The Joy of Sexism

This week, I've been embroiled in not one but two gender-based debates.

First up, I've been quoted in Delusions of Gender, the new book from Cordelia Fine, in which she examines the science of alleged sex differences in behaviour. The quote was from this 2008 post about Vicky Tuck, a teacher with odd ideas about the brains of boys and girls. I haven't had time to read the book yet, but a review's in the pipeline.

Then yesterday, I found out that I've been the subject of some research.

In this report, we detail research into the representation of women in science, engineering and technology (SET) within online media...

The research involved data collection and analysis from websites, web authors and young web users. We monitored SET content across 16 websites. Eight sites were generalist: BBC, Channel 4, SkyTV, The Guardian, The Daily Mail, Wikipedia, YouTube and Twitter.

Eight sites were SET-specific: New Scientist, Bad Science, The Science Museum, The Natural History Museum, Neuroskeptic Blog, Science – So What? So Everything, Watt’s Up With That? Blog and RichardDawkins.net.

Quite a line-up. Clearly they decided to look at the very best, most illustrious and most respected science blogs... and also Neuroskeptic. Anyway, unfortunately I can't access the paper, despite being in it, but according to the abstract they found that:

Online science informational content is male dominated in that far more men than women are present... we found that these women are:

• Subject to muting of their ‘voices’. This includes instances where SET women are pictured but remain anonymous and instances where they are used, mainly as science journalists, to ventriloquise other people's scientific work.
• Subject to clustering in specific SET fields and website sections, particularly those about ‘feminine’ subjects or specifically about women...
• Associated with ‘feminine’ attributes and activities, notably as caring, demonstrating empathy with children and animals...
• Predominantly White, middle-class, able-bodied and heterosexual.
• Peripheral to the main story and subordinated as students, young scientists, relatives of a male scientist ... we found less hyperlinking of women’s than men’s names in online SET.
• Discussed in terms of appearance, personality, sexuality and personal circumstances more often than men...
• More generally, constructed in ways that relocate them in the private domestic sphere, detract from their scientific contribution, and associate them, more often than men, with the new category of ‘bad science’.

Without knowing the details it's hard to evaluate these claims, but it's fair to say that some of it rings true.

There's been lots of buzz recently about the gender ratio of science bloggers - we're mostly male, who'd have guessed? - and I suppose this would be a good time to chip in. Does it matter?

I think it does, and moreover it's part of a bigger picture. As far as I can see, science bloggers are mostly: male, white, under 40... and almost all of the biggest ones are also native English speakers; I don't know if, overall, English-speakers are overrepresented, because not all blogs are written in English and I only know the ones that are - but English ones get the lions share of the traffic.

Back to gender, even in fields such as psychology and neuroscience in which there are lots of female researchers, bloggers are overwhelmingly male. Likewise, a lot of researchers, even those working in English-speaking countries, are non-native-English speakers, but they have an obvious disadvantage when it comes to blogging in English.

So science bloggers are drawn mostly from a narrow cross-section of the scientific community, which is a problem, because it greatly increases the chances of bloggers becoming an "echo chamber", or a clique, neither of which is likely to end well. Diversity is valuable, in this kind of thing, not because it's somehow morally good per se, but because it helps prevent stagnation.

Israel and Palestine are Both Fighting Back...?

There are three basic schools of thought on the Israel / Palestine thing.

• Those evil Israelis are out to destroy Palestine, and the Palestinians are just fighting back.
• Those evil Palestinians are out to destroy Israel, and the Israelis are just fighting back.
• It's a cycle of violence, where both sides are fighting back against the other.
  

Which one you subscribe to depends mostly on where you were born. I'm not aware of many people who've changed their minds on this issue, perhaps because doing so would require a study of the last 2,500 years of history, religion and politics.

Wouldn't it be handy if science could provide an answer? According to the authors of a new paper in Proceedings of the National Academy of Science, the "cycle" school is right: both sides are fighting back against the other: Both sides retaliate in the Israeli-Palestinian conflict.

The authors (from Switzerland, Israel and the USA) took data on daily fatalities on both sides, and also of daily launches of Palestinian "Qassam" rockets at Israel. The data run from 2001, the start of the current round of unpleasantness, to late 2008, the Gaza War.

They looked to see whether the number of events that happened on a certain day predicted the number of events caused by the other side on the following days, i.e. whether a Palestinian death caused the Palestinians to retaliate by firing more rockets and killing more Israelis, and vice versa.

What happened? They found that both sides were more likely to launch attacks on the days following a death on their own side. The exception to this rule was that Israel did not noticeably retaliate against Qassam launches. This is perhaps because Qassams are so ineffective: out of 3,645 recorded launches, they killed 15 people.

These graphs show the number of "extra" actions on the days following a event, averaged over the whole 8 years, according to a statistical method called the Impulse Response Function. Note that the absolute size of the effects is larger for the Israeli retaliations (the Y axis is bigger); there were a total of 4,874 Palestinian fatalities and 1,062 Israeli fatalities

The authors then used another method called Vector Autoregression to discover more about the relationship. In theory, this method controls for the past history of actions by a given side, so that it reveals the number of actions independently caused by the opposing side.

the number of Qassams fired increases by 6% on the first day after a single killing of a Palestinian by Israel; the probability of any Qassams being fired increases by 11%; and the probability of any Israelis being killed by Palestinians increases by 10%. Conversely, 1 day after the killing of a single Israeli by Palestinians, the number of Palestinians killed by Israel increases by 9%, and the probability of any Palestinians being killed increases by 20%

....retaliation accounts for a larger fraction of Palestinian compared with Israeli aggression: in the levels specification, 10% of all Qassam rockets can be attributed to prior Israeli attacks on Palestinians, but only 4% of killings of Palestinians by Israel can be attributed to prior Palestinian attacks on Israel.... 6% of all days on which Palestinians attack Israel with rockets, and 5% of all days on which they attack by killing Israelis, can be attributed to retaliation; in contrast, this is true for only 2% of all days on which Israel kills Palestinians.

What are we to make of this? This is a good paper as far as it goes, and it casts doubt on earlier analyses finding that Israel is retaliating against Palestinians but not vice versa. However, the inherent problem with all of this research (beyond the fact that it's all based on correlations and can only indirectly imply causation), is that it focuses on individual acts of violence. The authors say, citing surveys, that

Over one half of Israelis and three quarters of Palestinians think the other side seeks to take over their land. When accounting for their own acts of aggression, Israelis often claim to be merely responding to Palestinian violence, and Palestinians often see themselves as simply reacting to Israeli violence.

But I don't think many Israelis would argue that the IDF only kills individual Palestinians as a reflex reaction to a particular attack. They're claiming that the whole conflict is a defensive one, that the Palestinians are the aggressors, but that doesn't rule out their taking the initiative on a tactical level e.g. in destroying Palestinian military capabilities before they have a chance to attack. And vice versa on the other side.

WW2 was a war of aggression by the Axis powers, but that doesn't mean that the Allies only killed Axis soldiers after they'd attacked a certain place. The Allies were on the offensive for the second half of the war, and eventually invaded the Axis's own homelands, but it was still a defensive war, because the Axis were responsible for it.

For Israel and for Palestine, the other guys are to blame for the whole thing. Who's right, if anyone, is fundamentally a historical, political and ethical question, that can't be answered by looking at day-to-day variations in who's shooting when.

Comment Policy: Please only comment if you've got something to say about this paper, or related research. Comments that are just making the case for or against Israel will get deleted.

Haushofer J, Biletzki A, & Kanwisher N (2010). Both sides retaliate in the Israeli-Palestinian conflict. Proceedings of the National Academy of Sciences of the United States of America PMID: 20921415

Brand New Cortical Neurons

Are new neurons created in the adult brain?

For a long time, everyone thought the answer was "no". Then, about 15 years ago, we learned that neurogenesis does occur in the adult brain, but it was thought to be limited to two very small regions, the dentate gyrus and the sub-ventricular zone. Except in cases of injury, when adult neurogenesis had been reported elsewhere.

Now Guo et al look set to overturn this orthodoxy in a new Journal of Neuroscience paper, as they found ongoing neurogenesis in healthy adult brains in an area called the piriform cortex, part of the cerebral cortex.

The key to the discovery was oligodendrocyte progenitor cells (OPCs). OPCs were previously believed to only be able to turn into cells called oligodendrocytes, which are not neurons, but glia; glia are a kind of support crew for the brain.

But Guo et al show convincingly (with the help of genetically modified mice) that OPCs do become neurons in the piriform cortex of adult mice. Once they've been "born", these new neurons mature into functional pyramidal cells - they form synapses with other neurons, and otherwise seem to be perfectly happy, and they survived for hundreds of days (i.e. most of a mouse's lifetime).

The methods they used are complex but the crucial result was that they observed pyramidal cells expression yellow fluorescent protein, in mice genetically modified to express this protein only in OPCs; the picture above this post is one of these "yellow" (I know, it looks green to me) neurons.

This isn't the first paper to report neurogenesis in the adult mouse piriform cortex - a different group did so in 2008, but then two other experiments published later that year failed to confirm the result, so it's remained controversial. Whether this will end the controversy is uncertain but it looks pretty solid to me.

What does it all mean? The piriform cortex is a bit of a weird area, as while it's part of the cerebral cortex, the most "complex" part of the brain, it is evolutionary very old, and quite unlike the neocortex which is by far the largest part of the brain in humans.

The piriform is involved in the sense of smell, which is very important for mice, not so much in humans. We do have a piriform cortex, but it's tiny. Whether adult neurogenesis also occurs in the neocortex is the next big question...

Guo F, Maeda Y, Ma J, Xu J, Horiuchi M, Miers L, Vaccarino F, & Pleasure D (2010). Pyramidal neurons are generated from oligodendroglial progenitor cells in adult piriform cortex. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (36), 12036-49 PMID: 20826667

How To Sell An Idea

You've got an idea: a new way of doing things; a change; a paradigm shift. It might work, it might be no better than what we've got already, or it might end up being a disaster.

The honest way to present your proposal would be to admit its novelty, and hence the uncertainty: this is a new idea I had, I can't promise anything, but here are my reasons for thinking it's worth a try, here are the likely costs and benefits, here are the alternatives.

However, let's suppose you don't want to do that. That's hard work, and if your idea is crap, people could tell. How else could you convince them? By making it seem as though it's not a new idea at all.

You could dress your idea up as:

• the glorious past. Your idea is nothing more than how we did things back in the golden age, when everything was great. For some reason, people strayed from the true path, and things went bad. We should go back to the the good old days. It worked then, so it'll work now. You'll use words like: restoring, reviving, regaining, renewing... "re" is your friend.
• the next step. Your idea is just the logical progression of what we're already doing. Things used to be bad, and then they started to change, and get better. Let's make them even better, by doing more of the same. It's inevitable, anyway: you can't stop history. You'll use words like: progress, forward, advance, build, grow...
  
• catching up. You're just saying we should bring stuff into line with the way things are done elsewhere, which as we know, is working well. It's not even a matter of moving forward, so much as keeping up. It would be weird not to change. We don't want to be dinosaurs. You'll use words like: modernization, rationalization, reform...
  
• keeping things the same. Things are fine right now, and don't need improving. But in order for things to stay great, we must adapt to changing circumstances, so we'll have to make a few adjustments, but don't worry, fundamentally things are going to stay just as they are. You'll use words like: preserving, maintaining, protecting, upholding, strengthening...

The point in every case being to make an innovation seem like it's not one. New means untested, and uncertain, and risky. No-one likes that. Passing off ideas as already proven is a way of gaining acceptance for ideas that wouldn't stand up on their own merits. I'm sure I don't need to point out that this trick is a mainstay of politicians, ideologues and managers everywhere.

Of course, there are plenty of changes that really are these things, to various degrees. Sometimes the past was glorious, relatively speaking (France 1942 springs to mind); sometimes we do need to catch up.

But every new idea still has an element of risk. Nothing has ever been tried and tested in the exact circumstances that we face now, because those circumstances have never existed before. Just because it worked before, or elsewhere, in a situation that we think is similar, is no guarantee. There are only degrees of certainty.

This doesn't mean we can't decide what to do, or that we shouldn't change anything. Not changing things is a plan of action in itself, anyway. The point is that we ought to be willing to try stuff that might not work, our guide to what's likely to happen being the evidence on what's worked before, critically appraised. "I don't know" is not a dirty phrase.

Genes for ADHD, eh?

The first direct evidence of a genetic link to attention-deficit hyperactivity disorder has been found, a study says.

Wow! That's the headline. What's the real story?

The research was published in The Lancet, and it's brought to you by Wilson et al from Cardiff University: Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder.

The authors looked at copy-number variations (CNVs) in 410 children with ADHD, compared to 1156 healthy controls. A CNV is simply a catch-all term for when a large chunk of DNA is either missing ("deletions") or repeated ("duplications"), compared to normal human DNA. CNVs are extremely common - we all have a handful - and recently there's been loads of interest in them as possible causes for psychiatric disorders.

What happened? Out of everyone with high quality data available, 15.6% of the ADHD kids had at least one large, rare CNV, compared to 7.5% of the controls. CNVs were especially common in children with ADHD who also suffered mental retardation (defined as having an IQ less than 70) - 36% of this group carried at least one CNV. However, the rate was still elevated in those with normal IQs (11%).

A CNV could occur anywhere in the genome, and obviously what it does depends on where it is - which genes are deleted, or duplicated. Some CNVs don't cause any problems, presumably because they don't disrupt any important stuff.

The ADHD variants were very likely to affect genes which had been previously linked to either autism, or schizophrenia. In fact, no less than 6 of the ADHD kids carried the same 16p13.11 duplication, which has been found in schizophrenic patients too.

So...what does this mean? Well, the news has been full of talking heads only too willing to tell us. Pop-psychologist Oliver James was on top form - by his standards - making a comment which was reasonably sensible, and only involved one error:

Only 57 out of the 366 children with ADHD had the genetic variant supposed to be a cause of the illness. That would suggest that other factors are the main cause in the vast majority of cases. Genes hardly explain at all why some kids have ADHD and not others.

Well, there was no single genetic variant, there were lots. Plus, unusual CNVs were also carried by 7% of controls, so the "extra" mutations presumably only account for 7-8%. James also accused The Lancet of "massive spin" in describing the findings. While you can see his point, given that James's own output nowadays consists mostly of a Guardian column in which he routinely over/misinterprets papers, this is a bit rich.

The authors say that

the findings allow us to refute the hypothesis that ADHD is purely a social construct, which has important clinical and social implications for affected children and their families.

But they've actually proven that "ADHD" is a social construct. Yes, they've found that certain genetic variants are correlated with certain symptoms. Now we know that, say, 16p13.11-duplication-syndrome is a disease, and that its symptoms include (but aren't limited to) attention deficit and hyperactivity. But that doesn't tell us anything about all the other kids who are currently diagnosed with "ADHD", the ones who don't have that mutation.

"ADHD" is evidently an umbrella term for many different diseases, of which 16p13.11-duplication-syndrome is one. One day, when we know the causes of all cases of attention deficit and hyperactivity symptoms, the term "ADHD" will become extinct. There'll just be "X-duplication-syndrome", "Y-deletion-syndrome" and (because it's not all about genes) "Z-exposure-syndrome".

When I say that "ADHD" is a social construct, I don't mean that people with ADHD aren't ill. "Cancer" is also a social construct, a catch-all term for hundreds of diseases. The diseases are all too real, but the concept "cancer" is not necessarily a helpful one. It leads people to talk about Finding The Cure for Cancer, for example, which will never happen. A lot of cancers are already curable. One day, they might all be curable. But they'll be different cures.

So the fact that some cases of "ADHD" are caused by large rare genetic mutations, doesn't prove that the other cases are genetic. They might or might not be - for one thing, this study only looked at large mutations, affecting at least 500,000 bases. Given that even a deletion or insertion of just one base in the wrong place could completely screw up a gene, these could be just the tip of the iceberg.

But the other problem with claiming that this study shows "a genetic basis for ADHD" is that the variants overlapped with the ones that have recently been linked to autism, and schizophrenia. In other words, these genes don't so much cause ADHD, as protect against all kinds of problems, if you have the right variants.

If you don't, you might get ADHD, but you might get something else, or nothing, depending on... we don't know. Other genes and the environment, presumably. But "7% of cases of ADHD associated with mutations that also cause other stuff" wouldn't be a very good headline...

N. M. Williams et al (2010). Rare chromosomal deletions and duplications in attention deficit hyperactivity disorder: a genome-wide analysis The Lancet