Linguistic Structure: the Result of L2 Learners?

Wray and Grace (2007) propose that the structure of a language is dependent of the social structure of the population who speak it. Lupyan & Dale (2010) later showed this using statistical analysis. This has been discussed extensively on this blog before:

One of the proposed reasons for why large population size is thought to affect linguistic structure is that larger populations will have a larger ratio of second language (L2) speakers to first language (L1) speakers.

Languages within exoteric niches (large population and geographical spread with many language neighbors) have been shown to be more more morphologically isolating and, as a result, regular. This has proposed to be because of the biases of adult second language learners.

Esoteric languages are more irregular and morphologically complex and idiosyncratic. This is thought to be because of the biases of child learners.

There are studies which show that adult learners have a tendency to regularise languages but only under some circumstances. Hudson Kam & Newport (2009) show that adult learners will regularise unpredictable variability but only if it exists above a certain level of scatter and complexity.

As for the learning biases of children, Wray & Grace (2007) cite only one study which looked at children who were ‘native’ speakers of Esperanto (Bergen, 2001). Bergen (2001) found that the language that the children learnt displayed a loss of the accusative case and also displayed attrition in the tense system. Although Wray & Grace (2007) suggest that this explains patterns seen in esoteric communities, it may not be as straight forward as they suggest. The evidence suggests that esoteric conditions are going to display more morphological strategies in their languages which is the opposite to the biases the child learners of Esperanto are displaying. The children are rejecting morphological strategies in favour of attrition and word order.

I wanted to point out in this post that there is evidence to suggest that adult learners preserve irregularities and idiosyncrasies, while children learners regularize (suggesting the opposite to Wray & Grace).

Studies which have addressed these problems include Hudson Kam & Newport (2005) where adult learners of an artificial language preserved unpredictable variation and child learners of the same language regularized it. Hudson Kam & Newport (2009) show in a similar study that child learners of an artificial language will regularise unpredictable irregularity but, as mentioned above, adult learners will only do this where the irregularity passes a certain level of complexity.

However, some evidence does support Wray & Grace’s (2007) proposal about adult learners.  Smith & Wonnacott (2010) show that despite there being a tendency within individual adult learners to maintain the level of unpredicted variability within the language learning process, when put into a diffusion chain of adult learners the language regularises.  Smith & Wonnacott (2010) suggest that gradual processes such as this can explain the regularisation of languages over time. While this fits nicely with Wray & Grace’s (2007) theory there is still the problem that children are just as liable to regularise as adults if not more so.


This is just some relevant experiments which I thought lent something to the debate. I know there are other factors which have been proposed to have an effect on linguistic structure. I was just curious about people’s opinions on quite to what level L2 speakers have an effect.

Chris Knight Arrested

Sorry, this isn’t really Language Evolution related besides Chris Knight’s obvious connection to the subject but thought it would be of interest to readers of the blog.

Last night Chris Knight and Camilla Power were arrested after planning to execute effigies of Prince William at Westminster Abbey. They were arrested ahead of the royal wedding today.

A professor of anthropology at the University of East London, Chris Knight along with his partner, Camilla Power, also a anthropology lecturer at UEL, were arrested outside their home in southeast London at around 6.15pm.

They were arrested on suspicion of conspiracy to cause public nuisance and breach of the peace.

Dr Knight was seen laid down on the pavement during the arrest in an attempt to stop officers moving him into a police van. But the police prevailed and they were held in a police station overnight.

This is not the first time Dr Knight has caused trouble. He was sacked from his position in 2009, following claims that he incited violence at the G20 protests.

THE add that the camera man who was at the scene of the arrest asked Dr Knight: “Can I get your house keys so I can feed the rabbit?”

I do hope that the rabbit is OK.


Return of the Language Evolution Tree

A while ago, some collegues and I noticed that two prominent books on Language Evolution -Christiansen & Kirby’s Language Evolution and Fitch’s Evolution of Language – both included a picture of an acacia tree in the sunset on their covers.  On closer analysis, it turned out that they were the same tree:

Thus began the Acacia Tree Hypothesis of Language Evolution.

Following this up, I was thinking about Dediu & Ladd’s discovery that linguistic tone is has certain genetic correlates. Here’s the map of languages with linguistic tone:

However, I suspected the devious influence of acacia trees and so I found some information on their geographic distribution:

As I suspected, countries in which the acacia tree Acacia nilotica grows are significantly more likely to have tonal languages:

Tone No Tone
Acacia Trees 163 117
No Acacia Trees 104 237

(Chi-squared with Yates’ continuity correction = 47.1, df = 1, p < 0.0001, data from Crop Protection Consortium and the World Atlas of Language Structures).

The plot thickens …


Dediu, D., & Ladd, D. R. (2007). Linguistic tone is related to the population frequency of the adaptive haplogroups of two brain size genes, Microcephalin and ASPM. Proceedings of the National Academy of Sciences, 104, 10944–10949.

Fitch, W. T. 2010 The evolution of language. Cambridge, UK: Cambridge University Press.

Christiansen, M. and Kirby, S. (2003). Language Evolution. Oxford University Press.



I’ve added the images David mentioned to the post:

Also, The Babel’s Dawn blog banner

Language as a board game

I’ve just finished reading The Player of Games by Iain M. Banks.  Yes, I’m a little behind the times for a geek.  Anyway, I was struck by the concept of Azad in the book.  The protagonist visits an Imperial civilisation whose whole society revolves around the playing of a board game called Azad.  Except this is a vastly complicated board game, played on multiple, football-field-sized boards with semi-conscious pieces and developed over thousands of years.  In fact, the game is so complicated that you can’t play it well unless your cognitive structures have been shaped by the game from a very young age.  Here’s a little extract:

Continue reading “Language as a board game”

Anthropologists Trace Human Origins Back To One Large Goat

GoatsIn what is sure to be a more cited paper than Gould and Lewontin (1979), Douglas Ochs at Columbia University, together with a team of internationally renowned scientists (and probably a few internationally unknown graduate students), has found that all of humanity can be traced back to a large Pliocene-era goat.

More interesting, for this blog at least, is the finding that the roots of early Indo-European language were in goat bleating. Unfortunately, I couldn’t track down the actual paper myself to find the details of this argument, but if you’re interested, I would suggest looking at the original article where I found this wonderful and groundbreaking study, on the popular peer-reviewed site the Onion.

Full disclosure: This post has been listed in the Irrelevant and Irreverent category, because it probably fits there. We’re not seriously suggesting that humans do in fact go back to a single large goat species in the Pliocene – that’s much too early. Rather, it’s more likely that the goat species was around in the Silurian period. It feasted mainly on trilobites.

Possible Stroke on Live Television

I was alerted recently of this video. It’s short, and the rest of the post won’t make sense without watching it.

My mate Ally said that “I’m sure there’s some kind of linguistic point to be made here but I have no idea what it is.” My first few times through the video, I was also confused. However, the comment section is where things become clear. At the risk of being one of those reporters who mentions twitter-posts, TopGunMD1 stated:

“Its obvious she just had a STROKE! She is currently suffering from Wernicke’s aphasia, its a very serious problem. I hope her producer realized this and took her to the hospital immediately. If you ever see someone talk like that, call an ambulance or take them to the ER immediately.”

This is most likely a correct diagnosis. What’s happened here is that she’s had a stroke which dealt a debilitating blow to her Wernicke’s area, and she’s lost her recall for words. This might be seen as normal stumbling, but for the fact that she is a reporter, which would mean that she should historically stumble only very rarely, and never this much. Around a third of stroke sufferers develop speech problems, some of which can be reversed later. It is unclear here whether she is merely experiencing aphasia or speech production errors as well.

It looks like her fellows recognised her problem very quickly, and cut back to the next scheduled thing. As well, she’s been taken to the hospital for tests – let’s hope this isn’t permanent.

Poster Venn Diagram

Last week I presented an academic poster over at Edinburgh. Even though I’d argue it was reasonably successful, getting lots of good feedback and some useful recommendations, I still think it could have benefited from being trimmed down to highlight the main points. I’ve uploaded it to Scribd so you can see for yourself:
Phoneme Demography Poster

Since presenting I’ve come across this insanely useful poster Venn Diagram (H/T: John Hawks):

Now try and spot which aspects I didn’t cater for in my poster (hint: direct your eyes toward the right).

Matt Ridley’s contractual silence

This morning I just received my copy of Matt Ridley’s latest book, The Rational Optimist: How prosperity evolves. I must admit that, despite being a big fan of Ridley’s writings, I found myself somewhat disillusioned since his role in the subprime mortgage crisis at Northern Rock. In particular, I was always confused as to why Ridley never defended himself against scathing attacks from the likes of George Monbiot. Maybe it was an admission of guilt? Perhaps. But I now have a somewhat more satisfying explanation for the silence:

I am writing in times of unprecedented economic pessimism. The world banking system has lurched to the brink of collapse; an enormous bubble of debt has burst; world trade has contracted; unemployment is rising sharply all around the world as output falls. The immediate future looks bleak indeed, and some governments are planning further enormous public debt expansions that could hurt the next generation’s ability to prosper. To my intense regret I played a part in one phase of this disaster as non-executive chairman of Northern Rock, one of many banks that ran short of liquidity during the crisis. This is not a book about that experience (under terms of my employment there I am not at liberty to write about it). [my emphasis].

So there you have it: a contractual obligation to keep schtum. It’s a shame, really, as I would hate to be in a position where I am not even given the opportunity to defend my position, especially on a topic that generated a massive amount of news and speculation.

As for the book: so far, so good. It’s also a lot larger than I expected. I do have some minor quibbles, but they can wait until I write a more thorough review.

Some quick announcements

Just thought I’d make three quick announcements:

First, I decided to drag myself into the age of 140-characters and (albeit begrudgingly) joined Twitter. I say begrudgingly because my day is already packed with plenty of distractions besides adding Twitter into the mix… But I noticed it’s the place where all the cool science bloggers are gathering, and gradually coagulating into an amorphous cloud of science networking, so I thought I might as well sign up (ever the follower, never the trendsetter).

Second, if you happen to find yourself in Edinburgh on Friday October 1st, then you can come and see me and Sean presenting our respective posters (click here and here for the abstracts) at the 24th Language at Edinburgh Lunch. I’m sure, for me at least, it’ll be quite a sobering experience in highlighting how little I know about phonology, phonetics, sociolinguistics and demography. On the plus side I’ll get some free food 🙂 .

Lastly, if you happened to click on my poster abstract, then the more observant of you will have noticed I’m now affiliated with Cardiff University. Yes, that’s right, I’m doing yet another masters course. This time it’s at the Centre for Language and Communication Research, with the idea being that I’ll get a more solid foundation in research methodology etc before pursuing a PhD or research assistant position.

That is all.

Where does the myth of a gene for things like intelligence come from?

As a linguist I struggle with genetics, I am, however, as an evolution geek, very interested in it. This creates all sorts of problems and high levels of anxiety when talking about FOXP2 and other genes, due to fear that I misunderstand the very highly complex interactions which exist between genes, environmental effects or cascading effects which cannot be summed up in a simple “x gene causes x trait in humans” paradigm.

I would like to point everyone towards a new blog Dorothy Bishop’s written over at guardian science blogs:

Where does the myth of a gene for things like intelligence come from?

Which is about busting the widespread belief (for idiots like me) that individual genes determine traits such as intelligence, optimism, obesity and dyslexia. I find it interesting that this is presented in the blogs section and not as a mainstream article.

She points out on Twitter this morning that the Jedward pic was not her idea. (I add this point because I found it weirdly comforting)

And it’s also lovely to see that at the bottom of the pile of comments is a well articulated reply by Dorothy to individual users.

I love blogging, because there exists  the ability for individuals to reply to claims made about them, primary sources (papers &c.) are cited and checkable and there’s none of the unnecessary dumbing down found in mainstream media. Here’s an article by Ben Goldacre expanding on this subject (which incidentally includes work by Dorothy Bishop).

Here is a parable about how, as a blogger, my claims were checked, discussed and ultimately concluded to be bollocks. (I don’t have a contrastive parable about what would have happened if I’d instead made these claims in the mainstream media but many stories of this nature can be found here.)

If you read the blog post I wrote about links between Autism and SLI you would have seen me make this claim:

the CNTNAP2 gene has been found in independent samples to be associated with both ASD and SLI. This is interesting because it could show that gene mutations which cause improved social abilities could have also caused changes in our linguistic ability on a syntactic or phonological level.

This blog post cited the work of Dorothy Bishop quite heavily and she took the time out to come and tell me problems with it. Here’s what she said:

As you anticipated, I think there are some problems with the implications you draw from the work. There are two issues. The first is that the variants of CNTNAP2 associated with language level are not mutations. You would usually only use that term in the case where most people had the same DNA sequence in a gene, but rare individuals had a different DNA sequence. FOXP2 is a case in point: there is a family, the KE family, who have a mutation affecting around half the family members, where the DNA sequence is changed. For most people in the general population, and for most people with SLI, the FOXP2 sequence is the same.

The CNTNAP gene is very different. The DNA sequence has different versions in different people, and one version, which is pretty common in the general population, is associated with a small decrease in language abilities, but most people with this version would not be recognised as having any language impairment. Most researchers now think that SLI is probably the result of the combined effect of many genes, each of which may nudge language ability up or down a bit. In this regard, language ability is rather like height: there are rare mutations that may make a person drastically tall or short, but most variation in height arises from combined effect of many small influences of genes that show DNA variation in the normal population.

The second issue concerns the evidence for CNTNAP2 being involved in both SLI and autism. Many people in the field do think this means that the same gene that can cause SLI can also cause autism, and that the only difference is that people with autism have additional difficulties going beyond language – what I have termed the ‘autism as SLI plus’ model. I supported that model in the past, but there are some facts that are hard to square with it. First, although many people with autism have structural language problems (affecting grammar and phonology) similar to those in SLI, not all of them do. So people with high-functioning autism or Asperger syndrome may have well-developed skills in syntax and phonology, while still having difficulties with pragmatics. The second point, which is a big problem for a simple genetic account, is that whereas the relatives of people with SLI often have some difficulties with structural language, we don’t usually see that in relatives of people with autism, even if the person with autism has poor language skills. It was this latter point that I was particularly keen to try and explain in my paper. The bottom line is that to explain the pattern of data we need to think in terms of interactions between genes (technically known as epistasis). So there are genetic variants that increase risk of autism, and others that increase risk of SLI. Most of these will have an individually small effect. However, if you have a risk variant for a gene influencing SLI (such as CNTNAP2) in the context of having a genetic risk for autism, the effect on language will be much worse. According to this model CNTNAP2 doesn’t affect both social cognition and language; rather it affects language, but that effect will get multiplied if the person also has risk factors for autism.

Which is SOOOO interesting.

I’d really like to thank her for replying, it’s really lovely to know that high-flying academics are willing to help out when a sincere blogger tries to understand something and falls on their arse.