from chimps, and this seems to have happened only with the evolution of our own species at most 200,000 years ago.
The similarity between the human protein FOXP2 and that of other mammals puts it among the top 5 per cent of the most conserved of all our proteins. What’s more, different human populations show virtually no variation in their FOXP2 gene sequences. Last year, Enard’s colleague Svante Pääbo made the discovery that Neanderthals also had an identical gene, prompting questions over their linguistic abilities (see “Neanderthal echoes below).
“People sometimes think that the mutated FOXP2 in the KE family is a throwback to the chimpanzee version, but that’s not the case,” says Fisher. The KEs have the characteristically human form of the gene. Their mutation affects a part of the FOXP2 protein that interacts with DNA, which explains why it has trouble orchestrating the activity of other genes.
There must have been some evolutionary advantage associated with the human form of FOXP2, otherwise the two mutations would not have spread so quickly and comprehensively through the population. What this advantage was, and how it may have related to the rise of language, is more difficult to say. Nevertheless, clues are starting to emerge as we get a better picture of what FOXP2 does – not just in humans but in other animals too.
During development, the gene is expressed in the lungs, oesophagus and heart, but what interests language researchers is its role in the brain. Here there is remarkable similarity across species: from humans to finches to crocodiles, FOXP2 is active in the same regions. With no shortage of animal models to work with, several teams have chosen songbirds due to the similarities between their songs and human language: both build complex sequences from basic components such as syllables and riffs, and both forms of vocalisation are learned through imitation and practice during critical windows of development.
All bird species have very similar versions of FOXP2. In the zebra finch, its protein is 98 per cent identical to ours, differing by just eight amino acids. It is particularly active in a part of the basal ganglia dubbed “area X”, which is involved in song learning. Constance Scharff at the Max Planck Institute for Molecular Genetics in Berlin, Germany, reported that finches’ levels of FOXP2 expression in area X are highest during early life, which is when most of their song learning takes place. In canaries, which learn songs throughout their lives, levels of the protein shoot up annually and peak during the late summer months, which happens to be when they remodel their songs.
So what would happen to a bird’s songs if levels of the FOXP2 protein in its area X were to plummet during a crucial learning window? Scharff found out by injecting young finches with a tailored piece of RNA that inhibited the expression of the FOXP2 gene. The birds had difficulties in developing new tunes and their songs became garbled: they contained the same component “syllables” as the tunes of their tutors, but with syllables rearranged, left out, repeated incorrectly or sung at the wrong pitch.
The cacophony produced by these finches bears uncanny similarities to the distorted speech of the afflicted KE family members, making it tempting to pigeonhole FOXP2 as a vocal learning gene – influencing the ability to learn new communication sounds by imitating others. But that is no more accurate than calling it a “language gene”. For a start, songbird FOXP2 has no characteristic differences to the gene in non-songbirds. What’s more, among other species that show vocal learning, such as whales, dolphins and elephants, there are no characteristic patterns of mutation in their FOXP2 that they all share.
Instead, consensus is emerging that FOXP2 probably plays a more fundamental role in the brain. Its presence in the basal ganglia and cerebellums of different animals provides a clue as to what that role might be. Both regions help to produce precise sequences of muscle movements. Not only that, they are also able to integrate information coming in from the senses with motor commands sent from other parts of the brain. Such basic sensory-motor coordination would be vital for both birdsong and human speech. So could this be the key to understanding FOXP2?
New work by Fisher and his colleagues supports this idea. In 2008, his team engineered mice to carry the same FOXP2 mutation that affects the KE family, rendering the protein useless. Mice with two copies of the dysfunctional FOXP2 had shortened lives, characterised by motor disorders, growth problems and small cerebellums. Mice with one normal copy of FOXP2 and one faulty copy (as is the case in the affected members of the KE family) seemed outwardly healthy and capable of vocalisation, but had subtle defects.
For example, they found it difficult to acquire new motor skills such as learning to run faster on a tilted running wheel. An examination of their brains revealed the problem. The synapses connecting neurons within the cerebellum, and those in a part of the basal ganglia called the striatum in particular, were severely flawed. The signals that crossed these synapses failed to develop the long-term changes that are crucial for memory and learning. The opposite happened when the team engineered mice to produce a version of FOXP2 with the two characteristically human mutations. Their basal ganglia had neurons with longer outgrowths (dendrites) that were better able to strengthen or weaken the connections between them.
A battery of over 300 physical and mental tests showed that the altered mice were generally healthy. While they couldn’t speak like their cartoon equals, their central nervous system developed in different ways, and they showed changes in parts of the brain where FOXP2 is usually expressed (switched on) in humans.
Their squeaks were also subtly transformed. When mouse babies are moved away from their nest, they make ultrasonic distress calls that are too high for us to hear, but that their mothers pick up loudly and clearly. The altered Foxp2 gene subtly changed the structure of these alarm calls. We won’t know what this means until we get a better understanding of the similarities between mouse calls and human speech.
For now, the two groups of engineered mice tentatively support the idea that human-specific changes to FOXP2 affect aspects of speech, and strongly support the idea that they affect aspects of learning. “This shows, for the first time, that the [human-specific] amino-acid changes do indeed have functional effects, and that they are particularly relevant to the brain,” explains Fisher. “FOXP2 may have some deeply conserved role in neural circuits involved in learning and producing complex patterns of movement.” He suspects that mutant versions of FOXP2 disrupt these circuits and cause different problems in different species.
Pääbo agrees. “Language defects may be where problems with motor coordination show up most clearly in humans, since articulation is the most complex set of movements we make in our daily life,” he says. These circuits could underpin the origins of human speech, creating a biological platform for the evolution of both vocal learning in animals and spoken language in humans.
Holy diversity, Batman
The link between FOXP2 and sensory-motor coordination is bolstered further by research in bats. Sequencing the gene in 13 species of bats, Shuyi Zhang and colleagues from the East China Normal University in Shanghai discovered that it shows incredible diversity. Why would bats have such variable forms of FOXP2 when it is normally so unwavering in other species?
Zhang suspects that the answer lies in echolocation. He notes that the different versions seem to correspond with different systems of sonar navigation used by the various bat species. Although other mammals that use echolocation, such as whales and dolphins, do not have special versions of FOXP2, he points out that since they emit their sonar through their foreheads, these navigation systems have fewer moving parts. Furthermore, they need far less sensory-motor coordination than flying bats, which vocalise their ultrasonic pulses and adjust their flight every few milliseconds, based on their interpretation of the echoes they receive.
These bats suggest that FOXP2 is no more specific to basic communication than it is to language, and findings from other species tell a similar tale. Nevertheless, the discovery that this is an ancient gene that has assumed a variety of roles does nothing to diminish the importance of its latest incarnation in humans.
Since its discovery, no other gene has been convincingly implicated in overt language disorders. FOXP2 remains our only solid lead into the genetics of language. “It’s a molecular window into those kinds of pathways – but just one of a whole range of different genes that might be involved,” says Fisher. “It’s a starting point for us, but it’s not the whole story.” He has already used FOXP2 to hunt down other key players in language.
The executive’s minions
FOXP2 is a transcription factor, which activates some genes while suppressing others. Identifying its targets, particularly in the human brain, is the next obvious step. Working with Daniel Geschwind at the University of California, Los Angeles, Fisher has been trying to do just that, and their preliminary results indicate just what a massive job lies ahead. On their first foray alone, the team looked at about 5000 different genes and found that FOXP2 potentially regulates hundreds of these.
Some of these target genes control brain development in embryos and its continuing function in adults. Some affect the structural pattern of the developing brain and the growth of neurons. Others are involved in chemical signalling and the long-term changes in neural connections that enable to learning and adaptive behaviour. Some of the targets are of particular interest, including 47 genes that are expressed differently in human and chimpanzee brains, and a slightly overlapping set of 14 targets that have evolved particularly rapidly in humans.
Most intriguingly, Fisher says, “we have evidence that some FOXP2 targets are also implicated in language impairment.” Last year, Sonja Vernes in his group showed that FOXP2 switches off CNTNAP2, a gene involved in not one but two language disorders – specific language impairment (SLI) and autism. Both affect children, and both involve difficulties in picking up spoken language skills. The protein encoded by CNTNAP2 is deployed by nerve cells in the developing brain. It affects the connections between these cells and is particularly abundant in neural circuits that are involved in language.
Verne’s discovery is a sign that the true promise of FOXP2’s discovery is being fulfilled – the gene itself has been overly hyped, but its true worth lies in opening a door for more research into genes involved in language. It was the valuable clue that threw the case wide open. CNTNAP2 may be the first language disorder culprit revealed through FOXP2 and it’s unlikely to be the last.
Most recently, Dan Geschwind compared the network of genes that are targeted by FOXP2 in both chimps and humans. He found that the two human-specific amino acids within this executive protein have radically altered the set of genetic minions that it controls.
The genes that are directed by human FOXP2 are a varied cast of players that influence the development of the head and face, parts of the brain involved in motor skills, the growth of cartilage and connective tissues, and the development of the nervous system. All those roles fit with the idea that our version of FOXP2 has been a lynchpin in evolving the neural circuits and physical structures that are important for speech and language.
The FOXP2 story is far from complete, and every new discovery raises fresh questions just as it answers old ones. Already, this gene has already taught us important lessons about evolution and our place in the natural world. It shows that our much vaunted linguistic skills are more the result of genetic redeployment than out-and-out innovation. It seems that a quest to understand how we stand apart from other animals is instead leading to a deeper appreciation of what unites us.
Box – Neanderthal echoes
The unique human version of the FOXP2 gives us a surprising link with one extinct species. Last year, Svante Pääbo’s group at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted DNA from the bones of two Neanderthals, one of the first instances of geneticists exploring ancient skeletons for specific genes. They found that Neanderthal FOXP2 carries the same two mutations as those carried by us – mutations accrued since our lineage split from chimps between 6 and 5 million years ago.
Pääbo admits that he “struggled” to interpret the finding: the Neanderthal DNA suggests that the modern human’s version of FOXP2 arose much earlier than previously thought. Comparisons of gene sequences of modern humans with other living species had put the origins of human FOXP2 between 200,000 and 100,000 years ago, which matches archaeological estimates for the emergence of spoken language. However, Neanderthals split with humans around 400,000 years ago, so the discovery that they share our version of FOXP2 pushes the date of its emergence back at least that far.
“We believe there were two things that happened in the evolution of human FOXP2,” says Pääbo. “The two amino acid changes – which happened before the Neanderthal-human split – and some other change which we don’t know about that caused the selective sweep more recently.” In other words, the characteristic mutations that we see in human FOXP2 may indeed be more ancient than expected, but the mutated gene only became widespread and uniform later in human history. While many have interpreted Pääbo’s findings as evidence that Neanderthals could talk, he is more cautious. “There’s no reason to assume that they weren’t capable of spoken language, but there must be many other genes involved in speech that we yet don’t know about in Neanderthals.”
Telling the difference between a German and French speaker isn’t difficult. But you may be more surprised to know that you could have a good stab at distinguishing between German and French babies based on their cries. The bawls of French newborns tend to have a rising melody, with higher frequencies becoming more prominent as the cry progresses. German newborns tend to cry with a falling melody.
These differences are apparent just three days out of the womb. This suggests that they pick up elements of their parents’ language before they’re even born, and certainly before they start to babble themselves.
Birgit Mampe from the University of Wurzburg analysed the cries of 30 French newborns and 30 German ones, all born to monolingual families. She found that the average German cry reaches its maximum pitch and intensity at around 0.45 seconds, while French cries do so later, at around 0.6 seconds.
These differences match the melodic qualities of each respective language. Many French words and phrases have a rising pitch towards the end, capped only by a falling pitch at the very end. German more often shows the opposite trend – a falling pitch towards the end of a word or phrase.
These differences in “melody contours” become apparent as soon as infants start making sounds of their own. While Mampe can’t rule out the possibility that the infants learned about the sounds of their native tongue the few days following their birth, she thinks it’s more likely that they start tuning into the own language in the womb.
In some ways, this isn’t surprising. Features like melody, rhythm and intensity (collectively known as prosody) travel well across the wall of the stomach and they reach the womb with minimum disruption. We know that infants are very sensitive to prosodic features well before they start speaking themselves, which helps them learn their own mother tongue.
But this learning process starts as early as the third trimester. We know this because newborns prefer the sound of their mother’s voice compared to those of strangers. And when their mums speak to them in the saccharine “motherese”, they can suss out the emotional content of those words through analysing their melody.
Mampe’s data show that not only can infants sense the qualities of their native tongue, they can also imitate them in their first days of life. Previously, studies have found that babies can imitate the vowel sounds of adults only after 12 weeks of life, but clearly other features like pitch can be imitated much earlier. They’re helped by the fact that crying only requires them to coordinate their breathing and vocal cord movements, while making speech sounds requires far more complex feats of muscular gymnastics that are only possible after a few months.
Reference: Current Biology doi:10.1016/j.cub.2009.09.064
More on child development:
From a young age, children learn about the sounds that animals make. But even without teaching aides like Old Macdonald’s farm, it turns out that very young babies have an intuitive understanding of the noises that humans, and even monkeys, ought to make. Athena Vouloumanos from New York University found that at just five months of age, infants match human speech to human faces and monkey calls to monkey faces. Amazingly, this wasn’t a question of experience – the same infants failed to match quacks to duck faces, even though they had more experience with ducks than monkeys.
Voloumanos worked with a dozen five-month-old infants from English- and French-speaking homes. She found that they spent longer looking at human faces when they were paired with spoken words than with monkey or duck calls. They clearly expect human faces, and not animal ones, to produce speech, even when the words in question came from a language – Japanese – that they were unfamiliar with. However, the fact that it was speech was essential; human laughter failed to grab their attention in the same way, and they didn’t show any biases towards either human or monkey faces.
More surprisingly, the babies also understood the types of calls that monkeys ought to make. They spent more time staring at monkey faces that were paired with monkey calls, than those paired with human words or with duck quacks.
That’s certainly unexpected. These babies had no experience with the sight or sounds of rhesus monkeys but they ‘got’ that monkey calls most likely come from monkey faces. Similarly, they appreciated that a human face is an unlikely source of a monkey call even though they could hardly have experienced every possible sound that the human mouth can make.
Perhaps they were just lumping all non-human calls and faces into one category? That can’t be true, for they would have matched the monkey faces to either monkey or duck calls. Perhaps they matched monkeys to their calls because they ruled out a link to more familiar human or duck sounds? That’s unlikely too, for the infants failed to match ducks faces to quacks!
Instead, Vouloumanos believes that babies have an innate ability to predict the types of noises that come from certain faces, and vice versa. Anatomy shapes the sound of a call into a audio signature that’s specific to each species. A human vocal tract can’t produce the same repertoire of noises as a monkey’s and vice versa. Monkeys can produce a wider range of frequencies than humans can, but thanks to innovations in the shape of our mouth and tongue, we’re better at subtly altering the sounds we make within our narrower range.
So the very shape of the face can provide clues about the noises likely to emerge from it, and previous studies have found that infants are very sensitive to these cues. This may also explain why they failed to match duck faces with their quacks – their visages as so vastly different to the basic primate design that they might not even be registered as faces, let alone as potential clues about sound.
If that’s not enough, Vouloumanos has a second possible explanation – perhaps babies use their knowledge of human sounds to set up a sort of “similarity gradient”. Simply put, monkey faces are sort of like human faces but noticeably different, so monkey calls should be sort of like human calls but noticeably different.
Either way, it’s clear that very young babies are remarkably sensitive to the sounds of their own species, particularly those of speech. The five month mark seems to be an important turning point, not just for this ability but for many others. By five months, they can already match faces with voices on the basis of age or emotion, but only after that does their ear for voices truly develop, allowing them to tune in to specific voices, or to the distinct sounds of their native language.
Reference: PNAS doi: 10.1073/pnas.0906049106
More on child development: