I’ve a short review online with Prospect of The Future of the Brain (Princeton University Press), edited by Gary Marcus & Jeremy Freeman. Here’s a slightly longer version. But I will say more about the book and topic in my Prospect blog soon.
_________________________________________________________________________
If you want a breezy, whistle-stop tour of the latest brain science, look elsewhere. But if you’re up for chunky, rather technical expositions by real experts, this book repays the effort. The message lies in the very (and sometimes bewildering) diversity of the contributions: despite its dazzling array of methods to study the brain, from fMRI to genetic techniques for labeling and activating individual neurons, this is still a primitive field largely devoid of conceptual and theoretical frameworks. As the editors put it, “Where some organs make sense almost immediately once we understand their constituent parts, the brain’s operating principles continue to elude us.”
Among the stimulating ideas on offer is neuroscientist Anthony Zador’s suggestion that the brain might lack unifying principles, but merely gets the job done with a makeshift “bag of tricks”. There’s fodder too for sociologists of science: several contributions evince the spirit of current projects that aim to amass dizzying amounts of data about how neurons are connected, seemingly in the blind hope that insight will fall out of the maps once they are detailed enough.
All the more reason, then, for the skeptical voices reminding us that “data analysis isn’t theory”, that current neuroscience is “a collection of facts rather than ideas”, and that we don’t even know what kind of computer the brain is. All the same, the “future” of the title might be astonishing: will “neural dust” scattered through the brain record all our thoughts? And would you want that uploaded to the Cloud?
Thursday, December 18, 2014
Wednesday, December 17, 2014
The restoration of Chartres: second thoughts
Several people have asked me what I think about the “restoration” of Chartres Cathedral, in the light of the recent piece by Martin Filler for the New York Review of Books. (Here, in case you’re wondering, is why anyone should wish to solicit my humble opinion on the matter.) I have commented on this before here, but the more I hear about the work, the less sanguine I feel. Filler makes some good arguments against, the most salient, I think, being the fact that this contravenes normal conservation protocols: the usual approach now, especially for paintings, is to do what we can to rectify damage (such as reattaching flakes of paint) but otherwise to leave alone. In my earlier blog I mentioned the case of York Cathedral, where masons actively replace old, crumbling masonry with new – but this is a necessary affair to preserve the integrity of the building, whereas slapping on a lick of paint isn’t. And the faux marble on the columns looks particularly hideous and unnecessary. To judge from the photos, the restoration looks far more tacky than I had anticipated.
It is perhaps not ideal that visitors to Chartres come away thinking that the wonderful, stark gloom is what worshippers in the Middle Ages would have experienced too. But it seems unlikely that the new paint job is going to get anyone closer to an authentic experience. Worse, it’s the kind of thing that, once done, is very hard to undo. It’s good to recognize that the reverence with which we generally treat the fabric of old buildings now is very different from the attitudes of earlier times – bishops would demand that structures be knocked down when they looked too old-fashioned and replaced with something à la mode, and during the nineteenth-century Gothic revival architects like Eugène Viollet-le-Duc would take all kinds of liberties with their “restorations”. But this is no reason why we should act the same way. So while there is still a part of me that is intrigued by the thought of being able to see the interior of Chartres in something close to its original state, I have come round to thinking that the cathedral should have been left alone.
Monday, December 15, 2014
Beyond the crystal
Here’s my Material Witness column from the November issue of Nature Materials (13, 1003; 2014).
___________________________________________________________________________
The International Year of Crystallography has understandably been a celebration of order. From Rene-Just Haüy’s prescient drawings of stacked cubes to the convolutions of membrane proteins, Nature’s Milestones in Crystallography revealed a discipline able to tackle increasingly complex and subtle forms of atomic-scale regularity. But it seems fitting, as the year draws to a close, to recognize that the road ahead is far less tidy. Whether it is the introduction of defects to control semiconductor band structure [1], the nanoscale disorder that can improve the performance of thermoelectric materials [2], or the creation of nanoscale conduction pathways in graphene [3], the future of solid-state materials physics seems increasingly to depend on a delicate balance of crystallinity and its violation. In biology, the notion of “structure” has always been less congruent with periodicity, but ever since Schrödinger’s famous “aperiodic crystal” there has been a recognition that a deeper order may underpin the apparent molecular turmoil of life.
The decision to redefine crystallinity to encompass the not-quite-regularity of quasicrystals is, then, just the tip of the iceberg when it comes to widening the scope of crystallography. Even before quasicrystals were discovered, Ruelle asked if there might exist “turbulent crystals” without long-ranged order, exhibiting fuzzy diffraction peaks [4]. The goal of “generalizing” crystallography beyond its regular domain has been pursued most energetically by Mackay [5], who anticipated the link between quasicrystals and quasiperiodic tilings [6]. More recently, Cartwright and Mackay have suggested that structures such as crystals might be best characterized not by their degree of order as such but by the algorithmic complexity of the process by which they are made – making generalized crystallography an information science [7]. As Mackay proposed, “a crystal is a structure the description of which is much smaller than the structure itself, and this view leads to the consideration of structures as carriers of information and on to wider concerns with growth, form, morphogenesis, and life itself” [5].
These ideas have now been developed by Varn and Crutchfield to provide what they call an information-theoretic measure for describing materials structure [8]. Their aim is to devise a formal tool for characterizing the hitherto somewhat hazy notion of disorder in materials, thereby providing a framework that can encompass anything from perfect crystals to totally amorphous materials, all within a rubric of “chaotic crystallography”.
Their approach is again algorithmic. They introduce the concept of “ε-machines”, which are minimal operations that transform one state into another [9]: for example, one ε-machine can represent the appearance of a random growth fault. Varn and Crutchfield present nine ε-machines relevant to crystallography, and show how their operation to generate a particular structure is a kind of computation that can be assigned a Shannon entropy, like more familiar computations involving symbolic manipulations. Any particular structure or arrangement of components can then be specified in terms of an initially periodic arrangement of components and the amount of ε-machine computation needed to generate from it the structure in question. The authors demonstrate how, for a simple one-dimensional case, diffraction data can be inverted to reconstruct the ε-machine that describes the disordered material structure.
Quite how this will play out in classifying and distinguishing real materials structures remains to be seen. But it surely underscores the point made by D’Arcy Thompson, the pioneer of morphogenesis, in 1917: “Everything is what it is because it got that way” [10].
1. Seebauer, E. G. & Noh, K. W. Mater. Sci. Eng. Rep. 70, 151-168 (2010).
2. Snyder, G. J. & Toberer, E. S. Nat. Mater. 7, 105-114 (2008).
3. Lahiri, J., Lin, Y., Bozkurt, P., Oleynik, I. I. & Batzill, M., Nat. Nanotech. 5, 326-329 (2010).
4. Ruelle, D. Physica A 113, 619-623 (1982).
5. Mackay, A. L. Struct. Chem. 13, 215-219 (2002).
6. Mackay, A. L. Physica A 114, 609-613 (1982).
7. Cartwright, J. H. E. & Macaky, A. L., Phil. Trans. R. Soc. A 370, 2807-2822 (2012).
8. Varn, D. P. & Crutchfield, J. P., preprint http://www.arxiv.org/abs/1409.5930 (2014).
9. Crutchfield, J. P., Nat. Phys. 8, 17-24 (2012).
10. Thompson, D’A. W., On Growth and Form. Cambridge University Press, Cambridge, 1917.
___________________________________________________________________________
The International Year of Crystallography has understandably been a celebration of order. From Rene-Just Haüy’s prescient drawings of stacked cubes to the convolutions of membrane proteins, Nature’s Milestones in Crystallography revealed a discipline able to tackle increasingly complex and subtle forms of atomic-scale regularity. But it seems fitting, as the year draws to a close, to recognize that the road ahead is far less tidy. Whether it is the introduction of defects to control semiconductor band structure [1], the nanoscale disorder that can improve the performance of thermoelectric materials [2], or the creation of nanoscale conduction pathways in graphene [3], the future of solid-state materials physics seems increasingly to depend on a delicate balance of crystallinity and its violation. In biology, the notion of “structure” has always been less congruent with periodicity, but ever since Schrödinger’s famous “aperiodic crystal” there has been a recognition that a deeper order may underpin the apparent molecular turmoil of life.
The decision to redefine crystallinity to encompass the not-quite-regularity of quasicrystals is, then, just the tip of the iceberg when it comes to widening the scope of crystallography. Even before quasicrystals were discovered, Ruelle asked if there might exist “turbulent crystals” without long-ranged order, exhibiting fuzzy diffraction peaks [4]. The goal of “generalizing” crystallography beyond its regular domain has been pursued most energetically by Mackay [5], who anticipated the link between quasicrystals and quasiperiodic tilings [6]. More recently, Cartwright and Mackay have suggested that structures such as crystals might be best characterized not by their degree of order as such but by the algorithmic complexity of the process by which they are made – making generalized crystallography an information science [7]. As Mackay proposed, “a crystal is a structure the description of which is much smaller than the structure itself, and this view leads to the consideration of structures as carriers of information and on to wider concerns with growth, form, morphogenesis, and life itself” [5].
These ideas have now been developed by Varn and Crutchfield to provide what they call an information-theoretic measure for describing materials structure [8]. Their aim is to devise a formal tool for characterizing the hitherto somewhat hazy notion of disorder in materials, thereby providing a framework that can encompass anything from perfect crystals to totally amorphous materials, all within a rubric of “chaotic crystallography”.
Their approach is again algorithmic. They introduce the concept of “ε-machines”, which are minimal operations that transform one state into another [9]: for example, one ε-machine can represent the appearance of a random growth fault. Varn and Crutchfield present nine ε-machines relevant to crystallography, and show how their operation to generate a particular structure is a kind of computation that can be assigned a Shannon entropy, like more familiar computations involving symbolic manipulations. Any particular structure or arrangement of components can then be specified in terms of an initially periodic arrangement of components and the amount of ε-machine computation needed to generate from it the structure in question. The authors demonstrate how, for a simple one-dimensional case, diffraction data can be inverted to reconstruct the ε-machine that describes the disordered material structure.
Quite how this will play out in classifying and distinguishing real materials structures remains to be seen. But it surely underscores the point made by D’Arcy Thompson, the pioneer of morphogenesis, in 1917: “Everything is what it is because it got that way” [10].
1. Seebauer, E. G. & Noh, K. W. Mater. Sci. Eng. Rep. 70, 151-168 (2010).
2. Snyder, G. J. & Toberer, E. S. Nat. Mater. 7, 105-114 (2008).
3. Lahiri, J., Lin, Y., Bozkurt, P., Oleynik, I. I. & Batzill, M., Nat. Nanotech. 5, 326-329 (2010).
4. Ruelle, D. Physica A 113, 619-623 (1982).
5. Mackay, A. L. Struct. Chem. 13, 215-219 (2002).
6. Mackay, A. L. Physica A 114, 609-613 (1982).
7. Cartwright, J. H. E. & Macaky, A. L., Phil. Trans. R. Soc. A 370, 2807-2822 (2012).
8. Varn, D. P. & Crutchfield, J. P., preprint http://www.arxiv.org/abs/1409.5930 (2014).
9. Crutchfield, J. P., Nat. Phys. 8, 17-24 (2012).
10. Thompson, D’A. W., On Growth and Form. Cambridge University Press, Cambridge, 1917.
Friday, December 12, 2014
Why some junk DNA is selfish, but selfish genes are junk
“Horizontal gene transfer is more common than thought”: that's the message of a nice article in Aeon. I first came across it via a tweeted remark to the effect that this was the ultimate expression of the selfish gene. Why, genes are so selfish that they’ll even break the rules of inheritance by jumping right into the genomes of another species!
Now, that is some trick. I mean, the gene has to climb out of its native genome – and boy, those bonds are tough to break free from! – and then swim through the cytoplasm to the cell wall, wriggle through and then leap out fearlessly into the extracellular environment. There it has to live in hope of a passing cell before it gets degraded, and if it’s in luck then it takes out its diamond-tipped cutting tool and gets to work on…
Wait. You’re telling me the gene doesn’t do all this by itself? You’re saying that there is a host of genes in the donor cell that helps it happen, and a host of genes in the receiving cell to fix the new gene in place? But I thought the gene was being, you know, selfish? Instead, it’s as if it has sneaked into a house hoping to occupy it illegally, only to find a welcoming party offering it a cup of tea and a bed. Bah!
No, but look, I’m being far too literal about this selfishness, aren’t I? Well, aren’t I? Hmm, I wonder – because look, the Aeon page kindly directs me to another article by Itai Yanai and Martin Lercher that tells me all about what this selfishness business is all about.
And I think: have I wandered into 1976?
You see, this is what I find:
“Yet viewing our genome as an elegant and tidy blueprint for building humans misses a crucial fact: our genome does not exist to serve us humans at all. Instead, we exist to serve our genome, a collection of genes that have been surviving from time immemorial, skipping down the generations. These genes have evolved to build human ‘survival machines’, programmed as tools to make additional copies of the genes (by producing more humans who carry them in their genomes). From the cold-hearted view of biological reality, we exist only to ensure the survival of these travellers in our genomes... The selfish gene metaphor remains the single most relevant metaphor about our genome.”
Gosh, that really is cold-hearted isn’t it? It makes me feel so sad. But what leads these chaps to this unsparing conclusion, I wonder?
This: “From the viewpoint of natural selection, each gene is a long-lived replicator, its essential property being its ability to spawn copies.”
Then evolution, it seems, isn’t doing its job very well. Because, you see, I just took a gene and put it in a beaker and fed it with nucleotides, and it didn’t make a single copy. It was a rubbish replicator. So I tried another gene. Same thing. The funny thing was, the only way I could get the genes to replicate was to give them the molecular machinery and ingredients. Like in a PCR machine, say – but that’s like putting them on life support, right? The only way they’d do it without any real intervention was if I put the gene in a genome in a cell. So it really looked to me as though cells, not genes, were the replicators. Am I doing something wrong? After all, I am reliably informed that the gene “is on its own as a “replicator” – because “genes, but no other units in life’s hierarchy, make exact copies of themselves in a pool of such copies”. But genes no more “make exact copies of themselves in a pool of such copies” than printed pages (in a stack of other pages) make exact copies of themselves on the photocopier.
Oh, but silly me. Of course the genes don’t replicate by themselves! It is on its own as a replicator but doesn’t replicate on its own! (Got that?) No, you see, they can only do the job all together – ideally in a cell. “When looking at our genome”, say Yanai and Lercher, “we might take pride in how individual genes co-operate in order to build the human body in seemingly unselfish ways. But co-operation in making and maintaining a human body is just a highly successful strategy to make gene copies, perfectly consistent with selfishness.”
To be honest, I’ve never taken very much pride in what my genes do. But anyway: perfect consistent with selfishness? Let me see. I pay my taxes, I obey the laws, I contribute to charities that campaign for equality, I try to be nice to people, and a fair bit of this I do because I feel it is a pretty good thing to be a part of a society that functions well. I figure that’s probably best for me in the long run. Aha! – so what I do is perfectly consistent with selfishness. Well yes, but look, you’re not going to call me selfish just because I want to live in a well ordered society are you? No, but then I have intentions and thoughts of the future, I have acquired moral codes and so on – genes don’t have any of these things. Hmm… so how exactly does that make the metaphor of “selfishness” work? Or more precisely, how does it make selfishness a better metaphor than cooperativeness? If “genes don’t care”, then neither metaphor is better than the other. It’s just stuff that happens when genes get together.
But no, wait, maybe I’m missing the point. Genes are selfish because they compete with each other for limited resources, and only the best replicators – well no, only those housed in the cells or organisms that are themselves the best at replicating their genomes – survive. See, it says here: “Those genes that fail at replicating are no longer around, while even those that are good face stiff competition from other replicators. Only the best can secure the resources needed to reproduce themselves.”
This is the bullshit at the heart of the issue. “Good genes” face stiff competition from who exactly? Other replicators? So a phosphatase gene is competing with a dehydrogenase gene? (Yeah, who would win that fight?) No. No, no, no. This, folks, this is what I would bet countless people believe because of the bad metaphor of selfishness. Yet the phosphatase gene might well be doomed without the dehydrogenase gene. They need each other. They are really good friends. (These personification metaphors are great, aren’t they?) If the dehydrogenase gene gets better at its job, the phosphatase gene further down the genome just loves it, because she gets the benefit too! She just loves that better dehydrogenase. She goes round to his place and…
Hmm, these metaphors can get out of hand, can’t they?
No, if the dehydrogenase gene is competing with anyone, it’s with other alleles of the dehydrogenase gene. Genes aren’t in competition, alleles are.
(Actually even that doesn’t seem quite right. Organisms compete, and their genetic alleles affect their ability to compete. But this gives a sufficient appearance of competition among alleles that I can accept the use of the word.)
So genes only get replicated (by and large) in a genome. So if a gene is “improved” by natural selection, the whole genome benefits. But that’s just a side result – the gene doesn’t care about the others! Yet this is precisely the point. Because the gene “doesn’t care”, all you can talk about is what you see, not what you want to ascribe, metaphorically or otherwise, to a gene. An advantageous gene mutation helps the whole genome replicate. It’s not a question of who cares or who doesn’t, or what the gene “really” wants or doesn’t want. That is the outcome. “Selfishness” doesn’t help to elucidate that outcome – it confuses it.
“So why are we fooled into believing that humans (and animals and plants) rather than genes are what counts in biology?” the authors ask. They give an answer, but it’s not the right one. Higher organisms are a special case, of course, especially ones that reproduce sexually – it’s really cells that count. We’re “fooled” because cells can reproduce autonomously, but genes can’t.
So cells are where it’s at? Yes, and that’s why this article by Mike Lynch et al. calling for a meeting of evolutionary theory and cell biology is long overdue (PNAS 111, 16990; 2014). For one thing, it might temper erroneous statements like this one that Yanai and Lercher make: “Darwin showed that one simple logical principle [natural selection] could lead to all of the spectacular living design around us.” As Lynch and colleagues point out, there is abundant evidence that natural selection is one of several evolutionary processes that has shaped cells and simple organisms: “A commonly held but incorrect stance is that essentially all of evolution is a simple consequence of natural selection.” They point out, for example, that many pathways to greater complexity of both genomes and cells don’t confer any selective fitness.
The authors end with a tired Dawkinseque flourish: “we exist to serve our genome”. This statement has nothing to do with science – it is akin to the statement that “we are at the pinnacle of evolution”, but looking in the other direction. It is a little like saying that we exist to serve our minds – or that water falls on mountains in order to run downhill. It is not even wrong. We exist because of evolution, but not in order to do anything. Isn’t it strange how some who preen themselves on facing up to life’s lack of purpose then go right ahead and give it back a purpose?
The sad thing is that that Aeon article is actually all about junk DNA and what ENCODE has to say about it. It makes some fair criticisms of ENCODE’s dodgy definition of “function” for DNA. But it does so by examining the so-called LINE-1 elements in genomes, which are non-coding but just make copies of themselves. There used to be a word for this kind of DNA. Do you know what that word was? Selfish.
In the 1980s, geneticists and molecular biologists such as Francis Crick, Leslie Orgel and Ford Doolittle used “selfish DNA” in a strict sense, to refer to DNA sequences that just accumulated in genomes by making copies – and which did not itself affect the phenotype (W. F. Doolittle & C. Sapienza, Nature 284, p601, and L. E. Orgel & F. H. C. Crick, p604, 1980). This stuff not only had no function, it messed things up if it got too rife: it could eventually be deleterious to the genome that it infected. Now that’s what I call selfish! – something that acts in a way that is to its own benefit in the short term while benefitting nothing else, and which ultimately harms everything.
So you see, I’m not against the use of the selfish metaphor. I think that in its original sense it was just perfect. Its appropriation to describe the entire genome – as an attribute of all genes – wasn’t just misleading, it also devalued a perfectly good use of the term.
But all that seems to have been forgotten now. Could this be the result of some kind of meme, perhaps?
Now, that is some trick. I mean, the gene has to climb out of its native genome – and boy, those bonds are tough to break free from! – and then swim through the cytoplasm to the cell wall, wriggle through and then leap out fearlessly into the extracellular environment. There it has to live in hope of a passing cell before it gets degraded, and if it’s in luck then it takes out its diamond-tipped cutting tool and gets to work on…
Wait. You’re telling me the gene doesn’t do all this by itself? You’re saying that there is a host of genes in the donor cell that helps it happen, and a host of genes in the receiving cell to fix the new gene in place? But I thought the gene was being, you know, selfish? Instead, it’s as if it has sneaked into a house hoping to occupy it illegally, only to find a welcoming party offering it a cup of tea and a bed. Bah!
No, but look, I’m being far too literal about this selfishness, aren’t I? Well, aren’t I? Hmm, I wonder – because look, the Aeon page kindly directs me to another article by Itai Yanai and Martin Lercher that tells me all about what this selfishness business is all about.
And I think: have I wandered into 1976?
You see, this is what I find:
“Yet viewing our genome as an elegant and tidy blueprint for building humans misses a crucial fact: our genome does not exist to serve us humans at all. Instead, we exist to serve our genome, a collection of genes that have been surviving from time immemorial, skipping down the generations. These genes have evolved to build human ‘survival machines’, programmed as tools to make additional copies of the genes (by producing more humans who carry them in their genomes). From the cold-hearted view of biological reality, we exist only to ensure the survival of these travellers in our genomes... The selfish gene metaphor remains the single most relevant metaphor about our genome.”
Gosh, that really is cold-hearted isn’t it? It makes me feel so sad. But what leads these chaps to this unsparing conclusion, I wonder?
This: “From the viewpoint of natural selection, each gene is a long-lived replicator, its essential property being its ability to spawn copies.”
Then evolution, it seems, isn’t doing its job very well. Because, you see, I just took a gene and put it in a beaker and fed it with nucleotides, and it didn’t make a single copy. It was a rubbish replicator. So I tried another gene. Same thing. The funny thing was, the only way I could get the genes to replicate was to give them the molecular machinery and ingredients. Like in a PCR machine, say – but that’s like putting them on life support, right? The only way they’d do it without any real intervention was if I put the gene in a genome in a cell. So it really looked to me as though cells, not genes, were the replicators. Am I doing something wrong? After all, I am reliably informed that the gene “is on its own as a “replicator” – because “genes, but no other units in life’s hierarchy, make exact copies of themselves in a pool of such copies”. But genes no more “make exact copies of themselves in a pool of such copies” than printed pages (in a stack of other pages) make exact copies of themselves on the photocopier.
Oh, but silly me. Of course the genes don’t replicate by themselves! It is on its own as a replicator but doesn’t replicate on its own! (Got that?) No, you see, they can only do the job all together – ideally in a cell. “When looking at our genome”, say Yanai and Lercher, “we might take pride in how individual genes co-operate in order to build the human body in seemingly unselfish ways. But co-operation in making and maintaining a human body is just a highly successful strategy to make gene copies, perfectly consistent with selfishness.”
To be honest, I’ve never taken very much pride in what my genes do. But anyway: perfect consistent with selfishness? Let me see. I pay my taxes, I obey the laws, I contribute to charities that campaign for equality, I try to be nice to people, and a fair bit of this I do because I feel it is a pretty good thing to be a part of a society that functions well. I figure that’s probably best for me in the long run. Aha! – so what I do is perfectly consistent with selfishness. Well yes, but look, you’re not going to call me selfish just because I want to live in a well ordered society are you? No, but then I have intentions and thoughts of the future, I have acquired moral codes and so on – genes don’t have any of these things. Hmm… so how exactly does that make the metaphor of “selfishness” work? Or more precisely, how does it make selfishness a better metaphor than cooperativeness? If “genes don’t care”, then neither metaphor is better than the other. It’s just stuff that happens when genes get together.
But no, wait, maybe I’m missing the point. Genes are selfish because they compete with each other for limited resources, and only the best replicators – well no, only those housed in the cells or organisms that are themselves the best at replicating their genomes – survive. See, it says here: “Those genes that fail at replicating are no longer around, while even those that are good face stiff competition from other replicators. Only the best can secure the resources needed to reproduce themselves.”
This is the bullshit at the heart of the issue. “Good genes” face stiff competition from who exactly? Other replicators? So a phosphatase gene is competing with a dehydrogenase gene? (Yeah, who would win that fight?) No. No, no, no. This, folks, this is what I would bet countless people believe because of the bad metaphor of selfishness. Yet the phosphatase gene might well be doomed without the dehydrogenase gene. They need each other. They are really good friends. (These personification metaphors are great, aren’t they?) If the dehydrogenase gene gets better at its job, the phosphatase gene further down the genome just loves it, because she gets the benefit too! She just loves that better dehydrogenase. She goes round to his place and…
Hmm, these metaphors can get out of hand, can’t they?
No, if the dehydrogenase gene is competing with anyone, it’s with other alleles of the dehydrogenase gene. Genes aren’t in competition, alleles are.
(Actually even that doesn’t seem quite right. Organisms compete, and their genetic alleles affect their ability to compete. But this gives a sufficient appearance of competition among alleles that I can accept the use of the word.)
So genes only get replicated (by and large) in a genome. So if a gene is “improved” by natural selection, the whole genome benefits. But that’s just a side result – the gene doesn’t care about the others! Yet this is precisely the point. Because the gene “doesn’t care”, all you can talk about is what you see, not what you want to ascribe, metaphorically or otherwise, to a gene. An advantageous gene mutation helps the whole genome replicate. It’s not a question of who cares or who doesn’t, or what the gene “really” wants or doesn’t want. That is the outcome. “Selfishness” doesn’t help to elucidate that outcome – it confuses it.
“So why are we fooled into believing that humans (and animals and plants) rather than genes are what counts in biology?” the authors ask. They give an answer, but it’s not the right one. Higher organisms are a special case, of course, especially ones that reproduce sexually – it’s really cells that count. We’re “fooled” because cells can reproduce autonomously, but genes can’t.
So cells are where it’s at? Yes, and that’s why this article by Mike Lynch et al. calling for a meeting of evolutionary theory and cell biology is long overdue (PNAS 111, 16990; 2014). For one thing, it might temper erroneous statements like this one that Yanai and Lercher make: “Darwin showed that one simple logical principle [natural selection] could lead to all of the spectacular living design around us.” As Lynch and colleagues point out, there is abundant evidence that natural selection is one of several evolutionary processes that has shaped cells and simple organisms: “A commonly held but incorrect stance is that essentially all of evolution is a simple consequence of natural selection.” They point out, for example, that many pathways to greater complexity of both genomes and cells don’t confer any selective fitness.
The authors end with a tired Dawkinseque flourish: “we exist to serve our genome”. This statement has nothing to do with science – it is akin to the statement that “we are at the pinnacle of evolution”, but looking in the other direction. It is a little like saying that we exist to serve our minds – or that water falls on mountains in order to run downhill. It is not even wrong. We exist because of evolution, but not in order to do anything. Isn’t it strange how some who preen themselves on facing up to life’s lack of purpose then go right ahead and give it back a purpose?
The sad thing is that that Aeon article is actually all about junk DNA and what ENCODE has to say about it. It makes some fair criticisms of ENCODE’s dodgy definition of “function” for DNA. But it does so by examining the so-called LINE-1 elements in genomes, which are non-coding but just make copies of themselves. There used to be a word for this kind of DNA. Do you know what that word was? Selfish.
In the 1980s, geneticists and molecular biologists such as Francis Crick, Leslie Orgel and Ford Doolittle used “selfish DNA” in a strict sense, to refer to DNA sequences that just accumulated in genomes by making copies – and which did not itself affect the phenotype (W. F. Doolittle & C. Sapienza, Nature 284, p601, and L. E. Orgel & F. H. C. Crick, p604, 1980). This stuff not only had no function, it messed things up if it got too rife: it could eventually be deleterious to the genome that it infected. Now that’s what I call selfish! – something that acts in a way that is to its own benefit in the short term while benefitting nothing else, and which ultimately harms everything.
So you see, I’m not against the use of the selfish metaphor. I think that in its original sense it was just perfect. Its appropriation to describe the entire genome – as an attribute of all genes – wasn’t just misleading, it also devalued a perfectly good use of the term.
But all that seems to have been forgotten now. Could this be the result of some kind of meme, perhaps?
Monday, December 08, 2014
Chemistry for the kids - a view from the vaults
At some point this is all going to become a more coherently thought-out piece, but right now I just want to show you some of the Chemical Heritage Foundation’s fabulous collection of chemistry kits through the ages. It is going to form the basis of an exhibition at some point in the future, so consider this a preview.
There is an entire social history to be told through these boxes of chemistry for kids.
Here's one of the earliest examples, in which the chemicals come in rather fetching little wooden bottles. That’s the spirit, old chap!
I like the warning on this one: if you’re too little or too dumb to read the instructions, keep your hands off.
Sartorial tips here for the young chemist, sadly unheeded today. Tuck those ties in, mind – you don’t want them dipping in the acid. Lots of the US kits, like this one, were made by A. C. Gilbert Co. of New Haven, Connecticut, which became one of the biggest toy manufacturers in the world. The intriguing thing is that the company began in 1909 as a supplier of materials for magic shows – Alfred Gilbert was a magician. So even at this time, the link between stage magic and chemical demonstrations, which had been established in the nineteenth century, was still evident.
Girls, as you know, cannot grow up to be scientists. But if they apply themselves, they might be able to adapt their natural domestic skills to become lab technicians. Of course, they’ll only want this set if it is in pink.
But if that makes you cringe, it got far worse. Some chemistry sets were still marketed as magic shows even in the 1940s and 50s. Of course, this required that you dress up as some exotic Eastern fellow, like a “Hindu prince or Rajah”. And he needs an assistant, who should be “made up as an Ethiopian slave”. “His face and arms should be blackened with burned cork… By all means assign him a fantastic name such as Allah, Kola, Rota or any foreign-sounding word.” Remember now, these kits were probably being given to the fine young boys who would have been formulating US foreign policy in the 1970s and 80s (or, God help us, even now).
OK, so boys and girls can both do it in this British kit, provided that they have this rather weird amalgam of kitchen and lab.
Don’t look too closely, though, at the Periodic Tables pinned to the walls on either side. With apologies for the rubbish image from my phone camera, I think you can get the idea here.
This is one of my favourites. It includes “Safe experiments in atomic energy”, which you can conduct with a bit of uranium ore. Apparently, some of the Gilbert kits also included a Geiger counter. Make sure an adult helps you, kids!
Here are the manuals for it – part magic, part nuclear.
But we are not so reckless today. Oh no. Instead, you get 35 “fun activities”… with “no chemicals”. Well, I should jolly well hope not!
This one speaks volumes about its times, which you can see at a glance was the 1970s. It is not exactly a chemistry kit in the usual sense, because for once the kids are doing their experiments outside. Now they are not making chemicals, but testing for them: looking for signs of pollution and contamination in the air and the waters. Johnny Horizon is here to save the world from the silent spring.
There is still a whiff of the old connection with magic here, and with the alchemical books of secrets (which are the subject of the CHF exhibition that brought me here).
But here we are now. This looks a little more like it.
What a contrast this is from the clean, shiny brave new world of yesteryear.
Many thanks to the CHF folks for dragging these things from their vaults.
Wednesday, December 03, 2014
Pushing the boundaries
Here is my latest Music Instinct column for Sapere magazine. I collected some wonderful examples of absurdly complicated scores while working on this, but none with quite the same self-mocking wit as the one above.
___________________________________________________________________
There’s no accounting for taste, as people say, usually when they are deploring someone else’s. But there is. Psychological tests since the 1960s have suggested that what people tend to look for in music, as in visual art, is an optimal level of complexity: not too much, not too little. The graph of preference versus complexity looks like an inverted U [1].
Thus we soon grow weary of nursery rhymes, but complex experimental jazz is a decidedly niche phenomenon. So what is the ideal level of musical complexity? By some estimates, fairly low. The Beatles’ music has been shown to get generally more complex from 1962 to 1970, based on analysis of the rhythmic patterns, statistics of melodic pitch-change sequences and other factors [2]. And as complexity increased, sales declined. Of course, there’s surely more to the trend than that, but it implies that “All My Loving” is about as far as most of us will go.
But mightn’t there be value – artistic, if not commercial – in exploring the extremes of simplicity and complexity? Classical musicians evidently think so, whether it is the two-note drones of 1960s ultra-minimalist La Monte Young or the formidable, rapid-fire density of the “New Complexity” school of Brian Ferneyhough. Few listeners, it must be said, want to stay in these rather austere sonic landscapes for long.
But musical complexity needn’t be ideologically driven torture. J. S. Bach sometimes stacked up as many as six of his overlapping fugal voices, while the chromatic density of György Ligeti’s Atmosphères, with up to 56 string instruments all playing different notes, made perfect sense when used as the soundtrack to Stanley Kubrick’s 2001: A Space Odyssey.
The question is: what can the human mind handle? We have trouble following two conversations at once, but we seem able to handle musical polyphony without too much trouble. There are clearly limits to how much information we can process, but on the whole we probably sell ourselves short. Studies show that the more original and unpredictable music is, the more attentive we are to it – and often, relatively little exposure is needed before a move towards the complex end of the spectrum ceases to be tedious or confusing and becomes pleasurable. Acculturation can work wonders. Before pop music colonized Indonesia, gamelan was its pop music – and that, according to one measure of complexity rooted in information theory, is perhaps the most complex major musical style in the world.
1. Davies, J. B. The Psychology of Music. Hutchinson, London, 1978.
2. Eerola, T. & North, A. C. ‘Expectancy-based model of melodic complexity’, in Proceedings of the 6th International Conference of Music Perception and Cognition (Keele University, August 2000), eds Woods, C., Luck, G., Brochard, R., Seddon, F. & Sloboda, J. Keele University, 2000.
Wednesday, November 26, 2014
Hidden truths
I had meant to put up this piece – my October Crucible column for Chemistry World – some time back, so as to have the opportunity to show more of the amazing images of Liu Bolin. So anyway, here it is.
____________________________________________________________________
When I first set eyes on Liu Bolin, I didn’t see him at all. The Chinese artist has been dubbed the “Invisible Man”, because he uses extraordinarily precise body-painting to hide himself against all manner of backgrounds: shelves of magazines or tins in supermarkets, government propaganda posters, the Great Wall. What could easily seem in the West to be a clever gimmick becomes a deeply political statement in China, where invisibility serves as a metaphor for the way the state is perceived to ignore or “vanish” the ordinary citizen, while the rampant profiteering of the booming Chinese economy turns individuals into faceless consumers of meaningless products. In one of his most provocative works, Liu stands in front of the iconic portrait of Mao Zedong in Tiananmen Square, painted so that just his head and shoulders seem to be superimposed over those of the Great Helmsman. In another, a policeman grasps what appears to be a totally transparent, almost invisible Liu, or places his hands over the artist’s invisible eyes.
More recently Liu has commented on the degradation of China’s environment and the chemical adulteration of its food and drink. Some of these images are displayed in a new exhibition, A Colorful World?, at the Klein Sun Gallery in New York, which opened on 11 September. The title refers to “the countless multicolored advertisements and consumer goods that cloud today’s understanding of oppression and injustice.” But it’s not just their vulgarity and waste that Liu wants to point out, for in China there has sometimes been far more to fear from foods than their garish packaging. “The bright and colorful packaging of these snack foods convey a lighthearted feeling of joy and happiness, but what they truly provide is hazardous to human health”, the exhibition’s press release suggests. It’s bad enough that the foods are laden with carcinogens and additives, but several recent food scandals in China have revealed the presence of highly dangerous compounds. In 2008, some leading brands of powdered milk and infant formula were found to contain melamine, a toxic carcinogen added to boost the apparent protein content and so allow the milk to be diluted without failing quality standards. Melamine can cause kidney stones – several babies died from that condition, while many thousands were hospitalized.
There have been several other cases of foods treated with hormones and other hazardous cosmetic additives. The most recent involves the use of phthalate plasticizers in soft drinks as cheap replacements for palm oil. These compounds may be carcinogenic and are thought to disrupt the endocrine and reproductive systems by mimicking hormones. In his 2011 work Plasticizer, Liu commented on this use of such additives by “disappearing” in front of supermarket shelves of soft drinks.
So there is no knee-jerk chemophobia in these works, which represent a genuine attempt to highlight the lack of accountability and malpractice exercised within the food industry – and not just in China. The same is true of Liu’s Cancer Village, part of his Hiding in the City series in which he and others are painted to vanish against Chinese landscapes. The series began as a protest against the demolition of an artists’ village near Beijing in 2005 – Liu vanished amongst the rubble – but Cancer Village illustrates the invisibility and official “non-existence” of ordinary citizens in the face of a much more grievous threat: chemical pollution from factories, which seems likely to be the cause of a massive increase in cancer incidence in the village of the 23 people who Liu and his assistants have merged into a field behind which a chemical plant looms.
Such politically charged performance art walks a delicate line in China. Artists there have refined their approach to combine a lyrical, even playful obliqueness – less easily attacked by censors – with resonant symbolism. When in 1994 Wang Jin emptied 50 kg of red organic pigment into the Red Flag Canal in Henan Province for his work Battling the Flood, it was a sly comment not just on the uncritical “Red China” rhetoric of the Mao era (when the canal was dug) but also on the terrible bloodshed of that period.
It could equally have been a statement about the lamentable state of China’s waterways, where pollution, much of it from virtually unregulated chemicals plants, has rendered most of the river water fit only for industrial uses. That was certainly the concern highlighted by Yin Xiuzhen’s 1995 work Washing the River, in which the artist froze blocks of water from the polluted Funan River in Chengdu and stacked them on the banks. Passers-by were invited to “wash” the ice with clean water in an act that echoed the purifying ritual of baptism. This year Yin has recreated Washing the River on the polluted Derwent River near Hobart, Tasmania.
These are creative and sometimes moving responses to problems with both technological and political causes. They should be welcomed by scientists, who are good at spotting such problems but sometimes struggle to elicit a public reaction to them.
Thursday, November 20, 2014
The science and politics of gentrification
I figured that, after the tribulations of touching on the sensitive subject of genes and behaviour, it might be some light relief to turn to the interesting subject of urban development, and specifically a new paper looking at the morphological characteristics shared by parts of London that have recently undergone gentrification. I was attracted to the study partly because the locales it considers are so familiar to me – two of the areas, Brixton and Telegraph Hill, are just down the road from me in southeast London. But this also presented an opportunity to talk about the emerging approach to urban theory that regards cities as having “natural histories” amenable to exploration using scientific tools and concepts that were developed to understand morphological change and growth in the natural world. It’s an approach that I believe is proving very fruitful in terms of understanding how and why cities evolve.
Well, so I fondly imagined as I wrote the piece below for the Guardian. Now, I’m not totally naïve – I realise that gentrification is a sensitive subject given the decidedly mixed nature of the results. Districts might become safer and more family-friendly, not to mention the fact that they serve better coffee; but at the same time they can become unaffordable to many locals, stripped of some of their traditional character, and prey to predatory developers.
I’ve seen this happen in my own area of East Dulwich. I always feel that, when I say to Londoners that this is where I live, I have to quickly explain that we moved here 20 years ago when properties were cheap and the main street was fairly run-down and populated by a mixture of quirky but decidedly un-chi-chi shops. There is no way we could afford to move here today. So yes, the parks and cafés are all very nice, but I’ve mixed feelings about the demographic shifts and I’m dismayed by the stupid property prices.
So it was no surprise to find such mixed feelings reflected in the readers’ comments on my piece, many of which were pleasingly thoughtful and interesting compared to the snarky feedback one often gets on Comment is Free. But what I hadn’t anticipated was the Twitter response, where there seemed to be a sense in some quarters that my remarks on gentrification betrayed a rather sinister agenda. Admittedly, some of this was just ideological cant (ironically of a Marxist persuasion, I suspect), but some of the critical feedback offered food for thought on how notions of self-organization and complexity applied to urban growth can be received – responses that I hadn’t anticipated or encountered before.
Some felt that to regard gentrification, or any other aspect of urban development, as something akin to a “natural” process is to offer a convenient smokescreen for the fact that many such processes are driven by profit, greed and venality – or as some would say, by capital. To consider these processes in naturalistic terms, they said, is to risk disguising their political and economic origins, and to belittle the sometimes dismaying social consequences. Indeed, it seems that for some people this whole approach smacks of a kind of social Darwinism of the same ilk as that which proclaims that inequalities are natural and inevitable and that it is therefore fruitless to deplore them.
I can understand this point of view to some degree, for certainly a “naturalism” based on a misappropriation of Darwinian ideas has been used in the past to excuse the rapaciousness of capitalist economies. But to imagine that this is what a modern “complexity” approach to social phenomena is all about seems to me to reflect a deep and possibly even dangerous confusion. The aim of such work is, in general, to understand how certain consequences emerge from the social and institutional structures we create. These consequences might sometimes be highly non-intuitive in ways that simple cause-and-effect narratives can’t hope to capture. They are intended to be partly descriptive – what are the key features that characterize such phenomena; how are they different in different instances? – and partly explanatory. Often the methods involve agent-based modelling, starting from the question: if the agents are allowed or constrained to interact in such and such a way, what are the results likely to be? In the current case, the question is: why do some areas undergo gentrification, but not others? I can’t begin to imagine why, regardless of how you feel about gentrification or what its socio-political causes might be, that question would not be of interest.
But to see such explorations as a kind of justification of what it is they seek to understand is to totally misconstrue the object. Look at it this way. There has been a great deal of work done on traffic flows, in particular to understand how they break down and become congested. It would be bizarre to suggest that such studies are seeking to excuse or justify congestion. On the contrary, their aim is generally to find the causative influences of congestion, so that traffic rules or networks might be better designed to avoid it. Similarly, attempts to understand economic crashes and recessions using ideas from complex-systems theory don’t for a moment take as their starting point the idea that, if we can show why such events emerge from our existing economic systems, we have somehow shown that these are things we must just lie down and accept. (Indeed, amongst other things they can counter the foolish delusion, popular pre-2008, that such fluctuations are a thing of the past.)
Now, you might say that I did however begin my Guardian piece with the suggestion that (according to the researchers who did the work it describes) gentrification is “almost a law of nature”. This is certainly what the paper implies – that this phenomenon is simply a part of the cyclic change and renewal that cities experience. Surely one would hope – I would hope – that this change happens in terms of relatively deprived neighbourhoods experiencing an improvement in facilities and amenities, rather than by the kind of wholesale demolition that was deemed necessary for the Heygate estate. But the bad aspects of gentrification include inadequate provision for existing residents and businesses affected by the soaring prices, loss of local character, uninhibited property grabs, and so on. It’s complicated, for sure.
(A word here: some folks in the Guardian comments have deplored the Heygate development, and my impression has been that some residents were compelled to move against their wishes. I rather fear that there is some truth too in the suggestions that the people who will benefit most will be property developers. But I spent a considerable amount of time in the mid-1990s in the adjacent Aylesbury estate, a similarly hideous brutalist high-rise development plagued with social problems. Any sense of community that existed there – and there certainly was some – survived in spite of the disastrous social planning that had created these “living” spaces, not because of it. Moreover, I think we should be extremely wary of romanticizing a development that owed its existence to very similar circumstances: it was built on the ruins of postwar slums where deprivation coexisted with a sense of community, and from which residents were similarly rehoused or displaced.)
In any event, it is essential that studies of complexity and self-organization in social systems are never used to justify the status quo. They need to be accompanied by moral and ethical decisions about the kind of society we want to have. The whole point of much of this work, especially in agent-based modelling, is to show us the potential consequences of the choices we make: if we set things up this way, the result is likely to be this. They might save us from striving for solutions that are simply not attainable, or not unless we make some changes to the underlying rules. This, of course, is nothing more that Hume’s admonition not to confuse an “is” with an “ought”. The theories and models by no means absolve us from the responsibility of deciding what kind of society we want; indeed, they might hopefully challenge prejudices and dogmas about that. I hesitate to suggest that this approach is “apolitical”, since science rarely is, and in social science in particular it is very hard to be sure that we do not pose a question in a way that embodies or endorses certain preconceptions. And I feel that sometimes this kind of research operates in too much of a political vacuum, as though the researchers are reluctant to acknowledge or explore the real social and political implications of their work.
So I am glad that the issue came up. Here’s the article.
___________________________________________________________________________
Grumble all you like that Brixton’s covered market, once called a “24-hour supermarket” by the local police, has been colonised by trendy boutique restaurants. The fact is that the gentrification of what was once an edgy part of London is almost a law of nature.
“Urban gentrification”, say Sergio Porta, professor of urban design at Strathclyde University in Glasgow, and his coworkers in London and Italy in a new paper, “is a natural force underpinning the evolution of cities.” Their research reveals that Brixton shares features in common with other once down-at-heel London districts that have recently seen the invasion of farmer’s markets and designer coffee shops, such as Battersea and Telegraph Hill. These characteristics, they say, make such neighbourhoods ripe for gentrification.
Whether it is the Northern Quarter in Manchester, Harlem in New York or pretty much everywhere in central Paris, gentrification is rife in the world’s major cities. You know the signs: one minute the local pub gets a facelift, the next minute everyone is reading the Guardian and sipping lattes, and you daren’t even look at the property prices.
The implications for demographics, crime, transport and economics make it vital for planners and local authorities to get a grasp of what drives gentrification. Urban theorists have debated that for decades. According to one view the artists kick it off, as they did in Notting Hill, moving into cheap housing and transforming the area from poor to bohemian – then investors and families follow. Another view says that the developers and public agencies come first, buying up cheap property and then selling it for a profit to the middle classes.
Porta and his colleagues have focused instead on the physical attributes that seem to make an area ripe for – or vulnerable to, depending on your view – gentrification. Do different neighbourhoods share the same features? The team looked at five parts of London that have gone upmarket in the past decade or so: Brixton, Battersea, Telegraph Hill, Barnsbury and Dalston.
All of them are some distance from the city centre. The housing is typically dense but modest: undistinguished terraced houses two or three storeys high, often of Victorian vintage. “This picture is pretty much that of a traditional neighborhood, far away from the modernist model of big buildings”, says Porta.
But the key issue, the researchers say, is how the local street network is arranged, and how it is plugged into the rest of the city. Each street can be assigned a value of the awkwardly named “betweenness centrality”: a measure of how likely you are to pass along or across it on the shortest path between any two points in the area. It’s a purely geometric quantity that can be calculated directly from a map.
All of the five districts in the study have major roads with high betweenness centrality along their borders, but not through their centres. These roads provide good connections to the rest of the city without disrupting the neighbourhood. Smaller “local main” streets penetrate inside the district, providing easy access but not noise or danger. “It’s this balance between calmness and urban buzz within easy reach that is one of the conditions for gentrification”, says Porta. These conclusions rely only on geography: on what anyone can go and measure for themselves, not on the particular history of a neighbourhood or the plans of councillors and developers. Looked at this way, the researchers are studying city evolution much as biologists study natural evolution – almost as if the city itself were a natural organism.
This idea that cities obey laws beyond the reach of planning goes back to social theorist Lewis Mumford in the 1930s, who described the growth of cities as “amoeboid”. It was developed in the 1950s by the influential urban theorist Jane Jacobs, who argued that the forced redevelopment of American inner cities was destroying their inherent vibrancy.
Jacobs’ views on the spontaneous self-organization of urban environments anticipated modern work on ecosystems and other natural “complex systems”. Many urban theorists now believe that city growth should be considered a kind of natural history, and be studied scientifically using the tools of complexity theory rather than being forced to conform to some planner’s idea of how growth should occur.
Gentrification is not just “natural” but healthy for cities, Porta says: it’s a reflection of their ability to adapt, a facet of their resilience. The alternative for areas that lack the prerequisites – for example, modernist tower blocks, which cannot acquire the magic values of housing density and frontage height – is the wrecker’s ball, like that recently taken to the notorious Heygate estate in south London.
The new findings could have predicted that fate. By the same token, they might indicate where gentrification will happen next. Porta is wary of forecasting that without proper research, but he says that Lower Tooting is one area with all the right features, and looks set to become the new Balham, just as Balham was the new Clapham.
[Postscript: I told Sergio that I would give full credit to his coworkers. They are Alessandro Venerandi of University College London, Mattia Zanella of the University of Ferrara, and Ombretta Romice of the University of Strathclyde.]
Well, so I fondly imagined as I wrote the piece below for the Guardian. Now, I’m not totally naïve – I realise that gentrification is a sensitive subject given the decidedly mixed nature of the results. Districts might become safer and more family-friendly, not to mention the fact that they serve better coffee; but at the same time they can become unaffordable to many locals, stripped of some of their traditional character, and prey to predatory developers.
I’ve seen this happen in my own area of East Dulwich. I always feel that, when I say to Londoners that this is where I live, I have to quickly explain that we moved here 20 years ago when properties were cheap and the main street was fairly run-down and populated by a mixture of quirky but decidedly un-chi-chi shops. There is no way we could afford to move here today. So yes, the parks and cafés are all very nice, but I’ve mixed feelings about the demographic shifts and I’m dismayed by the stupid property prices.
So it was no surprise to find such mixed feelings reflected in the readers’ comments on my piece, many of which were pleasingly thoughtful and interesting compared to the snarky feedback one often gets on Comment is Free. But what I hadn’t anticipated was the Twitter response, where there seemed to be a sense in some quarters that my remarks on gentrification betrayed a rather sinister agenda. Admittedly, some of this was just ideological cant (ironically of a Marxist persuasion, I suspect), but some of the critical feedback offered food for thought on how notions of self-organization and complexity applied to urban growth can be received – responses that I hadn’t anticipated or encountered before.
Some felt that to regard gentrification, or any other aspect of urban development, as something akin to a “natural” process is to offer a convenient smokescreen for the fact that many such processes are driven by profit, greed and venality – or as some would say, by capital. To consider these processes in naturalistic terms, they said, is to risk disguising their political and economic origins, and to belittle the sometimes dismaying social consequences. Indeed, it seems that for some people this whole approach smacks of a kind of social Darwinism of the same ilk as that which proclaims that inequalities are natural and inevitable and that it is therefore fruitless to deplore them.
I can understand this point of view to some degree, for certainly a “naturalism” based on a misappropriation of Darwinian ideas has been used in the past to excuse the rapaciousness of capitalist economies. But to imagine that this is what a modern “complexity” approach to social phenomena is all about seems to me to reflect a deep and possibly even dangerous confusion. The aim of such work is, in general, to understand how certain consequences emerge from the social and institutional structures we create. These consequences might sometimes be highly non-intuitive in ways that simple cause-and-effect narratives can’t hope to capture. They are intended to be partly descriptive – what are the key features that characterize such phenomena; how are they different in different instances? – and partly explanatory. Often the methods involve agent-based modelling, starting from the question: if the agents are allowed or constrained to interact in such and such a way, what are the results likely to be? In the current case, the question is: why do some areas undergo gentrification, but not others? I can’t begin to imagine why, regardless of how you feel about gentrification or what its socio-political causes might be, that question would not be of interest.
But to see such explorations as a kind of justification of what it is they seek to understand is to totally misconstrue the object. Look at it this way. There has been a great deal of work done on traffic flows, in particular to understand how they break down and become congested. It would be bizarre to suggest that such studies are seeking to excuse or justify congestion. On the contrary, their aim is generally to find the causative influences of congestion, so that traffic rules or networks might be better designed to avoid it. Similarly, attempts to understand economic crashes and recessions using ideas from complex-systems theory don’t for a moment take as their starting point the idea that, if we can show why such events emerge from our existing economic systems, we have somehow shown that these are things we must just lie down and accept. (Indeed, amongst other things they can counter the foolish delusion, popular pre-2008, that such fluctuations are a thing of the past.)
Now, you might say that I did however begin my Guardian piece with the suggestion that (according to the researchers who did the work it describes) gentrification is “almost a law of nature”. This is certainly what the paper implies – that this phenomenon is simply a part of the cyclic change and renewal that cities experience. Surely one would hope – I would hope – that this change happens in terms of relatively deprived neighbourhoods experiencing an improvement in facilities and amenities, rather than by the kind of wholesale demolition that was deemed necessary for the Heygate estate. But the bad aspects of gentrification include inadequate provision for existing residents and businesses affected by the soaring prices, loss of local character, uninhibited property grabs, and so on. It’s complicated, for sure.
(A word here: some folks in the Guardian comments have deplored the Heygate development, and my impression has been that some residents were compelled to move against their wishes. I rather fear that there is some truth too in the suggestions that the people who will benefit most will be property developers. But I spent a considerable amount of time in the mid-1990s in the adjacent Aylesbury estate, a similarly hideous brutalist high-rise development plagued with social problems. Any sense of community that existed there – and there certainly was some – survived in spite of the disastrous social planning that had created these “living” spaces, not because of it. Moreover, I think we should be extremely wary of romanticizing a development that owed its existence to very similar circumstances: it was built on the ruins of postwar slums where deprivation coexisted with a sense of community, and from which residents were similarly rehoused or displaced.)
In any event, it is essential that studies of complexity and self-organization in social systems are never used to justify the status quo. They need to be accompanied by moral and ethical decisions about the kind of society we want to have. The whole point of much of this work, especially in agent-based modelling, is to show us the potential consequences of the choices we make: if we set things up this way, the result is likely to be this. They might save us from striving for solutions that are simply not attainable, or not unless we make some changes to the underlying rules. This, of course, is nothing more that Hume’s admonition not to confuse an “is” with an “ought”. The theories and models by no means absolve us from the responsibility of deciding what kind of society we want; indeed, they might hopefully challenge prejudices and dogmas about that. I hesitate to suggest that this approach is “apolitical”, since science rarely is, and in social science in particular it is very hard to be sure that we do not pose a question in a way that embodies or endorses certain preconceptions. And I feel that sometimes this kind of research operates in too much of a political vacuum, as though the researchers are reluctant to acknowledge or explore the real social and political implications of their work.
So I am glad that the issue came up. Here’s the article.
___________________________________________________________________________
Grumble all you like that Brixton’s covered market, once called a “24-hour supermarket” by the local police, has been colonised by trendy boutique restaurants. The fact is that the gentrification of what was once an edgy part of London is almost a law of nature.
“Urban gentrification”, say Sergio Porta, professor of urban design at Strathclyde University in Glasgow, and his coworkers in London and Italy in a new paper, “is a natural force underpinning the evolution of cities.” Their research reveals that Brixton shares features in common with other once down-at-heel London districts that have recently seen the invasion of farmer’s markets and designer coffee shops, such as Battersea and Telegraph Hill. These characteristics, they say, make such neighbourhoods ripe for gentrification.
Whether it is the Northern Quarter in Manchester, Harlem in New York or pretty much everywhere in central Paris, gentrification is rife in the world’s major cities. You know the signs: one minute the local pub gets a facelift, the next minute everyone is reading the Guardian and sipping lattes, and you daren’t even look at the property prices.
The implications for demographics, crime, transport and economics make it vital for planners and local authorities to get a grasp of what drives gentrification. Urban theorists have debated that for decades. According to one view the artists kick it off, as they did in Notting Hill, moving into cheap housing and transforming the area from poor to bohemian – then investors and families follow. Another view says that the developers and public agencies come first, buying up cheap property and then selling it for a profit to the middle classes.
Porta and his colleagues have focused instead on the physical attributes that seem to make an area ripe for – or vulnerable to, depending on your view – gentrification. Do different neighbourhoods share the same features? The team looked at five parts of London that have gone upmarket in the past decade or so: Brixton, Battersea, Telegraph Hill, Barnsbury and Dalston.
All of them are some distance from the city centre. The housing is typically dense but modest: undistinguished terraced houses two or three storeys high, often of Victorian vintage. “This picture is pretty much that of a traditional neighborhood, far away from the modernist model of big buildings”, says Porta.
But the key issue, the researchers say, is how the local street network is arranged, and how it is plugged into the rest of the city. Each street can be assigned a value of the awkwardly named “betweenness centrality”: a measure of how likely you are to pass along or across it on the shortest path between any two points in the area. It’s a purely geometric quantity that can be calculated directly from a map.
All of the five districts in the study have major roads with high betweenness centrality along their borders, but not through their centres. These roads provide good connections to the rest of the city without disrupting the neighbourhood. Smaller “local main” streets penetrate inside the district, providing easy access but not noise or danger. “It’s this balance between calmness and urban buzz within easy reach that is one of the conditions for gentrification”, says Porta. These conclusions rely only on geography: on what anyone can go and measure for themselves, not on the particular history of a neighbourhood or the plans of councillors and developers. Looked at this way, the researchers are studying city evolution much as biologists study natural evolution – almost as if the city itself were a natural organism.
This idea that cities obey laws beyond the reach of planning goes back to social theorist Lewis Mumford in the 1930s, who described the growth of cities as “amoeboid”. It was developed in the 1950s by the influential urban theorist Jane Jacobs, who argued that the forced redevelopment of American inner cities was destroying their inherent vibrancy.
Jacobs’ views on the spontaneous self-organization of urban environments anticipated modern work on ecosystems and other natural “complex systems”. Many urban theorists now believe that city growth should be considered a kind of natural history, and be studied scientifically using the tools of complexity theory rather than being forced to conform to some planner’s idea of how growth should occur.
Gentrification is not just “natural” but healthy for cities, Porta says: it’s a reflection of their ability to adapt, a facet of their resilience. The alternative for areas that lack the prerequisites – for example, modernist tower blocks, which cannot acquire the magic values of housing density and frontage height – is the wrecker’s ball, like that recently taken to the notorious Heygate estate in south London.
The new findings could have predicted that fate. By the same token, they might indicate where gentrification will happen next. Porta is wary of forecasting that without proper research, but he says that Lower Tooting is one area with all the right features, and looks set to become the new Balham, just as Balham was the new Clapham.
[Postscript: I told Sergio that I would give full credit to his coworkers. They are Alessandro Venerandi of University College London, Mattia Zanella of the University of Ferrara, and Ombretta Romice of the University of Strathclyde.]
Wednesday, November 19, 2014
Too funky in here
This piece for my Music Instinct column in Sapere magazine should be out and about in Italian any time now. I’ve talked about this deal before, but no harm in returning to it with the right soundtrack.
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I’ve got plans to discuss some seriously challenging music in the next column, so in this one I’m going to treat you. Look up Bootsy Collins’ song Stretchin’ Out and make sure you have room to dance. Pure hedonism, isn’t it? Well, maybe not, actually – because Bootsy is taking splendid advantage of our cognitive predispositions in order to do several things at once. That gusty and fabulously ornate bass guitar is laying down the syncopated groove that gets the feet twitching, the backing vocalists provide the blissed-out melody, and the sax and guitar solos ice the cake with their soaring improvisations.
Yes, there’s a lot going on. But the roles of each of these “voices” in the mix aren’t arbitrary. It now seems that the high-pitched vocals and solos take care of melodic duties because we hear melody best in the high register, while Bootsy’s bass thumps out the rhythm because our ears and minds are best attuned to rhythmic structures at low pitches.
This division of labour isn’t, after all, just a feature of funk: it seems to happen throughout the music of the world. The pianist’s left hand is usually her rhythmic anchor and her right is the source of melody, whether she’s playing Haydn or boogie-woogie. Low-pitched percussive instruments carry the rhythm in Indian classical music (where high-register sitar takes the melodic role) or Indonesian gamelan.
Psychologist Laurel Trainor and her collaborators in Canada have shed light on why this is. When they studied people listening to polyphonic music – which has several simultaneous melodic lines or “voices” – using magnetic sensors to monitor the subjects’ electrical brain activity, they found that each voice was stored as a separate “memory trace”, and that the most salient voice (the one listeners were most attuned to) was the one with the highest pitch.
In more recent experiments using electrical sensors to detect the characteristic brain responses to “errors” in what a listener hears, Trainor and colleagues found that the opposite is true for rhythm. The lower-pitched the tones are, the better we are at discriminating differences in their timing. This pitch-dependent sensitivity to rhythm, the researchers concluded, arises from the basic physiology of the inner ear, where the cochlea converts acoustic waves to nerve signals. We’re designed, it seems, for Bootsy’s freaky funk-outs.
Monday, November 17, 2014
Genes and IQ: some clarifications
I hadn’t anticipated that my article for Prospect on the “language of genes” would spark a discussion so focused on the question of the inheritability of IQ (which was just a small part of what the piece was about). Judging from the reverberations on Twitter, it looks as though some further clarifications might be useful.
The point of my article is not to contest whether cognitive abilities are heritable. Clearly they are. The point is that this fact does not necessarily imply it is meaningful to therefore talk about “genes for” that those abilities. Geneticists might argue that this is a straw man – that they recognize very well that the “genes for” trope is often unhelpful. This is true up to a point, but my argument is that this recognition came later than it needed to, and that even now the narratives and rhetoric used even in academic research on genetics and genomics fails to distance itself sufficiently from that legacy.
As for the issue of genes and IQ, I’ve said already that the evidence is contended, and it seems clear that there is a fair degree of polarization on the matter that is not helping the debate.
First, I should state clearly that there is very good reason to believe that, whatever cognitive abilities IQ tests measure, these abilities are inheritable to a significant degree. Of course one can argue about what exactly it is that IQ testing measures, and the limitations of those tests are widely (and rightly) advertised. But whatever the rights and wrong of using IQ as a measure of “intelligence”, or of using academic achievement as an indication of a person’s intellectual capacity, I believe that such “formal” measures tell us something about an individual’s cognitive abilities and that there is reason to believe that these are to some degree genetic.
There is nothing very surprising about that. The question is what the implications are – if any – for educational policy. One can debate the precise values, but there seems to be rather good reason to think that (1) academic achievement is strongly linked to socioeconomic status (SES), and (2) the relevance of genes to academic achievement becomes less evident as socioeconomic status declines. In cases of significant deprivation, it appears that the impact of genes on IQ might be close to negligible. A likely explanation for this is that, the fewer learning opportunities you have – the more obstructive your environment is to learning – the less you are going to benefit from any advantages your innate cognitive skills confer, since they are less likely to have a chance to manifest themselves. In an excellent learning environment, in contrast, innate differences are able to manifest themselves much more clearly. Again, there seems nothing terribly surprising about this. But the implications for education seem fairly plain: only when opportunities to learn are equal will one see clearly the extent of inherent genetic variation. This is of course very different from saying that when everyone has the same opportunities, everyone will do more or less equally well.
What this means is that, if a child with low SES is doing poorly at school, it would be wrong to say “well, obviously it is because of the disadvantages he faces through being poor.” It is possible that he has inherited limited cognitive resources that would hold him back even if he came from a wealthy background. That sounds harsh, and one might wish it wasn’t so – but it needs to be acknowledged, and it seems (though it’s hard to tell) that one of Dominic Cummings’ aims was to do so. But there are two crucial points to make here:
(1) If a child is doing poorly academically, it seems more likely to be due to inherent cognitive limitations if he has high SES than low SES, because in the former case genetic propensities are less masked by other factors.
(2) While the aforementioned statement might be true for individuals, it seems extremely unlikely as a generalized statement: one would expect inherited variations in cognition for low-SES children to be no different to those from high-SES children, so that any difference in academic achievement seen on average between these two groups would result from social and not genetic factors.
But wait – is that necessarily true? Might it not be that there is a correlation between low SES and genetically determined lower cognitive ability? To put it bluntly, might the poor be inherently dim – indeed, might not the causation actually work that way, i.e. they are poor because they are dim, not that they underachieve because they are poor?
Cummings seems to be raising this possibility. I say this warily because he seems to feel that he is constantly being misunderstood, but I can’t see how otherwise to interpret this passage in his paper (p.74):
“Raising school performance of poorer children is an inherently worthwhile thing to try to do but it would not necessarily lower parent-offspring correlations (nor change heritability estimates). When people look at the gaps between rich and poor children that already exist at a young age (3-5), they almost universally assume that these differences are because of environmental reasons (‘privileges of wealth’) and ignore genetics.”
If genetics is the reason for these gaps, he seems to be saying, then pouring money and resources into education for low-SES groups won’t help all that much, or at least won’t eliminate the gap. He certainly doesn’t say that we should not spend in that direction. Indeed, he suggests that one could argue we should put in more resources to the education of children from poorer backgrounds, precisely because they are more needed – but that we’d need to be realistic about the expected outcomes.
OK, so there are two ways to look at this. One is to say that surely hypothesizing that the correlation between low attainment and low SES is due to genetics shouldn’t be ruled out simply because it is “politically incorrect.” I’d agree with that. But it frustrates me endlessly that there are many scientists who would be content to stop there, i.e. with the notion that there are no questions in science that should not be asked. Science doesn’t work that way. Scientists don’t sit around dreaming up any hypothesis and then testing them. “I wonder if there might really be a race of aliens like the Clangers?” “I wonder if African nations really do have a genetic predisposition to bad government?” (Hello Nicholas Wade.) Hypotheses need to be motivated by observation, but they should also acknowledge what seems plausible on the basis of what we already know – yes, there are problems of governance in parts of Africa, but it is very hard to see how a genetic basis for that might arise, so why would you want to start from that possibility?
This was why I was so dismayed by the response of some scientists to the outcry about James Watson’s suggestions of a link between race and intelligence. If he had been proposing to set up a research programme to explore whether there were correlations between intelligence and some kind of genetic correlates of what we socially recognize as race (if such exist), then one could understand (just about) why criticisms of his comments and cancellations of his talks might seem like a kind of “politically correct” censorship, as some of Watson’s supporters asserted. But not only were Watson’s remarks apparently unmotivated by any well established scientific observations or theories, they were not advanced as a scientific hypothesis at all – they were supported by idle, bigoted anecdote.
Much the same applies here: given the apparent lack (to my knowledge) of any suggestion in the literature that the reasons that social class predicts educational achievement are genetic, it seems a strange (one might even argue dangerous) hypothesis to present a priori. Unless one has an underlying agenda, I’m puzzled by why one would suggest such a thing.
In any event, my real point was that, give the current state of play about links between genetics and measures of “intelligence” (for example, see this recent review), it isn’t clear why the matter should be terribly relevant to education policy at all. Cummings makes a big deal of Robert Plomin’s work – which, I hasten to point out, is totally respectable and worthwhile. Plomin’s hope is that, if one could identify genes linked to cognitive and academic abilities, it might be possible to personalize education to the individual’s inherent intellectual endowments. This is a reasonable and indeed praiseworthy goal. But what we have discovered so far on the matter seems to indicate that such ambitions are not only far from being realised but potentially misplaced in the first place – because there may not be a small set of genes that will predict those endowments. And that might be because we are thinking the wrong way – too linearly – about how many if not most genes actually operate. Personally, I find a little chilling the idea that we might try to predict children’s attainments by reading their genome, and gear their education accordingly – not least because we know (and Plomin would of course acknowledge this) that genes operate in conjunction with their environment, and so whatever genetic hand you have been dealt, its outcomes are contingent on experience. Given the current lack of a strong link between specific gene variants and IQ (and not for want of looking), right now it seems unlikely that we would learn anything more from genomics than smart teachers already discern from noting the strengths and limitations of each child. What’s more, evidence from neuroscience that early experiences affect the wiring of the brain make it seem far more profitable to place emphasis on a child’s learning environment (including that within the family), and not to worry about what your genes “say” about your future abilities.
It’s of course important to recognize that this situation might change in the future, but there seems little reason right now to anticipate that it will. This is why I feel that raising the matter of genetics in educational policy right now seems like a red herring – and worse, that it encourages this misleading and potentially damaging notion of “genes for”. Genetics should certainly not be a taboo subject in discussions about education, but I’ve yet to see a convincing argument for why it has anything to tell us about how to help children learn.
The point of my article is not to contest whether cognitive abilities are heritable. Clearly they are. The point is that this fact does not necessarily imply it is meaningful to therefore talk about “genes for” that those abilities. Geneticists might argue that this is a straw man – that they recognize very well that the “genes for” trope is often unhelpful. This is true up to a point, but my argument is that this recognition came later than it needed to, and that even now the narratives and rhetoric used even in academic research on genetics and genomics fails to distance itself sufficiently from that legacy.
As for the issue of genes and IQ, I’ve said already that the evidence is contended, and it seems clear that there is a fair degree of polarization on the matter that is not helping the debate.
First, I should state clearly that there is very good reason to believe that, whatever cognitive abilities IQ tests measure, these abilities are inheritable to a significant degree. Of course one can argue about what exactly it is that IQ testing measures, and the limitations of those tests are widely (and rightly) advertised. But whatever the rights and wrong of using IQ as a measure of “intelligence”, or of using academic achievement as an indication of a person’s intellectual capacity, I believe that such “formal” measures tell us something about an individual’s cognitive abilities and that there is reason to believe that these are to some degree genetic.
There is nothing very surprising about that. The question is what the implications are – if any – for educational policy. One can debate the precise values, but there seems to be rather good reason to think that (1) academic achievement is strongly linked to socioeconomic status (SES), and (2) the relevance of genes to academic achievement becomes less evident as socioeconomic status declines. In cases of significant deprivation, it appears that the impact of genes on IQ might be close to negligible. A likely explanation for this is that, the fewer learning opportunities you have – the more obstructive your environment is to learning – the less you are going to benefit from any advantages your innate cognitive skills confer, since they are less likely to have a chance to manifest themselves. In an excellent learning environment, in contrast, innate differences are able to manifest themselves much more clearly. Again, there seems nothing terribly surprising about this. But the implications for education seem fairly plain: only when opportunities to learn are equal will one see clearly the extent of inherent genetic variation. This is of course very different from saying that when everyone has the same opportunities, everyone will do more or less equally well.
What this means is that, if a child with low SES is doing poorly at school, it would be wrong to say “well, obviously it is because of the disadvantages he faces through being poor.” It is possible that he has inherited limited cognitive resources that would hold him back even if he came from a wealthy background. That sounds harsh, and one might wish it wasn’t so – but it needs to be acknowledged, and it seems (though it’s hard to tell) that one of Dominic Cummings’ aims was to do so. But there are two crucial points to make here:
(1) If a child is doing poorly academically, it seems more likely to be due to inherent cognitive limitations if he has high SES than low SES, because in the former case genetic propensities are less masked by other factors.
(2) While the aforementioned statement might be true for individuals, it seems extremely unlikely as a generalized statement: one would expect inherited variations in cognition for low-SES children to be no different to those from high-SES children, so that any difference in academic achievement seen on average between these two groups would result from social and not genetic factors.
But wait – is that necessarily true? Might it not be that there is a correlation between low SES and genetically determined lower cognitive ability? To put it bluntly, might the poor be inherently dim – indeed, might not the causation actually work that way, i.e. they are poor because they are dim, not that they underachieve because they are poor?
Cummings seems to be raising this possibility. I say this warily because he seems to feel that he is constantly being misunderstood, but I can’t see how otherwise to interpret this passage in his paper (p.74):
“Raising school performance of poorer children is an inherently worthwhile thing to try to do but it would not necessarily lower parent-offspring correlations (nor change heritability estimates). When people look at the gaps between rich and poor children that already exist at a young age (3-5), they almost universally assume that these differences are because of environmental reasons (‘privileges of wealth’) and ignore genetics.”
If genetics is the reason for these gaps, he seems to be saying, then pouring money and resources into education for low-SES groups won’t help all that much, or at least won’t eliminate the gap. He certainly doesn’t say that we should not spend in that direction. Indeed, he suggests that one could argue we should put in more resources to the education of children from poorer backgrounds, precisely because they are more needed – but that we’d need to be realistic about the expected outcomes.
OK, so there are two ways to look at this. One is to say that surely hypothesizing that the correlation between low attainment and low SES is due to genetics shouldn’t be ruled out simply because it is “politically incorrect.” I’d agree with that. But it frustrates me endlessly that there are many scientists who would be content to stop there, i.e. with the notion that there are no questions in science that should not be asked. Science doesn’t work that way. Scientists don’t sit around dreaming up any hypothesis and then testing them. “I wonder if there might really be a race of aliens like the Clangers?” “I wonder if African nations really do have a genetic predisposition to bad government?” (Hello Nicholas Wade.) Hypotheses need to be motivated by observation, but they should also acknowledge what seems plausible on the basis of what we already know – yes, there are problems of governance in parts of Africa, but it is very hard to see how a genetic basis for that might arise, so why would you want to start from that possibility?
This was why I was so dismayed by the response of some scientists to the outcry about James Watson’s suggestions of a link between race and intelligence. If he had been proposing to set up a research programme to explore whether there were correlations between intelligence and some kind of genetic correlates of what we socially recognize as race (if such exist), then one could understand (just about) why criticisms of his comments and cancellations of his talks might seem like a kind of “politically correct” censorship, as some of Watson’s supporters asserted. But not only were Watson’s remarks apparently unmotivated by any well established scientific observations or theories, they were not advanced as a scientific hypothesis at all – they were supported by idle, bigoted anecdote.
Much the same applies here: given the apparent lack (to my knowledge) of any suggestion in the literature that the reasons that social class predicts educational achievement are genetic, it seems a strange (one might even argue dangerous) hypothesis to present a priori. Unless one has an underlying agenda, I’m puzzled by why one would suggest such a thing.
In any event, my real point was that, give the current state of play about links between genetics and measures of “intelligence” (for example, see this recent review), it isn’t clear why the matter should be terribly relevant to education policy at all. Cummings makes a big deal of Robert Plomin’s work – which, I hasten to point out, is totally respectable and worthwhile. Plomin’s hope is that, if one could identify genes linked to cognitive and academic abilities, it might be possible to personalize education to the individual’s inherent intellectual endowments. This is a reasonable and indeed praiseworthy goal. But what we have discovered so far on the matter seems to indicate that such ambitions are not only far from being realised but potentially misplaced in the first place – because there may not be a small set of genes that will predict those endowments. And that might be because we are thinking the wrong way – too linearly – about how many if not most genes actually operate. Personally, I find a little chilling the idea that we might try to predict children’s attainments by reading their genome, and gear their education accordingly – not least because we know (and Plomin would of course acknowledge this) that genes operate in conjunction with their environment, and so whatever genetic hand you have been dealt, its outcomes are contingent on experience. Given the current lack of a strong link between specific gene variants and IQ (and not for want of looking), right now it seems unlikely that we would learn anything more from genomics than smart teachers already discern from noting the strengths and limitations of each child. What’s more, evidence from neuroscience that early experiences affect the wiring of the brain make it seem far more profitable to place emphasis on a child’s learning environment (including that within the family), and not to worry about what your genes “say” about your future abilities.
It’s of course important to recognize that this situation might change in the future, but there seems little reason right now to anticipate that it will. This is why I feel that raising the matter of genetics in educational policy right now seems like a red herring – and worse, that it encourages this misleading and potentially damaging notion of “genes for”. Genetics should certainly not be a taboo subject in discussions about education, but I’ve yet to see a convincing argument for why it has anything to tell us about how to help children learn.
Thursday, November 13, 2014
Genes and IQ - as touchy as I'd expected
Well, it’s clear that Dominic Cummings is not one to use one tweet when six will do. But his gist is clear: he does not like my article on genes in Prospect.
It is very clear that the issue of heritability of IQ and educational achievement, and environmental effects on these, is extremely contentious, and it’s not too hard to cherry-pick the data to support whatever conclusion you like. That said, the idea that “Social class remains the strongest predictor of educational achievement in the UK”, as this paper by a professor of education points out, seems fairly well established. I accept that I might have missed some acknowledgement of this in Cummings’ book-length document to Gove, but if so, I’ll need to have it pointed out to me. I find it very hard to see how anyone reading Cummings’ paper would have come away with that impression – rather, he argues rather strongly that genes, not socioeconomic status, are the central determinant.
But his claims are stronger than that. I have been rereading this particular passage to see if somehow I have got the wrong end of the stick:
“Raising school performance of poorer children is an inherently worthwhile thing to try to do but it would not necessarily lower parent-offspring correlations (nor change heritability estimates). When people look at the gaps between rich and poor children that already exist at a young age (3-5), they almost universally assume that these differences are because of environmental reasons (‘privileges of wealth’) and ignore genetics.”
So what is Cummings implying here, if not that the differences in school performance between rich and poor children might be, at least in large part, genetic? That the poor are, in other words, a genetic underclass as far as academic achievement is concerned – that they are poor presumably because they are not very bright? I am trying very hard to square this idea with the statement by Turkheimer and colleagues (2003 – paper here) that “in impoverished families, 60% of the variance in IQ is accounted for by the shared environment, and the contribution of genes is close to zero; in affluent families, the result is almost exactly the reverse.” (Yes, Cummings alludes briefly to Turkheimer’s work, but only by linking to a blog that mentions it and only in order to dismiss it as largely irrelevant to the debate.) Cummings does not say that we should give up on the poor simply because they are genetically disadvantaged in the IQ stakes – but comments like the one above surely give a message that neither better education nor less social disadvantage will make an awful lot of difference to academic outcomes.
Cummings advocates the potential value of “finding the genes responsible for cognitive abilities”. The entire point of my article is to challenge the assumption that there are “genes for” cognitive abilities. I point out that a large group of the world’s top researchers on genetics and cognition has just conducted a big study to identify such “genes”, and finds that most of the previous candidates are illusory. They find three genes linked to variations in IQ, and these account for differences of at most just 1.8 IQ points and are in the authors’ words “not useful for predicting any particular individual’s performance because the effect sizes are far too small”. Of course, it may be that the key “genes for” just haven’t yet been found. Or it may be - and Cummings has evidently failed to grasp this central point – that because a trait is somewhat inheritable does not imply that there are “genes for” this trait in any meaningful sense. That is why I find his comments misleading.
A little bit of reading comprehension here. Cummings complains about my remark that “So it’s not clear, pace Cummings, what this kind of study [i.e. the one mentioned in the paragraph above] adds to the conventional view that some kids are more academically able than others. It’s not clear why it should alter the goal of helping all children achieve what they can, to the best of their ability.” He says “I did not make the argument he implies – i.e. we should ‘alter the goal of helping all children’…”. Does “it should alter” refer to (A) the aforementioned academic study; (B) Dominic Cummings’ paper; (C) Michael Gove’s MP expenses claim? The point here is not that Cummings doesn’t want all children to achieve what they can – I genuinely believe he does want that – but that it is not at all clear from current findings on genes and IQ that that research has much to offer the formulation of educational policy.
I’m less concerned about Cummings’ accusations of “unprofessional journalism, riddled with errors”, since he doesn’t really explain what these errors are. His advice to Prospect – “do not publish journalism on this subject without having it checked by a genuine expert” – is a bit of a hostage to fortune, given that my article was read by Steve Jones and a colleague of Robert Plomin’s, who found none of these “errors”. If you do want the opinion of another real expert, rather than mine (and who could blame you?), you might want to look at what Steven Rose has to say on the topic, and then decide if there is any daylight between that and this.
It is very clear that the issue of heritability of IQ and educational achievement, and environmental effects on these, is extremely contentious, and it’s not too hard to cherry-pick the data to support whatever conclusion you like. That said, the idea that “Social class remains the strongest predictor of educational achievement in the UK”, as this paper by a professor of education points out, seems fairly well established. I accept that I might have missed some acknowledgement of this in Cummings’ book-length document to Gove, but if so, I’ll need to have it pointed out to me. I find it very hard to see how anyone reading Cummings’ paper would have come away with that impression – rather, he argues rather strongly that genes, not socioeconomic status, are the central determinant.
But his claims are stronger than that. I have been rereading this particular passage to see if somehow I have got the wrong end of the stick:
“Raising school performance of poorer children is an inherently worthwhile thing to try to do but it would not necessarily lower parent-offspring correlations (nor change heritability estimates). When people look at the gaps between rich and poor children that already exist at a young age (3-5), they almost universally assume that these differences are because of environmental reasons (‘privileges of wealth’) and ignore genetics.”
So what is Cummings implying here, if not that the differences in school performance between rich and poor children might be, at least in large part, genetic? That the poor are, in other words, a genetic underclass as far as academic achievement is concerned – that they are poor presumably because they are not very bright? I am trying very hard to square this idea with the statement by Turkheimer and colleagues (2003 – paper here) that “in impoverished families, 60% of the variance in IQ is accounted for by the shared environment, and the contribution of genes is close to zero; in affluent families, the result is almost exactly the reverse.” (Yes, Cummings alludes briefly to Turkheimer’s work, but only by linking to a blog that mentions it and only in order to dismiss it as largely irrelevant to the debate.) Cummings does not say that we should give up on the poor simply because they are genetically disadvantaged in the IQ stakes – but comments like the one above surely give a message that neither better education nor less social disadvantage will make an awful lot of difference to academic outcomes.
Cummings advocates the potential value of “finding the genes responsible for cognitive abilities”. The entire point of my article is to challenge the assumption that there are “genes for” cognitive abilities. I point out that a large group of the world’s top researchers on genetics and cognition has just conducted a big study to identify such “genes”, and finds that most of the previous candidates are illusory. They find three genes linked to variations in IQ, and these account for differences of at most just 1.8 IQ points and are in the authors’ words “not useful for predicting any particular individual’s performance because the effect sizes are far too small”. Of course, it may be that the key “genes for” just haven’t yet been found. Or it may be - and Cummings has evidently failed to grasp this central point – that because a trait is somewhat inheritable does not imply that there are “genes for” this trait in any meaningful sense. That is why I find his comments misleading.
A little bit of reading comprehension here. Cummings complains about my remark that “So it’s not clear, pace Cummings, what this kind of study [i.e. the one mentioned in the paragraph above] adds to the conventional view that some kids are more academically able than others. It’s not clear why it should alter the goal of helping all children achieve what they can, to the best of their ability.” He says “I did not make the argument he implies – i.e. we should ‘alter the goal of helping all children’…”. Does “it should alter” refer to (A) the aforementioned academic study; (B) Dominic Cummings’ paper; (C) Michael Gove’s MP expenses claim? The point here is not that Cummings doesn’t want all children to achieve what they can – I genuinely believe he does want that – but that it is not at all clear from current findings on genes and IQ that that research has much to offer the formulation of educational policy.
I’m less concerned about Cummings’ accusations of “unprofessional journalism, riddled with errors”, since he doesn’t really explain what these errors are. His advice to Prospect – “do not publish journalism on this subject without having it checked by a genuine expert” – is a bit of a hostage to fortune, given that my article was read by Steve Jones and a colleague of Robert Plomin’s, who found none of these “errors”. If you do want the opinion of another real expert, rather than mine (and who could blame you?), you might want to look at what Steven Rose has to say on the topic, and then decide if there is any daylight between that and this.
The gene delusion
This is an extended version of my piece in the December issue of Prospect.
__________________________________________________________________________
Metaphors in science are notoriously slippery, but biologists seem particularly poorly attuned to the implications of theirs. The tenacity of the misleading “genes for” picture is one of their legacies.
You might think it’s sheer bad luck to be struck by lightning. But some of us are cursed with a struck-by-lightning (SBL) gene. Sure, as with many genetic conditions, if you have the SBL gene it doesn’t mean you will be struck by lightning, just that your chances are higher (here by a factor of about three or four) than those without it. But that seems a fairly big risk factor to me – and I should know, because I’ve got the gene.
Yet no one is working on a genetic remedy. Scandalous? Not really, because SBL can be identified as the gene better known as SRY, the sex-determining gene on the Y chromosome, which makes an embryo develop into a male. Yes, men get hit by lightning more often, because their behaviour – rushing about on golf courses and football pitches in the rain, that sort of thing – makes it more likely. Call it stereotyping all you like: the statistics don’t lie.
Geneticist Steve Jones has used this example to point to the absurdity of the concept of a “gene for”. If we knew nothing else about what SRY does, and it fell out of a statistical search for genetic associations with being hit by lightning, we might indeed conclude that warrants the label SBL. But the association with lightning strikes is merely a side-product of the way the gene’s effects play out in a particular environment. SRY could equally be misattributed as a gene for criminality, murder, baldness, watching Top Gear.
“The most dangerous word in genetics is ‘for’”, Jones has said. “Only fifteen years ago people expected that they would find genes for cancer, heart disease or diabetes. But medicine’s big secret is that we haven’t found them. And we haven’t found them because they are not there.” Compare that with Bill Clinton promising, next to smiling scientists in 2000, that the decoding of the human genome means “doctors increasingly will be able to cure diseases like Alzheimer's, Parkinson's, diabetes and cancer by attacking their genetic roots.”
What does this mean for the much vaunted age of “personalized medicine” – of health care tailored to our individual genome, which can now be decoded for a few thousand dollars and might soon be as common a feature as blood group and cholesterol index on everyone’s health records? The answer is complicated. Genetic data do reveal a lot about our inherent predispositions to certain medical conditions. But that doesn’t necessarily mean we have the “genes for” those conditions in any meaningful sense – genes that can be considered to lie at the “roots”.
The tendency to assign genes the responsibility for well defined personal attributes doesn’t just muddy the waters of post-genomic medicine. It distorts the whole public discourse around genetics, and arguably around the way genomes are shaped by natural selection. And it takes us down some dark avenues, from the notorious history of eugenics to the recurring minefield of how genes are influenced by race. The furore over the views expressed by former New York Times science reporter Nicholas Wade in his book A Troublesome Inheritance: Genes, Race and Human History is just the latest skirmish in this ongoing saga. Wade suggests that differences in social behaviour and characteristics among human societies may be genetically encoded. It’s an old argument, although expressed less crudely than in the anthropology of yore: the intellectual and economic hegemony of Western culture is down to innate biological differences. Scientists have lined up to savage Wade’s book, but the contentious questions it asks – are differences in, say, intelligence, rationality and social cohesion down to our genes? – won’t go away. Nor should they – but we’re not going to make much headway with them until we get to grips with the distinctions between what genes do and what genes are “for”.
Born that way
Geneticists now gnash their teeth at the bad journalism that proclaims the discovery of a “gene for”. But the burden of guilt for this trope lies with the research community itself. It’s not hard to find both implicit and explicit references to “genes for” in the literature or pronouncements of biologists. They are not always as ill-judged as DNA pioneer James Watson’s suggestion that genetic testing for “gay genes” could offer a woman the opportunity to abort a child that carried them. But the implication that traits such as personality and susceptibility to disease are necessarily determined by one or a few genes permeates the field. Without that sort of functional autonomy, for example, it is hard to see how the notion of selfish genes can be coherent. References to blueprints, lists of parts and instruction manuals during the Human Genome Project carried the same baggage.
It’s understandable how this habit began. As the modern era of genetics dawned and it became possible to probe the effects of particular genes by mutating, adding or silencing them (the latter being called “knockout” experiments) in flies, mice and other laboratory animals, researchers began to find clear links between the presence or absence of a gene variant – for brevity I’ll follow the sloppy convention and just say “gene” – in an organism’s genome and certain traits of the whole organism. Surely it stands to reason that, if you see a particular trait in the presence of a gene but not in its absence, that gene is in some sense a gene “for” the trait?
Well, yes and no. So-called coding genes contain the instructions for making particular proteins: enzymes that comprise the biomolecular machinery, and protein fabrics of the body. That’s the only thing they are really “for”. Spiders have a “gene for silk”; humans have a “gene for digesting the milk sugar lactose”. Mutations of these genes can be responsible for inheritable conditions.
But the lack or malfunction of a particular enzyme due to a genetic mutation can have complex knock-on effects in the body. What’s more, most genes are non-coding: they don’t encode proteins, but instead regulate the activity of other genes, creating complex networks of gene interactions. Most human traits arise out of this network, which blurs the picture a “genes for” picture. As the spurious “SBL gene” shows, it’s then wrong to infer causation from correlation. That’s not just a difficulty of finding the right genes within the network. For some traits, even if they are genetically encoded it can be inappropriate to talk of causative mechanisms and explanations at the genetic level.
Indeed, gene knockout studies tended to undermine the “gene for” picture more than they confirmed it. Time and again geneticists would find that, if they knocked out a gene apparently “for” a feature indispensible to an organism’s vitality, the organism hardly seemed to bat an eyelid. We now know that this is at least partly because of the immense complexity of gene networks, which have redundancy built in. If there’s a failure in one part of the network then, just as with closing a station on the London Underground, there may be an alternative route to the same goal.
Nothing here would surprise engineers. They know that such redundancy and failsafe mechanisms are an essential part of the robustness of any complex system, whether it is a chemicals plant or a computer. There is nothing that need have surprised geneticists either, who have known since the 1960s that genes work in self-regulating networks. All the same, I sat through countless editorial meetings at Nature in the early 1990s in which a newly accepted paper would be described breathlessly as showing that a gene thought to do this had now been shown to do that too. The language remained resolutely that of “genes for”: such genes were just multi-tasking.
One of the most notorious episodes of “genes for” from that period was a 1993 study by a team of geneticists at the US National Cancer Institute, who published in the premier journal Science the claim that with “99.5% certainty there is a gene (or genes) in [a particular] area of the X chromosome that predisposes a male to become a heterosexual” – in other words, in effect a “gay gene”.
Anyone interested in genes was already primed to accept that idea. Geneticists had been talking about a genetic basis for homosexuality since the 1970s, and in his 1982 book The Extended Phenotype Richard Dawkins used the possibility (“for the sake of argument”) to explore the notion of how a gene might exert different effects in different environments. For Dawkins, this environmental influence shows only that we must recognize a contingency about what a gene is “for”, not that the whole idea of it being “for” a particular trait or behaviour may be meaningless.
This complexity in the emerging view of what genes do is tellingly, and perhaps inadvertently, captured in Matt Ridley’s book Genome, published in 1999 as the completion of the Human Genome Project was about to be announced. Ridley offered little portraits of inheritable traits associated with each of the 23 human chromosomes. He began with a confident description of how the gene associated with Huntington’s chorea was tracked down. Here, surely, is a “gene for” – if you are unlucky enough to have the particular mutation, you’ll develop the disease.
But then Ridley gets to asthma, intelligence, homosexuality and “novelty-seeking”. All do seem to have an inherited component. “In the late 1980s, off went various groups of scientists in confident pursuit of the ‘asthma gene’”, Ridley writes. By 1998 they had found not one, but fifteen. Today some researchers admit that hundreds might be involved. In the other cases, Ridley admitted, the jury is still out. But it’s not any more: today, all the candidate “genes for” he mentioned in relation to intelligence, homosexuality and novelty-seeking have been ruled out. Isn’t this odd? There was Ridley, an (unusually well informed) science writer, declaring the futility of quests for specific genes “for” complex personality traits, yet finding himself compelled to report on geneticists’ efforts find them. So who was to blame?
Intelligence tests
On genes for intelligence, Ridley mentioned the work of Robert Plomin, who in 1998 reported an association between IQ and a gene called IGF2R. The fact that the gene was known to encode a protein responsible for a very routine and mundane cell function might have been a clue that the connection was at best indirect. That the gene had previously been associated with liver cancer might have been another. Still, Ridley said, we’ll have to see. In 2002 we saw: Plomin and others reported (to scant press attention) that they had not been able to replicate the association of IGF2R with IQ. “It doesn’t look like that has panned out,” he said in 2008.
“Anybody who gets evidence of a link between a disease and a gene has a duty to report it”, Ridley wrote. “If it proves an illusion, little harm is done.” Isn’t that just the way science works, after all? Surely – but whether innocent errors and false trails cause harm depends very much on how they are reported. Studies like Plomin’s are well motivated and valuable, and he has deplored the “genes for” picture himself. But there’s little hope that this research will avoid such associations unless biologists can do a better job of correcting the deeply misleading narrative that exists about what genes do, which has flourished amidst their often complacent attitude towards explaining it.
If you want to see the hazards of illusory gene associations, take the recent claim by Michael Gove’s education adviser Dominic Cummings that findings on the inherited, innate aspect of intelligence (in particular the work of Plomin) are being ignored. For a start, the very mention of genetics seemed to send rational argument out of the window. Some on the left sucked their teeth and muttered darkly about eugenics, or declared the idea “incendiary” and outrageous without bothering to explain why. That’s why Jill Boucher, writing in Prospect, had a point when she excoriated the “politically correct” attacks on Cummings’ comments. But unless Boucher can point to an educationalist or teacher who denies that children differ in their innate abilities, or who regards them all as potential Nobel laureates, she is erecting something of a straw man.
A real problem with Cummings’ comments was not that they attribute some of our characteristics to our genes but that they gave the impression of genetics as a fait accompli – if you don’t have the right genes, nothing much will help. This goes against the now accepted consensus that genes exert their effects in interaction with their environment. And the precise extent of inheritability is unclear. While IQ is often quoted as being about 50% inheritable, there is some evidence that the association with genetics is much weaker in children from poor backgrounds: that good genes won’t help you much if the circumstances are against it. (This finding is seemingly robust in the US, but not in Europe, where social inequalities might not be pronounced enough to produce the effect.)
Nonetheless, there’s nothing wrong in principle with Cummings’ suggestion that research to identify “high IQ” genes should be encouraged. But if he were to look a little more deeply into what it has already discovered (and sometimes un-discovered again), he might wonder what it offers education policy. A 2012 study pointed out that most previous claims of an association between intelligence and specific genes don’t stand up to scrutiny. Nor is there much encouragement from ones that do. In September an international consortium led by Daniel Benjamin of Cornell University in New York reported on a search for genes linked to cognitive ability using a new statistical method that overcomes the weaknesses of traditional surveys. The method cross-checks such putative associations against a “proxy phenotype” – a trait that can ‘stand in’ for the one being probed. In this case the proxy for cognitive performance was the number of years that the tens of thousands of test subjects spent in education.
From several intelligence-linked genes claimed in previous work, only three survived this scrutiny. More to the point, those three were able to account for only a tiny fraction of the inheritable differences in IQ. Someone blessed with two copies of all three of the “favourable” gene variants could expect a boost of just 1.8 IQ points relative to someone with none of these variants. As the authors themselves admitted, the three gene variants are “not useful for predicting any particular individual’s performance because the effect sizes are far too small”.
Perhaps, then, the media would be best advised not to call these “IQ genes”. But you could forgive them for doing so, for they’d only have been echoing one of the paper’s authors, the influential cognitive scientist Steven Pinker of Harvard University. The proper response to a study showing that most existing candidates for gene-intelligence associations were wrong, and that the few that weren’t contribute almost negligibly to inheritability, surely isn’t “Here they are at last”, but “Jesus, is this all there is?”
Where, then, is the remainder of the inherited component? It must presumably reside among a host of genes whose effects are too subtle to be detected by current methods. Those genes will surely be involved in other physiological functions, their effects in intelligence being highly indirect. They are in no meaningful sense “genes for intelligence”, any more than SRY is a gene for being struck by lightning.
So it’s not clear, pace Cummings, what this kind of study adds to the conventional view that some kids are more academically able than others. It’s not clear why it should alter the goal of helping all children achieve what they can, to the best of their ability. Such findings offer very dim prospects for Plomin’s hope, laudable in principle, that education might be tailored to the strengths and weaknesses of individual pupils’ genetic endowment.
Race matters
So, then, to Wade’s claims that genetics causes racial differences in traits such as the propensity for violence or the organization of social institutions. As Wade’s book has shown, the issue of race and genes remains as tendentious as ever. On the one hand, of the total genetic variation between random individuals, around 90% is already present in populations on a single continent – Asia, say – and only 10% more would accrue from pooling Europeans, Africans and Asians together. Some biologists argue that this makes the notion of race biologically meaningless. Yet ancestry does leave an imprint in our genomes: for example, lactose intolerance is more common in Africa and Asia, sickle-cell anemia in people of African origin, and cystic fibrosis in white northern Europeans. That’s why the concept of race is useful as a proxy for medical risk assessment and diagnosis. Besides, arguments about statistical clusters of gene variation don’t alter the fact that culturally conventional indicators of race – pigmentation and eye shape, say – are genetically determined.
What you choose to emphasize and ignore in this matter is largely a question of ideology, not science. But arguments like those Wade puts forward draw their strength from the simplistic notions of how genes relate to phenotype. We know that what we can, in this case, reasonably call cystic-fibrosis or sickle-cell genes (because the conditions derive from a single gene mutation) differ in incidence among racial groups. We also know that genetic variation, while gradual, is not geographically uniform. Might it not be that those variations could encompass genes for intelligence, say?
Yet if the genetic constitution of such traits is really so dispersed, this is a little like grabbing a hundred Scrabble tiles from some huge pile and expecting them to spell out this sentence. Ah, but such random grabs are then filtered into meaningful configurations by natural selection, Wade argues: genes producing a predisposition to capitalism or tribalism might be more useful in some populations than others. Setting aside the improbability of those particular genes existing in the first place, this idea relies on the assumption that every inheritable trait can be selected for, because it stems from genes “for” that trait. That’s precisely the fallacy that once supported eugenic arguments for the betterment of the human race: that we can breed out genes for criminality, stupidity, mendacity.
While it has been reassuring to watch Wade’s thesis be comprehensively dismantled (here and here and here, say) by scientists and other knowledgeable commentators, it’s hard not to contrast their response with that to James Watson’s claim in 2007 that the idea that all races share “equal powers of reason” is a delusion. Despite the fact that Watson adduced as “evidence” only the alleged experience of “people who have to deal with black employees”, he was defended as the victim of a witch-hunt by an “illiberal and intolerant thought police”. Even though it is hard to disentangle genuine prejudice from habitual liberal-baiting in Watson’s remarks, all we are really seeing here is one natural endpoint of the “genes for” and “instruction book” mentality underpinning the Human Genome Project that Watson helped establish and initially led.
The dark genome
The dispersed, “polygenic” nature of inheritable intelligence is likely to be the norm in genetics, at least for many traits we care about. Much the same applies to many inheritable medical conditions, such as schizophrenia and multiple sclerosis: like asthma, they seem to arise from the action of many, perhaps even hundreds, of genes, and there’s not one gene, or even a small number, that can be identified as the main culprits. This “missing heritability”, sometimes called the “dark matter” of the genome, is one of the biggest challenges to the promised personalized medicine of the post-genome era. But it should also be seen as challenging our understanding of genetics per se. Jones, who has been energetic about puncturing the worse misunderstandings of the “genes for” picture, admits that he wouldn’t now attempt to explain how genetics really works, in a manner akin to his brilliant The Language of the Genes (1994), because the field has got so damned complicated.
Yet the linguistic analogy – with genes as words and genomes as books – might remain a serviceable one, if only it were taken more seriously. Combing the genome for genes for many (not all) complex traits seems a little like analyzing Hamlet to look for the words in which Hamlet’s indecision resides. Sure, there’s a lot riding on the cluster “To be or not to be”, but excise it and his wavering persists. Meanwhile, “to” does a lot of other work in the play, and is in no meaningful sense an “indecisive Hamlet” word.
The irony is that a study like the latest “IQ genes” report, while showing yet again the inadequacy of the “gene for” picture, is likely to perpetuate it. As Jones has pointed out, such work has the unfortunate side-effect of feeding our fascination with the putative genetic basis of social problems such as discrimination or differences in educational achievement, about which we can do rather little, while distracting us from the often more significant socioeconomic causes, about which we could do a great deal.
__________________________________________________________________________
Metaphors in science are notoriously slippery, but biologists seem particularly poorly attuned to the implications of theirs. The tenacity of the misleading “genes for” picture is one of their legacies.
You might think it’s sheer bad luck to be struck by lightning. But some of us are cursed with a struck-by-lightning (SBL) gene. Sure, as with many genetic conditions, if you have the SBL gene it doesn’t mean you will be struck by lightning, just that your chances are higher (here by a factor of about three or four) than those without it. But that seems a fairly big risk factor to me – and I should know, because I’ve got the gene.
Yet no one is working on a genetic remedy. Scandalous? Not really, because SBL can be identified as the gene better known as SRY, the sex-determining gene on the Y chromosome, which makes an embryo develop into a male. Yes, men get hit by lightning more often, because their behaviour – rushing about on golf courses and football pitches in the rain, that sort of thing – makes it more likely. Call it stereotyping all you like: the statistics don’t lie.
Geneticist Steve Jones has used this example to point to the absurdity of the concept of a “gene for”. If we knew nothing else about what SRY does, and it fell out of a statistical search for genetic associations with being hit by lightning, we might indeed conclude that warrants the label SBL. But the association with lightning strikes is merely a side-product of the way the gene’s effects play out in a particular environment. SRY could equally be misattributed as a gene for criminality, murder, baldness, watching Top Gear.
“The most dangerous word in genetics is ‘for’”, Jones has said. “Only fifteen years ago people expected that they would find genes for cancer, heart disease or diabetes. But medicine’s big secret is that we haven’t found them. And we haven’t found them because they are not there.” Compare that with Bill Clinton promising, next to smiling scientists in 2000, that the decoding of the human genome means “doctors increasingly will be able to cure diseases like Alzheimer's, Parkinson's, diabetes and cancer by attacking their genetic roots.”
What does this mean for the much vaunted age of “personalized medicine” – of health care tailored to our individual genome, which can now be decoded for a few thousand dollars and might soon be as common a feature as blood group and cholesterol index on everyone’s health records? The answer is complicated. Genetic data do reveal a lot about our inherent predispositions to certain medical conditions. But that doesn’t necessarily mean we have the “genes for” those conditions in any meaningful sense – genes that can be considered to lie at the “roots”.
The tendency to assign genes the responsibility for well defined personal attributes doesn’t just muddy the waters of post-genomic medicine. It distorts the whole public discourse around genetics, and arguably around the way genomes are shaped by natural selection. And it takes us down some dark avenues, from the notorious history of eugenics to the recurring minefield of how genes are influenced by race. The furore over the views expressed by former New York Times science reporter Nicholas Wade in his book A Troublesome Inheritance: Genes, Race and Human History is just the latest skirmish in this ongoing saga. Wade suggests that differences in social behaviour and characteristics among human societies may be genetically encoded. It’s an old argument, although expressed less crudely than in the anthropology of yore: the intellectual and economic hegemony of Western culture is down to innate biological differences. Scientists have lined up to savage Wade’s book, but the contentious questions it asks – are differences in, say, intelligence, rationality and social cohesion down to our genes? – won’t go away. Nor should they – but we’re not going to make much headway with them until we get to grips with the distinctions between what genes do and what genes are “for”.
Born that way
Geneticists now gnash their teeth at the bad journalism that proclaims the discovery of a “gene for”. But the burden of guilt for this trope lies with the research community itself. It’s not hard to find both implicit and explicit references to “genes for” in the literature or pronouncements of biologists. They are not always as ill-judged as DNA pioneer James Watson’s suggestion that genetic testing for “gay genes” could offer a woman the opportunity to abort a child that carried them. But the implication that traits such as personality and susceptibility to disease are necessarily determined by one or a few genes permeates the field. Without that sort of functional autonomy, for example, it is hard to see how the notion of selfish genes can be coherent. References to blueprints, lists of parts and instruction manuals during the Human Genome Project carried the same baggage.
It’s understandable how this habit began. As the modern era of genetics dawned and it became possible to probe the effects of particular genes by mutating, adding or silencing them (the latter being called “knockout” experiments) in flies, mice and other laboratory animals, researchers began to find clear links between the presence or absence of a gene variant – for brevity I’ll follow the sloppy convention and just say “gene” – in an organism’s genome and certain traits of the whole organism. Surely it stands to reason that, if you see a particular trait in the presence of a gene but not in its absence, that gene is in some sense a gene “for” the trait?
Well, yes and no. So-called coding genes contain the instructions for making particular proteins: enzymes that comprise the biomolecular machinery, and protein fabrics of the body. That’s the only thing they are really “for”. Spiders have a “gene for silk”; humans have a “gene for digesting the milk sugar lactose”. Mutations of these genes can be responsible for inheritable conditions.
But the lack or malfunction of a particular enzyme due to a genetic mutation can have complex knock-on effects in the body. What’s more, most genes are non-coding: they don’t encode proteins, but instead regulate the activity of other genes, creating complex networks of gene interactions. Most human traits arise out of this network, which blurs the picture a “genes for” picture. As the spurious “SBL gene” shows, it’s then wrong to infer causation from correlation. That’s not just a difficulty of finding the right genes within the network. For some traits, even if they are genetically encoded it can be inappropriate to talk of causative mechanisms and explanations at the genetic level.
Indeed, gene knockout studies tended to undermine the “gene for” picture more than they confirmed it. Time and again geneticists would find that, if they knocked out a gene apparently “for” a feature indispensible to an organism’s vitality, the organism hardly seemed to bat an eyelid. We now know that this is at least partly because of the immense complexity of gene networks, which have redundancy built in. If there’s a failure in one part of the network then, just as with closing a station on the London Underground, there may be an alternative route to the same goal.
Nothing here would surprise engineers. They know that such redundancy and failsafe mechanisms are an essential part of the robustness of any complex system, whether it is a chemicals plant or a computer. There is nothing that need have surprised geneticists either, who have known since the 1960s that genes work in self-regulating networks. All the same, I sat through countless editorial meetings at Nature in the early 1990s in which a newly accepted paper would be described breathlessly as showing that a gene thought to do this had now been shown to do that too. The language remained resolutely that of “genes for”: such genes were just multi-tasking.
One of the most notorious episodes of “genes for” from that period was a 1993 study by a team of geneticists at the US National Cancer Institute, who published in the premier journal Science the claim that with “99.5% certainty there is a gene (or genes) in [a particular] area of the X chromosome that predisposes a male to become a heterosexual” – in other words, in effect a “gay gene”.
Anyone interested in genes was already primed to accept that idea. Geneticists had been talking about a genetic basis for homosexuality since the 1970s, and in his 1982 book The Extended Phenotype Richard Dawkins used the possibility (“for the sake of argument”) to explore the notion of how a gene might exert different effects in different environments. For Dawkins, this environmental influence shows only that we must recognize a contingency about what a gene is “for”, not that the whole idea of it being “for” a particular trait or behaviour may be meaningless.
This complexity in the emerging view of what genes do is tellingly, and perhaps inadvertently, captured in Matt Ridley’s book Genome, published in 1999 as the completion of the Human Genome Project was about to be announced. Ridley offered little portraits of inheritable traits associated with each of the 23 human chromosomes. He began with a confident description of how the gene associated with Huntington’s chorea was tracked down. Here, surely, is a “gene for” – if you are unlucky enough to have the particular mutation, you’ll develop the disease.
But then Ridley gets to asthma, intelligence, homosexuality and “novelty-seeking”. All do seem to have an inherited component. “In the late 1980s, off went various groups of scientists in confident pursuit of the ‘asthma gene’”, Ridley writes. By 1998 they had found not one, but fifteen. Today some researchers admit that hundreds might be involved. In the other cases, Ridley admitted, the jury is still out. But it’s not any more: today, all the candidate “genes for” he mentioned in relation to intelligence, homosexuality and novelty-seeking have been ruled out. Isn’t this odd? There was Ridley, an (unusually well informed) science writer, declaring the futility of quests for specific genes “for” complex personality traits, yet finding himself compelled to report on geneticists’ efforts find them. So who was to blame?
Intelligence tests
On genes for intelligence, Ridley mentioned the work of Robert Plomin, who in 1998 reported an association between IQ and a gene called IGF2R. The fact that the gene was known to encode a protein responsible for a very routine and mundane cell function might have been a clue that the connection was at best indirect. That the gene had previously been associated with liver cancer might have been another. Still, Ridley said, we’ll have to see. In 2002 we saw: Plomin and others reported (to scant press attention) that they had not been able to replicate the association of IGF2R with IQ. “It doesn’t look like that has panned out,” he said in 2008.
“Anybody who gets evidence of a link between a disease and a gene has a duty to report it”, Ridley wrote. “If it proves an illusion, little harm is done.” Isn’t that just the way science works, after all? Surely – but whether innocent errors and false trails cause harm depends very much on how they are reported. Studies like Plomin’s are well motivated and valuable, and he has deplored the “genes for” picture himself. But there’s little hope that this research will avoid such associations unless biologists can do a better job of correcting the deeply misleading narrative that exists about what genes do, which has flourished amidst their often complacent attitude towards explaining it.
If you want to see the hazards of illusory gene associations, take the recent claim by Michael Gove’s education adviser Dominic Cummings that findings on the inherited, innate aspect of intelligence (in particular the work of Plomin) are being ignored. For a start, the very mention of genetics seemed to send rational argument out of the window. Some on the left sucked their teeth and muttered darkly about eugenics, or declared the idea “incendiary” and outrageous without bothering to explain why. That’s why Jill Boucher, writing in Prospect, had a point when she excoriated the “politically correct” attacks on Cummings’ comments. But unless Boucher can point to an educationalist or teacher who denies that children differ in their innate abilities, or who regards them all as potential Nobel laureates, she is erecting something of a straw man.
A real problem with Cummings’ comments was not that they attribute some of our characteristics to our genes but that they gave the impression of genetics as a fait accompli – if you don’t have the right genes, nothing much will help. This goes against the now accepted consensus that genes exert their effects in interaction with their environment. And the precise extent of inheritability is unclear. While IQ is often quoted as being about 50% inheritable, there is some evidence that the association with genetics is much weaker in children from poor backgrounds: that good genes won’t help you much if the circumstances are against it. (This finding is seemingly robust in the US, but not in Europe, where social inequalities might not be pronounced enough to produce the effect.)
Nonetheless, there’s nothing wrong in principle with Cummings’ suggestion that research to identify “high IQ” genes should be encouraged. But if he were to look a little more deeply into what it has already discovered (and sometimes un-discovered again), he might wonder what it offers education policy. A 2012 study pointed out that most previous claims of an association between intelligence and specific genes don’t stand up to scrutiny. Nor is there much encouragement from ones that do. In September an international consortium led by Daniel Benjamin of Cornell University in New York reported on a search for genes linked to cognitive ability using a new statistical method that overcomes the weaknesses of traditional surveys. The method cross-checks such putative associations against a “proxy phenotype” – a trait that can ‘stand in’ for the one being probed. In this case the proxy for cognitive performance was the number of years that the tens of thousands of test subjects spent in education.
From several intelligence-linked genes claimed in previous work, only three survived this scrutiny. More to the point, those three were able to account for only a tiny fraction of the inheritable differences in IQ. Someone blessed with two copies of all three of the “favourable” gene variants could expect a boost of just 1.8 IQ points relative to someone with none of these variants. As the authors themselves admitted, the three gene variants are “not useful for predicting any particular individual’s performance because the effect sizes are far too small”.
Perhaps, then, the media would be best advised not to call these “IQ genes”. But you could forgive them for doing so, for they’d only have been echoing one of the paper’s authors, the influential cognitive scientist Steven Pinker of Harvard University. The proper response to a study showing that most existing candidates for gene-intelligence associations were wrong, and that the few that weren’t contribute almost negligibly to inheritability, surely isn’t “Here they are at last”, but “Jesus, is this all there is?”
Where, then, is the remainder of the inherited component? It must presumably reside among a host of genes whose effects are too subtle to be detected by current methods. Those genes will surely be involved in other physiological functions, their effects in intelligence being highly indirect. They are in no meaningful sense “genes for intelligence”, any more than SRY is a gene for being struck by lightning.
So it’s not clear, pace Cummings, what this kind of study adds to the conventional view that some kids are more academically able than others. It’s not clear why it should alter the goal of helping all children achieve what they can, to the best of their ability. Such findings offer very dim prospects for Plomin’s hope, laudable in principle, that education might be tailored to the strengths and weaknesses of individual pupils’ genetic endowment.
Race matters
So, then, to Wade’s claims that genetics causes racial differences in traits such as the propensity for violence or the organization of social institutions. As Wade’s book has shown, the issue of race and genes remains as tendentious as ever. On the one hand, of the total genetic variation between random individuals, around 90% is already present in populations on a single continent – Asia, say – and only 10% more would accrue from pooling Europeans, Africans and Asians together. Some biologists argue that this makes the notion of race biologically meaningless. Yet ancestry does leave an imprint in our genomes: for example, lactose intolerance is more common in Africa and Asia, sickle-cell anemia in people of African origin, and cystic fibrosis in white northern Europeans. That’s why the concept of race is useful as a proxy for medical risk assessment and diagnosis. Besides, arguments about statistical clusters of gene variation don’t alter the fact that culturally conventional indicators of race – pigmentation and eye shape, say – are genetically determined.
What you choose to emphasize and ignore in this matter is largely a question of ideology, not science. But arguments like those Wade puts forward draw their strength from the simplistic notions of how genes relate to phenotype. We know that what we can, in this case, reasonably call cystic-fibrosis or sickle-cell genes (because the conditions derive from a single gene mutation) differ in incidence among racial groups. We also know that genetic variation, while gradual, is not geographically uniform. Might it not be that those variations could encompass genes for intelligence, say?
Yet if the genetic constitution of such traits is really so dispersed, this is a little like grabbing a hundred Scrabble tiles from some huge pile and expecting them to spell out this sentence. Ah, but such random grabs are then filtered into meaningful configurations by natural selection, Wade argues: genes producing a predisposition to capitalism or tribalism might be more useful in some populations than others. Setting aside the improbability of those particular genes existing in the first place, this idea relies on the assumption that every inheritable trait can be selected for, because it stems from genes “for” that trait. That’s precisely the fallacy that once supported eugenic arguments for the betterment of the human race: that we can breed out genes for criminality, stupidity, mendacity.
While it has been reassuring to watch Wade’s thesis be comprehensively dismantled (here and here and here, say) by scientists and other knowledgeable commentators, it’s hard not to contrast their response with that to James Watson’s claim in 2007 that the idea that all races share “equal powers of reason” is a delusion. Despite the fact that Watson adduced as “evidence” only the alleged experience of “people who have to deal with black employees”, he was defended as the victim of a witch-hunt by an “illiberal and intolerant thought police”. Even though it is hard to disentangle genuine prejudice from habitual liberal-baiting in Watson’s remarks, all we are really seeing here is one natural endpoint of the “genes for” and “instruction book” mentality underpinning the Human Genome Project that Watson helped establish and initially led.
The dark genome
The dispersed, “polygenic” nature of inheritable intelligence is likely to be the norm in genetics, at least for many traits we care about. Much the same applies to many inheritable medical conditions, such as schizophrenia and multiple sclerosis: like asthma, they seem to arise from the action of many, perhaps even hundreds, of genes, and there’s not one gene, or even a small number, that can be identified as the main culprits. This “missing heritability”, sometimes called the “dark matter” of the genome, is one of the biggest challenges to the promised personalized medicine of the post-genome era. But it should also be seen as challenging our understanding of genetics per se. Jones, who has been energetic about puncturing the worse misunderstandings of the “genes for” picture, admits that he wouldn’t now attempt to explain how genetics really works, in a manner akin to his brilliant The Language of the Genes (1994), because the field has got so damned complicated.
Yet the linguistic analogy – with genes as words and genomes as books – might remain a serviceable one, if only it were taken more seriously. Combing the genome for genes for many (not all) complex traits seems a little like analyzing Hamlet to look for the words in which Hamlet’s indecision resides. Sure, there’s a lot riding on the cluster “To be or not to be”, but excise it and his wavering persists. Meanwhile, “to” does a lot of other work in the play, and is in no meaningful sense an “indecisive Hamlet” word.
The irony is that a study like the latest “IQ genes” report, while showing yet again the inadequacy of the “gene for” picture, is likely to perpetuate it. As Jones has pointed out, such work has the unfortunate side-effect of feeding our fascination with the putative genetic basis of social problems such as discrimination or differences in educational achievement, about which we can do rather little, while distracting us from the often more significant socioeconomic causes, about which we could do a great deal.
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