Some Links #18: GxExC
The depression map: genes, culture, serotonin, and a side of pathogens. Another new science blog network (Wired) and once again a new stable of good science writers. I’m particularly pleased to see that David Dobbs, a former SciBling and top science writer, has found a new home for Neuron Culture. I was also pleased to see he had written an article on studies into the interactions between genes and culture, namely: Chiao & Blizinsky (2009) and Way & Lieberman (2010). And I was even more pleased to see that he’d mentioned both mine and Sean’s posts on the social sensitivity hypothesis. Suffice to say, I was pleased.
Take home paragraph:
In a sense, these studies are looking not at gene-x-environment interactions, or GxE, but at genes x (immediate) environment x culture — GxExC. The third variable can make all the difference. Gene-by-environment studies over the last 20 years have contributed enormously to our understanding of mood and behavior. Without them we would not have studies, like these led by Chiao and Way and Kim, that suggest broader and deeper dimensions to what makes us struggle, thrive, or just act differently in different situations. GxE is clearly important. But when we leave out variations in culture, we risk profoundly misunderstanding how these genes — and the people who carry them — actually operate in the big wide world.
Razib also has some thoughts on the topic:
The same issues are not as operative when it comes to culture. Two tribes can speak different dialects or languages. If a woman moves from one tribe to another her children don’t necessarily speak a mixture of languages, rather, they may speak the language of their fathers. The nature of cultural inheritance is more flexible, and so allows for the persistence of more heritable variation at different levels of organization. Differences of religion, language, dress, and values, can be very strong between two groups who have long lived near each other and may be genetically similar.
Homo was born vocalizing. Babel’s Dawn links to a recently finished PhD thesis that supposedly argues for a relatively recent emergence for language (approx. 120,000 years ago). She defends her assertions by stating: “[…] all of the unique cognitive traits attributed to humans arose as the consequence of one crucial mutation, which radically altered the architecture of the ancestral primate brain.” I haven’t read the thesis, and I probably won’t as I’m already stretched in regards to my reading, but I’m completely unconvinced by the hopeful mutation hypothesis. Plus, as Bolles notes in his post, there is plenty of available evidence to the contrary.
Primed for Reading. Robert Boyd reviews Stanislas Dehane’s new book, Reading in the Brain: The Science and Evolution of a Human Invention, which I’ll be picking up soon. In the meantime, to give you a bit of background, I suggest you read Dehane’s (2007) paper on the Neuronal Recycling Hypothesis: the Cultural recycling of cortical maps. H/T: Gene Expression.
Through the looking glass (part 1). The Lousy Linguist reviews Guy Deutscher’s new book, Through the Language Glass: Why the World Looks Different in Other Languages, with the general takeaway message being that, in part one at least, one where the book is a bit science-lite. What really interested me, though, were these two paragraphs:
We discover quite quickly what Deutscher is doing as he begins to walk through complexity issues of “particular areas of language” (page 109), namely morphology, phonology, and subordination. And these last 15 pages are really the gem of Part 1. He shows that there is an interesting, somewhat illogical, entirely engaging but as yet unexplained set of correlations between speaker population size and linguistic complexity.
For example, languages with small numbers of speakers tend to have more morphologically rich grammars (hence one could claim that small = more complex). However, small languages with small numbers of speakers also tend to have small phonological inventories. Hmmm, weird, right? [My emphasis]
As those of you who read this blog will know: I don’t think it’s weird that small speaker populations also tend to have small phonological inventories.
Clothing lice out of Africa. A cool new paper by Troups et al which looks at the evolutionary history of clothing lice to provide specific estimates on the origin of clothing. Using a Bayesian coalescent modelling approach, they estimate that clothing lice diverged from head louse ancestors between 83,000 and 170,000 years ago. H/T: Dienekes.
Language, Thought and Space (III): Frames of Reference in Language and Cognition
In the second chapter of his 2003 book Space in Language and Cognition: Explorations in Cognitive Diversity, Stephen Levinson discusses a concept that has been crucial to discussions of space and ‘perspectivation’ in language: frames of reference. (see e.g. these posts on my blog Shared Symbolic Storage) The term as it is used today was coined by Gestalt theorists of perception in the 1920s and was used to signify the steady and constant background against which other objects could be made out and identified. It can be defined as
“‘a unit or organization of units that collectively serve to identify a coordinate system with respect to which certain properties of objects, including the phenomenal self, are gauged’ (Rock 1992: 404, emphasis in Levinson 2003: 24).
Language and Complexity: Evolution Inside Out
Here is a video of Terrence Deacon, someone who needs no introduction on this website, giving a talk at Irving K. Barber Learning Centre about his latest research into language evolution:
Continue reading “Language and Complexity: Evolution Inside Out”
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.
Memetic Sophistry
Over at the Psychology Today blog complex, Joseph Carroll is taking Norman Holland to task on remarks that Holland made concerning the relationship between the reader of a literary text and the text itself. Though I disagree with Carroll on many matters, I agree with him on this one particular issue. Beyond that, I think his critique of Holland can also be applied to Susan Blackmore’s equivocations on memes. Here’s what Carroll says about Holland:
This whole way of thinking is a form of scholastic sophistry, useless and sterile. It produces verbal arguments that consist only in fabricated and unnecessary confusions, confusions like that which you produce as your conclusion in the passage you cited from your book: “the reader constructs everything” (p. 176). This conclusion seems plausible because it slyly blends two separate meanings of the word “constructs.” One meaning is that our brains assemble percepts into mental images. That meaning is correct. The other meaning is that our brains assemble percepts that are not radically constrained by the signals produced in the book. That meaning is incorrect. Once you have this kind of ambiguity at work for you, you can shuffle back and forth between the two meanings, sometimes suggesting the quite radical notion that books don’t “impose” any constraints—any meanings—on readers; and sometimes retreating into the safety of the correct meaning: that our brains assemble percepts.
Blackmore equivocates in a similar fashion on the question of whether or not memes are active agents. Here’s a snippet from a TED talk she gave last year:
The way to think about memes, though, is to think, why do they spread? They’re selfish information, they get copied if they can. But some of them will be copied because they’re good, or true, or useful, or beautiful. Some of them will be copied even though they’re not. Some, it’s quite hard to tell why.
Here she talks of memes as though they are agents of some kind, they’re selfish and they try to get copied. A bit later she says:
So think of it this way. Imagine a world full of brains and far more memes than can possibly find homes. The memes are trying to get copied, trying, in inverted commas, i.e., that’s the shorthand for, if they can get copied they will. They’re using you and me as their propagating copying machinery, and we are the meme machines.
Here memes are using us as machines for propagating themselves. And then we have this passage where she talks about a war between memes and genes:
So you get an arms race between the genes which are trying to get the humans to have small economical brains and not waste their time copying all this stuff, and the memes themselves, like the sounds that people made and copied – in other words, what turned out to be language – competing to get the brains to get bigger and bigger. So the big brain on this theory of driven by the memes.
The term “meme,” as we know, was coined by Richard Dawkins, who is also responsible for anthropomorphizing genes as selfish agents in biological evolution. Dawkins knows perfectly well that genes aren’t agents, and is quite capable of explicating that selfishness in terms that eliminate the anthropomorphism, which is but a useful shorthand, albeit a shorthand that has caused a great deal of mischief.
More on The Social Sensitivity Hypothesis
In a recent post, James wrote about the Social Sensitivity hypothesis. Given findings that certain genetic variants will make a person more sensitive to social contact and more reliant on social contact under stress, it proposes that certain genetic variants ‘fit’ better with certain social structures. In support of this idea, Way and Lieberman (2010) find a correlation between the prevalence of this variant and the level of collectivism (as opposed to individualism) in a society.
An alternative explanation I’ve been thinking about is migration patterns. If genetic differences make a person less reliant on social networks, they may be more likely to migrate. This would predict that areas settled later in human history will have more ‘non socially sensitive’ individuals.
Continue reading “More on The Social Sensitivity Hypothesis”
A Replicated Word Cloud
I found this cool website for generating really awesome looking word clouds: http://www.wordle.net/. Here is a word cloud for this website:
Apparently, the clouds are based on word frequency, but I don’t think it can be pulling much data from this website if Levinson is coming out as one of the most frequently used words. Still, it entertained me for a few minutes. H/T: Glossographia.
Language, Thought, and Space (II): Universals and Variation
Spatial orientation is crucial when we try to navigate the world around us. It is a fundamental domain of human experience and depends on a wide array of cognitive capacities and integrated neural subsystems. What is most important for spatial cognition however, are the frames of references we use to locate and classify ourselves, others, objects, and events.
Often, we define a landmark (say ourselves, or a tree, or the telly) and then define an object’s location in relation to this landmark (the mouse is to my right, the bike lies left of the tree, my keys have fallen behind the telly). But as it turns out, many languages are not able to express a coordinate system with the meaning of the English expression “left of.” Instead, they employ a compass-like system of orientation.
They do not use a relative frame of reference, like in the English “the cat is behind the truck” but instead use an absolute frame of reference that can be illustrated in English by sentences such as “the cat is north of the truck.” (Levinson 2003: 3). This may seem exotic for us, but for many languages it is the dominant – although often not the only – way of locating things in space.
What cognitive consequences follow from this?
Continue reading “Language, Thought, and Space (II): Universals and Variation”
More on Phoneme Inventory Size and Demography
On the basis of Sean’s comment, about using a regression to look at how phoneme inventory size improved as geographic spread was incorporated along with population size, I decided to look at the stats a bit more closely (original post is here). It’s fairly easy to perform multiple regression in R, which, in the case of my data, resulted in highly significant results (p<0.001) for the intercept, area and population (residual standard error = 9.633 on 393 degrees of freedom; adjusted R-Squared = 0.1084). I then plotted all the combinations as scatterplots for each pair of variables. As you can see below, this is fairly useful as a quick summary but it is also messy and confusing. Another problem is that the pairs plot is on the original data and not the linear model.
Continue reading “More on Phoneme Inventory Size and Demography”