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.

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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.

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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.

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.

The gene delusion

This is an extended version of my piece in the December issue of Prospect.

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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.

Friday, November 07, 2014

Who are you calling a journalist?

When from time to time I’m fortunate enough to be asked to give a talk at a scientific meeting in a country that requires a visa, I always anticipate a bit of wary quizzing.
“So which institution are you from, Dr Ball?”
“Well, I’m not.”
“So you’re writing about this meeting?”
“Well, I might, but I’m going to give a talk…”
[US version: Sardonic glance, which says “Who is this joker?”]
[Chinese version: “Whatever. We’re giving you a short-term journalist visa, pal.”]
It’s pretty much the only time I have to think about my professional status within the scientific community. I’m generally content to call myself a writer, often a “science writer”, but I don’t trouble too much about whether this merges into a kind of quasi-scientist role. Well, I suppose the other time is when I write a paper for the academic literature, and feel oddly exposed when the only thing I can write for my address is “25 Brenchley Grove SE23” [not really], without the shield of an institution. Otherwise I have no real reason to think about this stuff, not least because, with extremely rare exceptions (a spectacularly insecure Nobel laureate being one), scientists themselves seem supremely unconcerned about whether you are a “scientist”, “writer”, “journalist” or whatever – in my experience they are true to the egalitarian spirit of science in being glad to talk to you or listen to you without the need for any kind of label, so long as they are interested in what you have to say.

All this springs to mind not just because I’ve recently returned from speaking at a conference in China but because of the latest round in the spat between Richard Dawkins and E. O. Wilson. I have felt very little sympathy previously for the rather intemperate way that Dawkins has launched into Wilson for his support of group selection – an argument that Wilson makes in collaboration with Martin Nowak on the back of some serious mathematics. But Wilson now does himself no credit at all by dismissing Dawkins’ challenges on the ground that Richard is a “journalist” – “and journalists are people that report what the scientists have found.” For one thing, this is just a part of what science journalists do; they also provide context for and sometimes critique of what the scientists have found. They are not just PR monkeys. But it is patently absurd to call Richard a journalist, even though sometimes he does write journalistic pieces. We all know that he has not really conducted original research for many years now. We know that this is pretty much true too of various other scientists in academic positions whose main job now is the communication of science. And so what? To suggest that that activity disqualifies them as real scientists is not just silly but speaks of the kind of snobbish disdain for popularization that Carl Sagan long suffered from. I can’t believe for a moment that Wilson feels that disdain, since he is such a splendid popularizer himself, and so I can only suppose that this humane man had a moment of irritation that got the better of him. If he thinks Dawkins is wrong, he needs to say why, not to discount the arguments on the grounds that Richard doesn’t do research. (By the same token, of course, if other evolutionary biologists think Wilson is wrong , they shouldn’t be saying so by going round drumming up signatures for mass letters to Nature saying how he’s let the side down. Arguments from authority or weight of numbers are precisely what scientists are meant to eschew.)

I suppose one could argue, however, that Richard is only getting a taste of his own medicine. When he compiled the Oxford Book of Modern Science Writing, he didn’t even acknowledge the existence of scientifically trained people who write about science for a living. Rather, his choices were apparently made between “professional scientists” and “excursions into science by professional writers” (he excludes the latter). This implies that, if you’re not a “professional scientist” then you are a dilettante – a suggestion that I don’t take personally but which strikes me as spectacularly insulting to the truly great science writers such as James Gleick, Carl Zimmer, Deborah Blum, and, oh sorry guys, loads of others I should mention. The mighty Thomas Levenson saw this attitude off more comprehensively and persuasively than I ever could. Maybe it would do Richard no harm to join us for a bit. There’s no shame in it. After all, his writing has precisely the kind of writerly virtues that Robin McKie says in this Guardian science podcast (on the Royal Society Winton Book Prize) that he finds much more often in the works of professional writers than in those of scientists writing books about their pet topic.

Oh, and by the way: visa officials aren’t the only ones who insist that you’re only to be taken seriously if you have “Department of…” after your name. I know for a fact that this is the criterion for inclusion on Radio 4’s In Our Time too. But I suppose the folks making those choices are arts graduates – and while I love the humanities, I know how strongly the argument from authority still holds sway there.

The science of artificial olives


My Chemistry World Crucible column for November... And I really do want to give this a go one day.

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How would you like your soup, madam – one lump or two? If you ever had the chance (and financial resources) to dine at elBulli on the Catalonian Costa Brava before it closed in 2011, you’ll understand how soup can be served this way. The celebrity chef Ferran Adrià has worked for years to perfect the technique of spherification, a method of encapsulating liquid foods in an edible polymer skin. It is one of the most striking coups of molecular gastronomy – cooking based on advanced chemistry – and I am reliably informed that elBulli’s spherificated olives, made from puréed olive, were out of this world.

[Actually the recommendation, from the RSC’s Phil Robinson, deserves to be quoted in full: “The spherificated olives certainly were good. But the rabbit brain and sea anemone dish was surf and turf too far removed for my taste.”]

Spherification goes back a long way. It was invented in the 1940s and patented for the production of “artificial edible cherries”. Innovative chefs such as Hervé This, the doyen of molecular gastronomy, explored it in later decades. It uses sodium alginate, a natural food thickener extracted from brown seaweed, which is gelated from solution when exposed to calcium ions. The usual method is to place a dollop of the food ingredient, mixed with sodium alginate, into a bath of a calcium salt such as calcium lactate gluconate. As it gels, the blob is pulled into a sphere by surface tension.

Adrià came across the technique in 2003 and began at once to experiment with it, creating ravioli-like dishes from puréed pea and mango and varying the recipes to tune the texture of the gel. But in 2005 the “scientific department” of his restaurant came up with a new approach that turned the chemistry inside out. Adrià realized that the liquid core could be kept more fluid by allowing it to grow a thin skin within a solution of sodium alginate. In other words, instead of adding alginate droplets to a calcium bath, he began adding liquids naturally rich in calcium (or supplemented with it if necessary) into an alginate bath. Within just a few minutes of this reverse spherification, the droplets develop a membrane tough enough for them to be lifted out gently on a spoon. After rinsing in water, they’re ready to eat: one bite releases a flood of the flavoursome ingredients, whether it’s tomato soup, puréed strawberries or olives. It works for just about any liquid, and is a rare example of haute cuisine that you can do at home – Adrià even supplies kits with all the ingredients.

The basic process of gelation is no mystery. But the details haven’t been clear. Why is calcium alginate a gel whereas the sodium salt is soluble? And what effect does the chemistry of the encapsulated fluid have on the membrane? To answer such questions, Adrià is collaborating with biophysicist Christophe Chipot of the University of Illinois at Urbana-Champaign and a team at Nankai University in Tianjin, China. In their first foray they used molecular dynamics simulations to study the process (H. Fu et al., J. Phys. Chem. B 118, 11747 (2014)).

Since it’s not feasible either to investigate a full-sized hors d’oeuvre this way or to include the chemical complexity of puréed olive, the researchers have looked at nanospheres of representative liquids such as a hydrocarbon (dodecane), a fatty acid (oleic) and its sodium and calcium salts. Alginate is a polysaccharide, a somewhat random copolymer of two sugars, and in the simulations these polymers encapsulated the core droplets in a hydrogel matrix. With calcium ions present the alginate forms a well-defined membrane, but with sodium oleate as the core the membrane failed to cohere into a compact form. Evidently the calcium ions are essential. Why? The researchers find that, while both sodium and calcium ions are coordinated to electron-donating oxygen atoms in the alginate chains, the average coordination number for calcium is a little over 3, while that for sodium is about 2. This means that calcium ions are considerably better at cross-linking the polysaccharide chains by chelation and thereby stabilizing the membrane network – a conclusion supported by thermodynamic calculations of the binding free energies.

A pure hydrocarbon core doesn’t easily grow a stable membrane either, even with calcium ions present, since it can neither sequester the ions to its surface nor benefit from direct interactions with the alginate, for example by hydrogen bonding, so as to adsorb a coating that the calcium ions can then cross-link. That’s why, if you want to make a spherificated morsel with an oily filling, the researchers say that “some avant-garde cuisine techniques” are needed – as Adrià has apparently already discovered.

elBulli closed because of the massive losses it was incurring, despite typical dining costs of around $250 per head and an absurdly oversubscribed booking list. It’s not clear what will spring from it now. The elBullifoundation announces that the restaurant will be replaced with an “exhibition centre” to “help understand its historical and culinary evolution”, to archive the history of cooking generally, and to “provide facilities related to the process of creativity.” It all sounds mysteriously intriguing, but I suspect most visitors will be hoping that there’s a café attached.

Particle Fever: nearly all good

I finally got around to watching all of Particle Fever. It’s great, and makes me all the happier that Fabiola Gianotti will be the new director. I fully agree with Peter Woit that “if you want to get someone turned on to high energy particle physics, or just convince a young person that a career in science is an attractive idea, the CERN footage in this film should do the job better than anything I’ve seen from even the highly competent CERN press office.” I don’t withdraw my complaint about how the director has spoken about the role of the LHC in physics more generally, but that’s a minor quibble given what a splendid job he’s done.

But I was intrigued to discover this comment from Woit:

“As for the really bad idea, it’s the introduction of the multiverse into the theory part of the film. Kaplan is shown claiming that the multiverse predicts a 140 GeV Higgs, based on this paper of Yasunori Nomura and Lawrence Hall (who was Arkani-Hamed’s advisor). This is at a time when there were experimental hints of a 140 GeV Higgs. After they went away, and the mass came out at 125 GeV, the “prediction” is forgotten, but a long segment still has Arkani-Hamed going on about the CC and arguing for the multiverse. Just before this segment though, Dunford the experimentalist is shown Skyping with the filmmaker, warning them “Don’t listen to theorists”. At the film showing, Kaplan and Arkani-Hamed were there and answered questions at the end. One of the first questions (not from me…) was from an audience member who asked why they had put the material about the multiverse in the film, even though it had no real link to the Higgs or the LHC experiments. Arkani-Hamed admitted that the 140 Gev prediction was tenuous, there was no “sharp” link of the multiverse to the Higgs, and that no way is now known to get predictions out of the multiverse idea or test it. Kaplan explained that the intention was to make an “experiential” film, focusing on what theorists were talking about and thinking about, without getting into really trying to fully explain the scientific issues. The problem with this is that the film comes through as promoting the Dimopoulos/Arkani-Hamed view that no SUSY means a multiverse, without showing any challenge to such an argument.”

I’m no expert, to understate absurdly, but Woit is, and it does rather sound as though there was a little bit of an agenda here. After all, everyone loves a good multiverse. Or do they? Watch this space.

Sunday, October 12, 2014

Mind control

Here's a pre-edited version of my piece for the Observer today, with a little bit more stuff still in it and some links. This was a great topic to research, and a bit disconcerting at times too.

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Be careful what you wish for. That’s what Joel, played by Jim Carrey, discovers in Charlie Kaufmann’s 2004 film Eternal Sunshine of the Spotless Mind, when he asks a memory-erasure company Lacuna Inc. to excise the recollections of a painful breakup from his mind. While the procedure is happening, Joel realizes that he doesn’t want every happy memory of the relationship to vanish, and seeks desperately to hold on to a few fragments.

The movie offers a metaphor for how we are defined by our memories, how poignant is both their recall and their loss, and how unreliable they can be. So what if Lacuna’s process is implausible? Just enjoy the allegory.

Except that selective memory erasure isn’t implausible at all. It’s already happening.

Researchers and clinicians are now using drugs to suppress the emotional impact of traumatic memories. They have been able to implant false memories in flies and mice, so that innocuous environments or smells seem to be “remembered” as threatening. They are showing that memory is not like an old celluloid film, fixed but fading; it is constantly being changed and updated, and can be edited and falsified with alarming ease.

“I see a world where we can reactivate any kind of memory we like, or erase unwanted memories”, says neuroscientist Steve Ramirez of the Massachusetts Institute of Technology. “I even see a world where editing memories is something of a reality. We’re living in a time where it’s possible to pluck questions from the tree of science fiction and ground them in experimental reality.” So be careful what you wish for.

But while it’s easy to weave capabilities like this into dystopian narratives, most of which the movies have already supplied – the authoritarian memory-manipulation of Total Recall, the mind-reading police state of Minority Report, the dream espionage of Inception – research on the manipulation of memory could offer tremendous benefits. Already, people suffering from post-traumatic stress disorder (PTSD), such as soldiers or victims of violent crime, have found relief from the pain of their dark memories through drugs that suppress the emotional associations. And the more we understand about how memories are stored and recalled, the closer we get to treatments for neurodegenerative conditions such as Alzheimer’s and other forms of dementia.

So there are good motivations for exploring the plasticity of memory – how it can be altered or erased. And while there are valid concerns about potential abuses, they aren’t so very different from those that any biomedical advance accrues. What seems more fundamentally unsettling, but also astonishing, about this work is what it tells us about us: how we construct our identity from our experience, and how our recollections of that experience can deceive us. The research, says Ramirez, has taught him “how unstable our identity can be.”

Best forgotten

Your whole being depends on memory in ways you probably take for granted. You see a tree, and recognize it as a tree, and know it is called “tree” and that it is a plant that grows. You know your language, your name, your loved ones. Few things are more devastating, to the individual and those close to them, than the loss of these everyday facts. As the memories fade, the person seems to fade with them. Christopher Nolan’s film Memento echoes the case of Henry Molaison, who, after a brain operation for epilepsy in the 1950s, lost the ability to record short-term memories. Each day his carers had to introduce themselves to him anew.

Molaison’s surgery removed a part of his brain called the hippocampus, giving a clue that this region is involved in short-term memory. Yet he remembered events and facts learnt long ago, and could be taught new ones, indicating that long-term memory is stored somewhere else. Using computer analogies for the brain is risky, but it’s reasonable here to compare our short-term memory with a computer’s ephemeral working memory or RAM, and the long-term memory with the hard drive that holds information more durably. While short-term memory is associated with the hippocampus, long-term memory is more distributed throughout the cortex. Some information is stored long-term, such as facts and events we experience repeatedly or that have an emotional association; other items vanish within hours. If you look up the phone number of a plumber, you’ll probably have forgotten it by tomorrow, but you may remember the phone number of your family home from childhood.

What exactly do we remember? Recall isn’t total – you might retain the key aspects of a significant event but not what day of the week it was, or what you were wearing, or exactly what was said. Your memories are a mixed bag: facts, feelings, sights, smells. Ramirez points out that, while Eternal Sunshine implies that all these features of a memory are bundled up and stored in specific neurons in a single location in the brain, in fact it’s now clear that different aspects are stored in different locations. The “facts”, sometimes called episodic memory, are filed in one place, the feelings in another (generally in a brain region called the amygdala). All the same, those components of the memory do each have specific addresses in the vast network of our billions of neurons. What’s more, these fragments remain linked and can be recalled together, so that the event we reconstruct in our heads is seamless, if incomplete. “Memory feels very cohesive, but in reality it’s a reconstructive process”, says Ramirez.

Given all this filtering and parceling out, it’s not surprising that memory is imperfect. “The fidelity of memory is very poor”, says psychologist Alain Brunet of McGill University in Montreal. “We think we remember exactly what happens, but research demonstrates that this is a fallacy.” It’s our need for a coherent narrative that misleads us: the brain elaborates and fills in gaps, and we can’t easily distinguish the “truth” from the invention. You don’t need fancy technologies to mess with memory – just telling someone they experienced something they didn’t, or showing them digitally manipulated photos, can be enough to seed a false conviction. That, much more than intentional falsehood, is why eye-witness accounts may be so unreliable and contradictory.

It gets worse. One of the most extraordinary findings of modern neuroscience, reported in 2000 by neurobiologist Joseph LeDoux and his colleagues at New York University, is that each time you remember something, you have to rebuild the memory again. LeDoux’s team reported that when rats were conditioned to associate a particular sound with mild electric shocks, so that they showed a “freezing” fear response when they heard the sound subsequently, this association could be broken by infusing the animals’ amygdala with a drug called anisomycin. The sound then no longer provoked fear – but only if the drug was administered within an hour or so of the memory being evoked. Anisomycin disrupts biochemical processes that create proteins, and the researchers figured that this protein manufacture was essential for restoring a memory after it has arisen. This is called reconsolidation: it starts a few minutes after recall, and takes a few hours to complete.

So those security questions asking you for the name of your first pet are even more bothersome than you thought, because each time you have to call up the answer (sorry if I just made you do it again), your brain then has to write the memory back into long-term storage. A computer analogy is again helpful. When we work on a file, the computer makes a copy of the stored version and we work on that – if the power is cut, we still have the original. But as Brunet explains, “When we remember something, we bring up the original file.” If we don’t write it back into the memory, it’s gone.

This rewriting process can, like repeated photocopying, degrade the memory a little. But LeDoux’s work showed that it also offers a window for manipulating the memory. When we call it up, we have the opportunity to change it. LeDoux found that a drug called propranolol can weaken the emotional impact of a memory without affecting the episodic content. This means that the effect of painful recollections causing PTSD can be softened. Propranolol is already known to be safe in humans: it is a beta blocker used to treat hypertension, and (tellingly) also to combat anxiety, because it blocks the action of the stress hormone epinephrine in the amygdala. A team at Harvard Medical School has recently discovered that xenon, the inert gas used as an anaesthetic, can also weaken the reconsolidation of fear memories in rats. An advantage of xenon over propranolol is that it gets in and out of the brain very quickly, taking about three minutes each way. If it works well for humans, says Edward Meloni of the Harvard team, “we envisage that patients could self-administer xenon immediately after experiencing a spontaneous intrusive traumatic memory, such as awakening from a nightmare.” The timing of the drug relative to reactivation of the trauma memory may, he says, be critical for blocking the reconsolidation process.

These techniques are now finding clinical use. Brunet uses propranolol to treat people with PTSD, including soldiers returned from active combat, rape victims and people who have suffered car crashes. “It’s amazingly simple,” he says. They give the patients a pill containing propranolol, and then about an hour later “we evoke the memory by having patients write it down and then read it out.” That’s often not easy for them, he says – but they manage it. The patients are then asked to continue reading the script regularly over the next several weeks. Gradually they find that its emotional impact fades, even though the facts are recalled clearly.

“After three or four weeks”, says Brunet, “our patients say things like ‘I feel like I’m smiling inside, because I feel like I’m reading someone else’s script – I’m no longer personally gripped by it.’” They might feel empathy with the descriptions of the terrible things that happened to this person – but that person no longer feels like them. No “talking cure” could do that so quickly and effectively, while conventional drug therapies only suppress the symptoms. “Psychiatry hasn’t cured a single patient in sixty years”, Brunet says.

These cases are extreme, but aren’t even difficult memories (perhaps especially those) part of what makes us who we are? Should we really want to get rid of them? Brunet is confident about giving these treatments to patients who are struggling with memories so awful that life becomes a torment. “We haven’t had a single person say ‘I miss those memories’”, he says. After all, there’s nothing unnatural about forgetting. “We are in part the sum of our memories, and it’s important to keep them”, Brunet says. “But forgetting is part of the human makeup too. We’re built to forget.”

Yet it’s not exactly forgetting. While propranolol and xenon can modify a memory by dampening its emotional impact, the memory remains: PTSD patients still recall “what happened”, and even the emotions are only reduced, not eliminated. We don’t yet really understand what it means to truly forget something. Is it ever really gone or just impossible to recall? And what happens when we learn to overcome fearful memories – say, letting go of a childhood fear of dogs as we figure that they’re mostly quite friendly? “Forgetting is fairly ill-defined”, says neuroscientist Scott Waddell at the University of Oxford. “Is there some interfering process that out-competes the original memory, or does the original memory disappear altogether?” Some research on flies suggests that forgetting isn’t just a matter of decay but an active process in which the old memory is taken apart. Animal experiments have also revealed the spontaneous re-emergence of memories after they were apparently eliminated by re-training, suggesting that memories don’t vanish but are just pushed aside. “It’s really not clear what is going on”, Waddell admits.

Looking into a fly’s head

That’s not so surprising, though, because it’s not fully understood how memory works in the first place. Waddell is trying to figure that out – by training fruit flies and literally looking into their brains. What makes flies so useful is that it’s easy to breed genetically modified strains, so that the role of specific genes in brain activity can be studied by manipulating or silencing them. And the fruit fly is big and complex enough to show sophisticated behavior, such as learning to associate a particular odour with a reward like sugar, while being simple enough to comprehend – it has around 100,000 neurons, compared to our many billions.

What’s more, a fruit fly’s brain is transparent enough to look right through it under the microscope, so that one can watch neural processing while the fly is alive. By attaching fluorescent molecules to particular neurons, Waddell can identify the neural circuitry linked to a particular memory. In his lab in Oxford he showed me an image of a real fly’s brain: a haze of bluish-coloured neurons, with bright green spots and filaments that are, in effect, a snapshot of a memory. The memory might be along the lines of “Ah, that smell – the last time I followed it, it led to something tasty.”

How do you find the relevant neurons among thousands of others? The key is that when neurons get active to form a memory, they advertise their state of busyness. They produce specific proteins, which can be tagged with other light-emitting proteins by genetic engineering of the respective genes. One approach is to inject benign viruses that stitch the light-emission genes right next to the gene for the protein you want to tag; another is to engineer particular cells to produce a foreign protein to which the fluorescent tags will bind. When these neurons get to work forming a memory, they light up. Ramirez compares it to the way lights in the windows of an office block at night betray the location of workers inside.

This ability to identify and target individual memories has enabled researchers like Waddell and Ramirez to manipulate them experimentally in, well, mind-boggling ways. Rather than just watching memories form by fluorescent tagging, they can use tags that act as light-activated switches to turn gene activity on or off with laser light directed down an optical fibre into the brain. This technique, called optogenetics, is driving a revolution in neuroscience, Ramirez says, because it gives researchers highly selective control over neural activity – enabling them in effect to stimulate or suppress particular thoughts and memories.

Waddell’s lab is not a good place to bring a banana for lunch. The fly store is packed with shelves of glass bottles, each full of flies feasting on a lump of sugar at the bottom. Every bottle is carefully labeled to identify the genetic strain of the insects it contains: which genes have been modified. But surely they get out from time to time, I wonder – and as if on cue, a fly buzzes past. Is that a problem? “They don’t survive for long on the outside,” Waddell reassures me.

Having spent the summer cursing the plague of flies gathering around the compost bin in the kitchen, I’m given fresh respect for these creatures when I inspect one under the microscope and see the bejeweled splendor of its red eyes. It’s only sleeping: you can anaesthetize fruit flies with a puff of carbon dioxide. That’s important for mapping neurons to memories in the microscope, because there’s not much going on in the mind of a dead fly.

These brain maps are now pretty comprehensive. We know, for example, which subset of neurons (about 2,000 in all) is involved in learning to recognize odours, and which neurons can give those smells good or bad associations. And thanks to optogenetics, researchers have been able to switch on some of these “aversive” neurons while flies smell a particular odour, so that they avoid it even though they have actually experienced nothing bad (such as shock treatment) in its presence – in other words, you might say, to stimulate a fictitious false memory. For a fly, it’s not obvious that we can call this “fear”, Waddell says, but “it’s certainly something they don’t like”. In the same way, by using molecular switches that are flipped with heat rather than light, Waddell and his colleagues were able to give flies good vibes about a particular smell. Flies display these preferences by choosing to go in particular directions when they are placed in little plastic mazes, some of them masterfully engineered with little gear-operated gates courtesy of the lab’s 3D printer.

Ramirez, working in a team at MIT led by Susumu Tonegawa, has practiced similar deceptions on mice. In an experiment in 2012 they created a fear memory in a mouse by putting it in a chamber where it experienced mild electric shocks to the feet. While this memory was being laid down, the researchers used optogenetic methods to make the corresponding neurons, located in the hippocampus, switchable with light. Then they put the mouse in a different chamber, where it seemed perfectly at ease. But when they reactivated the fear memory with light, the mouse froze: suddenly it had bad feelings about this place.

That’s not exactly implanting a false memory, however, but just reactivating a true one. To genuinely falsify a recollection, the researchers devised a more elaborate experiment. First, they placed a mouse in a chamber and labeled the neurons that recorded the memory of that place with optogenetic switches. Then the mouse was put in a different chamber and given mild shocks – but while these were delivered, the memory of the first chamber was triggered using light. When the mouse was then put back in the first chamber it froze. Its memory insisted, now without any artificial prompting, that the first chamber was a nasty place, even though nothing untoward had ever happened there. It is not too much to say that a false reality had been directly written into the mouse’s brain.

You must remember this

The problem with memory is often not so much that we totally forget something or recall it wrongly, but that we simply can’t find it even though we know it’s in there somewhere. What triggers memory recall? Why does a fly only seem to recall a food-related odour when it is hungry? Why do we feel fear only if we’re in actual danger, and not all the time? Indeed, it is the breakdown of these normal cues that produces PTSD, where the fear response gets triggered in inappropriate situations.

A good memory is largely about mastering this triggering process. Participants in memory competitions that involve memorizing long sequences of arbitrary numbers are advised to “hook” the information onto easily recalled images. A patient named Solomon Shereshevsky, studied in the early twentieth century by the neuropsychologist Alexander Luria, exploited his condition of synaesthesia – the crosstalk between different sensory experiences such as sound and colour – to tag information with colours, images, sounds or tastes so that he seemed able to remember everything he heard or read. Cases like this show that there is nothing implausible about Jorge Luis Borges’ fictional character Funes the Memorious, who forgets not the slightest detail of his life. We don’t forget because we run out of brain space, even if it sometimes feels like that.

Rather than constructing a complex system of mnemonics, perhaps it is possible simply to boost the strength of the memory as it is imprinted. “We know that emotionally arousing situations are more likely to be remembered than mundane ones”, LeDoux has explained. “A big part of the reason is that in significant situations chemicals called neuromodulators are released, and they enhance the memory storage process.” So memory sticks when the brain is aroused: emotional associations will do it, but so might exercise, or certain drugs. And because of reconsolidation, it seems possible to enhance memory after it has already been laid down. LeDoux has found that a chemical called isoproterenol has the opposite effect from propranolol on reconsolidation of memory in rats, making fear memories even stronger as they are rewritten into long-term storage in the amygdala. If it works for humans too, he speculates that the drug might help people who have “sluggish” memories.

Couldn’t we all do with a bit of that, though? Ramirez regards chemical memory enhancement as perfectly feasible in principle, and in fact there is already some evidence that caffeine can enhance long-term memory. But then what is considered fair play? No one quibbles about students going into an exam buoyed up by an espresso, but where do we draw the line?

Mind control

It’s hard to come up with extrapolations of these discoveries that are too far-fetched to be ruled out. You can tick off the movies one by one. The memory erasure of Eternal Sunshine is happening right now to some degree. And although so far we know only how to implant a false memory if it has actually been experienced in another context, as our understanding of the molecular and cellular encoding of memory improves Ramirez thinks it might be feasible to construct memories “from the ground up”, as in Total Recall or the implanted childhood recollections of the replicant Rachael in Blade Runner. As Rachael so poignantly found out, that’s the way to fake a whole identity.

If we know which neurons are associated with a particular memory, we can look into a brain and know what a person is thinking about, just by seeing which neurons are active: we can mind-read, as in Minority Report. “With sufficiently good technology you could do that”, Ramirez affirms. “It’s just a problem of technical limitations.” By the same token, we might reconstruct or intervene in dreams, as in Inception (Ramirez and colleagues called their false-memory experiment Project Inception). Decoding the thought processes of dreams is “a very trendy area, and one people are quite excited about”, says Waddell.

How about chips implanted in the brain to control neural activity, Matrix-style? Theodore Berger of the University of Southern California has implanted microchips in rats’ brains that can duplicate the role of the hippocampus in forming long-term memories, recording the neural signals involved and then playing them back. His most recent research shows that the same technique of mimicking neural signals seems to work in rhesus monkeys. The US Defense Advanced Research Projects Agency (DARPA) has two such memory-prosthesis projects afoot. One, called SUBNETS, aims to develop wireless implant devices that could treat PTSD and other combat-related disorders. The other, called RAM (Restoring Active Memories), seeks to restore memories lost through brain injury that are needed for specialized motor skills, such as how to drive a car or operate machinery. The details are under wraps, however, and it’s not clear how feasible it will be to record and replay specific memories. LeDoux professes that he can’t imagine how it could work, given that long-term memories aren’t stored in a single location. To stimulate all the right sites, says Waddell, “you’d have to make sure that your implantation was extremely specific – and I can’t see that happening.”

Ramirez says that it’s precisely because the future possibilities are so remarkable, and perhaps so unsettling, that “we’re starting this conversation today so that down the line we have the appropriate infrastructure.” Are we wise enough to know what we want to forget, to remember, or to think we remember? Do we risk blanking out formative, instructive and precious experiences, or finding ourselves one day being told, as Deckard tells Rachael in Blade Runner, “those aren’t your memories – they’re someone else’s”?

“The problems are not with the current research, but with the question of what we might be able to do in 10-15 years,” says Brunet. It’s one thing to bring in legislation to restrict abuses, just as we do for other biomedical technologies. But the hardest arguments might be about not what we prohibit but what we allow. Should individuals be allowed to edit their own memories or have false ones implanted? Ramirez is upbeat, but insists that the ethical choices are not for scientists alone to thrash out. “We all have some really big decisions ahead of us,” he says.