Which is why I was completely flummoxed by a recent Nature headline screaming “Disputed results a fresh blow for social psychology”. The article relates to a recent study published in PLOS ONE, which looked at the concept of ‘intelligence priming’ - that thinking about someone perceived to be smart (or stupid) can affect your performance on an intelligence test. Over the course of 9 experiments, the study attempted to replicate the findings of a 1998 paper by Dijksterhuis and van Knippenberg, and the results all pointed towards intelligence priming providing no advantage in subsequent intelligence tests (i.e. in contention with the original results). I’m not going to go into the nitty-gritty of the specific studies - if you’re interested, it’s worth reading the paper along with responses in the comments. But there are two points to note here. One, as already mentioned, is that replication studies are important, and should be forming a huge part of scientific research - so it’s a good thing that this study was conducted (and published). The second is that one failure to replicate does not constitute a death blow for a particular theory.

To echo Gary Marcus’ recent post on the matter, social psychology does not equal priming, and priming does not equal social psychology. To say that one failure to replicate one particular phenomenon is a blow for the entire field is disingenuous, and tarnishes the many admirable attempts currently being made to not just turn psychology around, but also to lead the way in reforming scientific research practices. Initiatives like the Reproducibility Project, Cortex’s Registered Reports (which went live this week), and BMC Psychology’s open access approach to reviewing are all shining examples of the positive and beneficial moves currently being made.

Perhaps another, more worrying problem, is the association between failures to replicate and fraud. Again, to be clear on this, there are two completely separate conversations to be had. One is the need to replicate psychological studies to determine whether the effects we see are genuine and robust. The other is whether questionable research practices (QRP) are leading to over-inflated and erroneous results. Again, others have gone into excellent details on these matters recently, but it’s worth remembering that this isn’t a two-way street. Replication is part of the answer to preventing or discouraging QRPs. QRPS are not an inherent part of failures to replicate. In my opinion, to discuss any failure to replicate with specific reference to the fraud of Stapel and Smeesters, as the Nature article did, unfairly and unnecessarily calls into question the integrity of honest researchers.

In short, I don’t think every failure to replicate a study is news-worthy, and I certainly don’t think it helps anyone to persistently link such failures to extreme cases of fraud. Many psychologists are actively trying to reform the field in innovative and interesting ways, for the benefit of everyone. Let’s concentrate on that being a positive thing.

She's on Twitter as @trufflesquirrel and blogs about life as a PhD student at: http://squirreledthoughts.wordpress.com/

The way researchers, clinicians and society think about child mental health problems is constantly evolving as we discover and come to understand more about the nature of human mental health. This is a particularly topical issue with the forthcoming release of the DSM-5, the latest version of the Diagnostic and Statistical Manual, which is a book used by psychiatrists to diagnose mental health problems across the lifespan. One fairly subtle change which we can expect to see is the removal of a restriction under attention deficit hyperactivity disorder (ADHD). Under the current version of the manual (the DSM-IV), ADHD cannot be diagnosed in the presence of a pervasive developmental disorder (which is an umbrella term for autism spectrum disorder (ASD) and related conditions like Rett’s syndrome).

Why this restriction was in there in the first place is not entirely clear, except that it was assumed that if a child has ASD, their social and communication deficits and stereotyped behaviours somehow account for any problems they might show with hyperactivity, impulsivity or attention. The difficulty with such a restriction is that the children with ASD who do have problems with hyperactivity, impulsivity or attention might not get any treatment for these, if they were not also diagnosed with ADHD. Unlike with ASD, medications (particularly stimulants, like the well-known Ritalin) are actually frequently quite effective in lessening the behavioural and attention difficulties associated with ADHD. So being able to diagnose and treat both problems should be a change for the good.

Indeed, the rate of ADHD problems in children with ASD and vice versa is a lot higher than just the rate of ADHD or ASD in the general population. But because of the restriction under DSM-IV, so far not a huge amount of research has gone into trying to understand the relationship between these different but co-occurring conditions.

I chose to study this topic for my PhD, in the hope that I could learn more about children who have both ADHD and ASD problems. I started by looking at a large sample of children who had been diagnosed with ADHD, which had been recruited from around the UK (mostly Wales) over a number of years (see here for some background information on the study). In fact, before I started my PhD, I helped to collect data from some of the final families to take part in this study. Parents completed a fairly lengthy interview about their children’s ADHD problems and also about other difficulties, namely behavioural problems (such as stealing or fighting), anxiety (for example fear of separation from parents) and depression (for example low mood or self-harming). Parents also filled out some questionnaires, including the Social Communication Questionnaire, which asked 40 questions about autistic traits, and others which asked about children’s language and motor abilities (such as when they started walking and talking). Meanwhile, the children completed a battery of tests, including an IQ test to assess cognitive abilities and some reading and spelling tests.

Unlike in many studies researching ADHD and ASD, we did not collect data from typically developing children. This is mostly because the sample was recruited for a genetic study of ADHD and we already had control genetic data from the population (thanks to an international collaboration with other researchers). However, given the amount of information collected, the sample provides us with exciting opportunities to address many other interesting questions too. So instead of comparing the children with ADHD to their typical peers and looking for group differences, we looked at variation within the ADHD sample. In total, there were 711 children whose parents completed enough of the interview and questionnaires for us to be able to analyse the data they provided.

What we found is that the more autistic traits children had, the more severe their ADHD symptoms were. What’s more, even after accounting for how severe their ADHD was, more autistic traits predicted more anxiety and behavioural problems, as well as more cognitive difficulties (particularly working memory problems) and a greater chance of having language and motor delays. There was no relationship between autistic traits and reading or spelling abilities in these children with ADHD. Although autistic traits also predicted more depressive symptoms, these were actually accounted for by the greater rate of ADHD symptoms (that is, more severe ADHD predicted worse depression symptoms and so autistic traits only really predicted more depression by virtue of being related to ADHD severity).

One important point to mention about the study is that although we looked across a wide range of ages (from 5-18 years) we can’t draw any conclusions about cause and effect because we looked cross-sectionally (that is, only at a single time point in each child’s life and not across time). Also, although we found a general pattern that more autistic traits indicated more of the other problems, not all children who had autistic traits had these other difficulties.

Based on these results, we concluded that it is important for clinicians assessing and diagnosing a child with ADHD to also be actively aware of the child’s social and communication abilities and to determine whether they display any stereotyped or repetitive behaviours. The presence of such autistic traits may be a marker of greater symptom severity and possibly additional, more complex needs. Our results also support the change in the DSM-5, which will allow a dual diagnosis of ADHD and ASD in a child, hopefully resulting in more research into and support for both sets of problems in children.

This research has been published today in European Child and Adolescent Psychiatry, where I am pleased to say it is available Open Access (a requirement of the Wellcome Trust who funded the study). I will also be presenting it as a poster at the upcoming International Meeting for Autism Research next week (poster session on May 4^th). As my PhD continues, I hope to find out more about how ADHD and autistic traits relate to one another and what the common risk factors for these problems might be.

Screen time, as I’ve banged on about before, is a fairly simply concept - the number of hours per day some sort of screen-based technology (smartphone, TV, computer, games console) is used. There are lots of studies out there (mostly based in the US), that look at long-term data on the effects of screen time, and have found all sorts of things - for example, it’s been associated with obesity, reductions in hip bone mineral density in girls, more aggressive and antisocial behaviour, and problems in educational performance. And, as I’ve banged on about before, people like Aric Sigman have produced opinion pieces selectively citing some of the more worrying outcomes of these studies, arguing for limits to be imposed (2 hours max) on the amount of time that kids spend using screen-based technology.

This week, a new study has come out in the Archives of Disease in Childhood, looking at the effects of watching TV and playing video games on childhood development in the UK. This is excellent news - one thing that I’ve noted as a problem with previous arguments about imposing limits on screen time is that there are studies out there suggesting that legislation that might work in one country might not necessarily work in another. So it’s about time that we got a decent handle on what’s going on in the UK. This new study, by researchers at the MRC’s Public Health Sciences Unit (PHSU) at the University of Glasgow, paints a rather more balanced picture than some people would have you believe.

The study used data from the Millennium Cohort Study, which is a prospective study of children born in parts of the UK between September 2000 and January 2002. A prospective cohort study is a type of observational study where lots of people (over 11,000 in this case) are followed over the course of their lives, and are assessed at various time points (in this case 9 months, 3, 5 and 7 years) to collect information on a wealth of topics - everything from what they do in their spare time, to how they’re performing at school, to what’s going on in their family home life. The idea is that you can plan to look at various sorts of outcomes, and so take as much relevant information as possible to see which factors are most important in influencing said outcomes. For example, say you’re interested in factors associated with the development of depression, and maybe you suspect that eating sprouts is a major cause. The best way to test for this would be to take two sets of people that don’t differ from each other in any way, except that one set is given sprouts and the other is given fake sprouts (a placebo), and see whether more people are diagnosed with depression in the sprout group than in the fake sprout group. However, for obvious reasons you can’t do this in real life - it’s completely unethical to deliberately expose people to things that you suspect cause diseases or disorders (sprouts, as far as I know, aren’t associated with depression, but they do taste awful). What you can do instead though, is take a massive group of people, some of whom will eat sprouts anyway (lord knows why), and see whether those people, after controlling for as many other factors as possible, end up with a higher risk of developing depression than people who don’t eat sprouts. That’s a prospective cohort study.

The PHSU study used this type of data set to look at whether watching TV or playing video games at age 5 was associated with behavioural or emotional problems at age 7 - things like hyperactivity, peer relationship problems, conduct disorder, that sort of thing. The important thing is that they controlled for quite a wide range of potentially confounding factors - things like sleeping difficulties, health, family socioeconomic status, the mum’s mental and physical health, frequency of parent-child activities, and the wonderfully-named ‘confusion, hubbub and order scale’ - a measure of ‘household chaos’.

The results are complex. Initially, for those children that used either TV or video games for more than three hours a day, there was an association between this amount of screen time and increases in all of the problems assessed. However, this result pretty much disappears when you include all of the above covariates (and more) in the analysis - the only association that remains significant is between TV viewing and conduct disorder. In other words, taking lots of things into consideration, 5 year olds who watch TV for more than three hours a day were no more likely than others to develop emotional or peer relationship problems by age 7, but they were slightly more likely to develop aggressive behaviours. Video games, conversely, almost seem to have the opposite effect - children who played games for less than an hour a day were actually less likely to show problems than those who play no games at all. For children who play games or watch TV for between 1 and 3 hours a day, there don’t seem to be any consistent or significant effects.

Now, there are a couple of problems with this study. The main one harks back to this generalised concept of screen time - we don’t know what types of games these children were playing, or what type of TV they were watching. Presumably, for outcomes like conduct disorder (i.e. aggression), we might expect to see a greater effect of violent media than, say, watching Teletubbies or playing My Little Pony sudoku. As a result, we don’t know whether the children who watch more than three hours of TV are watching qualitatively different types of programs than those who watch less than three hours.  This also introduces a hidden confound into the data - you might also expect that those children with poorer scores on measures like the ‘household chaos’ questionnaire might also play or watch systematically different types of media than those that have more positive scores. Arguably, in a more structured and positively family environment, parents may be more likely to heed to things like film or video game age classifications, making it less likely for those children to be playing violent video games or watching movies inappropriate for their age. With a measure as generalised as screen time, we simply don’t know.

At any rate, this study is a promising first step in providing a balanced, data-driven view of the effects of modern technology on childhood development. In May of last year, Aric Sigman was quoted in various news outlets as suggesting that the parents who constantly use screen-based technology around their kids are guilty of neglect, and that more than two hours a day of TV or video game use should be banned. What we see in this present study, is a complete lack of evidence to back that claim up - we don’t see consistent negative problems in those children who watch TV of play games for between 1 and 3 hours per day. Even for those who spend more time than that, the results aren’t anywhere near as catastrophic as some would suggest. But the results also show how we need to go beyond this vague notion of ‘screen time’, and start to discuss more nuanced, detailed aspects of video game and TV genres. Childhood development is complex; likewise, our concepts of what affects it need to show complexity.

Luckily, the chemical’s curious properties were rediscovered, again by accident, in 1945. Dr Erik Jacobsen was a researcher based at a pharmaceutical company in Copenhagen. After the war, he became interested in medicines that could counteract scabies and intestinal worms, developed by British researchers earlier that decade - medicines that contained disulfiram. Taking a somewhat risky approach to testing new drugs, Jacobsen was known for administering new drugs to himself. The Dec 6, 1949 issue of Time details what happened next:

“One night before going to a dinner party he swallowed a couple of pills made of tetraethyl-thiuram-disulfide; they were supposed to be good for intestinal worms. To his surprise, Dr. Jacobsen found that any form of alcohol revolted him. When he sipped even a small glass of beer, his face got red, his heart started to pound and he had trouble getting his breath.”

Jacobsen unwittingly had rediscovered the deleterious effects of disulfiram on alcohol. Over the course of the next few years, he studiously laboured over developing the drug now known as ‘antabuse’, used in the treatment of chronic alcoholism.

The story of disulfiram echoes the story of many other drugs, especially in the early days of pharmaceutical development. Serendipitous situations, happy accidents, and lucky coincidences all contributed to the discovery of treatments for a wide range of problems. Iproniazid, the first antidepressant, was originally used in the treatment of tuberculosis, until doctors and researchers started to notice that it also seemed to make people much happier. Chlorpromazine, a drug used in the treatment of schizophrenia, was originally trialed as a treatment used to reduce shock during surgical procedures. Potassium bromide has a somewhat stranger history, in that it was used as an effective treatment for epilepsy, but for all the wrong reasons. Sir Charles Locock is generally credited (although there is disagreement) with noting a link between the administration of bromide and a reduction in sex drive. At the time (the 1850s), masturbation was regarded as major cause of epilepsy, so Locock theorised that by reducing sexual drive, the seizures associated with epilepsy would be abated. Of course, we know now that there’s no such link between epilepsy and masturbation, yet by happenstance, bromides still seemed to be effective, and were used to treat epilepsy well into the 20^th Century. But the story of drug development doesn’t just stop at serendipity. If it did, pharmacology - and science in general - would be all over the place. What should always follow is scientific rigour and strictly controlled, incremental study. As the story of John Cade explains, without that rigour, you might just miss something important.

Cade was an Australian physician, graduating from the University of Melbourne in the early half on the 1930s. Although he specialised as a psychiatrist, when he joined the armed services as a Captain in 1940, he served has a surgeon. Luck was not on his side though, and after the fall of Singapore in 1942, he spent the rest of the war as a prisoner in Changi Prison. During his time there, Cade noticed a pattern emerging: following the death of fellow prisoners who suffered from psychiatric illness, post-mortem examinations revealed they all had internal physical abnormalities, such as tumours. After the end of the war, Cade returned to Australia to once again practice as a psychiatrist, and began to search for the presence of toxins in the urine of manic patients that might belie a physical cause. His studies, rather gruesomely, involved injecting guinea pigs with the urine from patients with various forms of psychiatric illness, including mania, and noting the toxicity of each. After trial and error, he eventually hypothesised that it was the presence of uric acid that appeared to be enhancing the toxic effects of urine.

Isolating and administering uric acid was not a trivial task, as it wasn’t soluble in water. Through an apparently happy accident, Cade mixed the acid with lithium salt in order to help it to dissolve, and subsequently tested the new solution. Surprisingly, instead of enhancing the toxicity of the uric acid, the compound - lithium urate - reduced it. Now, in some biological psychology textbooks, the story then goes that Cade also noticed that administering the solution resulted in the relief of mania and depression in human patients, and that for a time, Cade mistakenly believed it was the uric acid that was the cause. However, this version of events is somewhat unfair; by all accounts Cade was a meticulous man. After discovering the counterintuitive effects of the lithium urate solution, he instead used lithium carbonate, and again noted the same effects. So very early on in the process, and as any rigorous scientist would do, he isolated the separate compounds in order to systematically determine where the true effect came from. The result was the development of lithium as the first - and still one of the most widely used - treatments for bipolar disorder.

In a way, stories like those of Cade and Jacobsen paint a lovely picture of how research, in reality, often works. Yes, sometimes there are happy coincidences, and chance encounters, and sometimes they’re critical to new discoveries. But on their own, they’re meaningless. Without the years of rigorous work that follow them up (or in some cases precede them), like Williams’ account of disulfiram, they become consigned to forgotten history books.

Ingredients: eight carbon atoms. Eleven hydrogen atoms. One nitrogen atom. Two oxygen atoms. Mix together well, and bake for 45 minutes at 200 degrees or gas mark 6. For news stories, add a healthy dose of controversy. Best served with a pinch of salt.

Dopamine, at face value, is a pretty simple little chemical. What is surprising about it is how complex and varied its effects are on the body. When introduced to the kidneys, it can have a diuretic effect. It can be used to increase heart rate and blood pressure following heart failure. More commonly, it is implicated in various motivational and attentional processes in the brain – but even there, the story is not so simple. As Vaughan Bell has recently and brilliantly pointed out, dopamine can have varied – even opposite – effects, depending on the receptor it is interacting with. It can have different effects depending on the area of the brain it is activated in, and it can sometimes have different effects in the same brain area. What is perhaps also surprising then, is how this wonderful complexity gets completely lost in any news story that involves dopamine.

Back in January, an article appeared on the Forbes magazine website called “Addicted to bang: the neuroscience of the gun” (protip: guns don’t have a nervous system, and there aren’t any guns in our nervous system, so you can’t have a ‘neuroscience’ of it). Of the effects of dopamine on addiction, it had this to say:

“First, because the human brain evolved in an era of immediacy—when threats and rewards were of the lions, tigers and food variety—the dopamine circuitry has an inborn timing mechanism. If the reward follows the stimulus by roughly 100-200 milliseconds, it’s sitting in dopamine’s sweet spot. Firing a muzzle loader—for example—would certainly release dopamine, but it takes too long between multiple firings for a significant reward loop to be created. Firing an automatic weapon, though, sits close to the sweet spot—an assault weapon can fire a round every 100 milliseconds. Meaning not only are guns addictive, but automatic weaponry is far more addictive than most.”

So in other words, every time someone fires an automatic weapon, through the actions of dopamine as a reward chemical, they become increasingly and incrementally addicted to it. It plays well into the popular conception of ‘reward’. Usually when we think of reward, we think of something nice – you do a good deed at home, and to incentivise that behaviour, you get a chocolate. In the popular press, this is where the story for dopamine ends; something nice happens, which causes a flood of dopamine, which reinforces the behaviour and makes it more appealing. The more this happens, the more dopamine gets released, and the more likely you are to become addicted. It’s a neat and tidy, simple story, that sounds serious and probable because it involves a neurotransmitter that we know lots about.

The trouble is that because brains are really complex, there’s never going to be a one-to-one mapping between a particular neurotransmitter and a particular function or behaviour. Ed Yong’s response to the article put it best when he said it was a story about “derpamine” - dumbed down and stupid. So while we do know a considerable amount about dopamine, the effects that it has (even on motivation and addiction) are not simplistic. Scicurious has recently and eloquently explained research looking at how dopamine can also be released when you’re just expecting something nice to happen. And as John Salamone and Mercè Correa highlight in an excellent review article, it is also involved in ‘aversive’ motivations – in other words, the need to avoid things that you find unpleasant. And yes, dopamine can in some cases be considered to be a ‘reward’ chemical, but the caveat here is that there doesn’t appear to be any consensus in the scientific literature about what reward specifically means.

So all of this is going to be confusing to someone encountering dopamine for the first time, but the answer to that is not, as so often happens in the media, to dumb the story down. However, the reason for the sheer number of poor neuroscience articles out there goes deeper than that. In part, it’s because simple stories are more enticing than convoluted ones. It’s also, I think, because there’s a reluctance among the scientific community to engage people in difficult, complex issues, particularly about the brain – and this is a real shame. There are some fantastic people like Vaughan Bell, Scicurious and Neuroskeptic, who are doing a great job of explaining neuroscience in an interesting, engaging, and (critically) accurate manner, and it would be brilliant to see more researchers try their hand at it. It may not necessarily stop the onslaught of wishy-washy, “dopamine = pleasure”-type articles, but reactive and intelligent blogging can certainly help to redress the balance.

On the 14^th March, SpotOn is hosting a session on ‘Communication and the Brain’ that will look at the challenges of explaining various aspects of the brain to the public, and I sincerely hope that the session inspires more neuroscientists to take up blogging. Part of the answer to those challenges is to be honest, and not feel the need to oversimplify research to the point that it’s basically wrong. Much the opposite, in fact – for example, the complexity of dopamine’s story highlights just how cool this simple little neurotransmitter is. Think about it for a second. Isn’t it amazing that a single chemical can have such profound and widespread effects on the brain and human behaviour – everything from motor control, to heart rate, to motivation? To me, that’s much more interesting than tediously mapping it onto a single function and not giving it a second thought.

Your project’s been featured on gaming websites like WoW Insider, which is pretty amazing! What’s the response from the gaming community been like? Has it helped?
The majority of people who donated to my crowdfunding project were from the gaming community. I marketed that project specifically to get gamers interested in showing the positive side of the community. I had a really great response from gamers who have autism themselves, have children with autism, or know someone with autism. The feedback that I received from the gaming community was overwhelmingly positive.  The biggest spikes in my crowdfunding progress happened on days that WoW Insider highlighted my research project. I’m incredibly thankful for their publicity.

Have you met any resistance or negativity from anyone with regards to incorporating video games into research?
Over the last few years, there has been an explosion of interest in the use of games for improving health and education outcomes. The autism research community in particular has actually been slow to adopt this growing trend. The research field as a whole is starting to be much more accepting of “gamification” processes for improving learning and health outcomes.  Public figures in gaming research, such as Jane McGonigal and Daphne Bavelier, have done a really great job of opening the door for other researchers to get into educational game design. At Penn State, there are two different centers that promote innovation and gamification in research, including the “Educational Gaming Commons”. So, the autism intervention game that we are developing is just a natural extension of research interests at Penn State and beyond.

How has your gaming background helped in developing the project? Do you think it’s something you could have developed without being a gamer?
My gaming background is the reason why I am working on creating a game for individuals with autism. I am working with Dr. Scherf (an autism researcher with no gaming experience) and Dr. Smyth (a researcher who has created educational games, but has not previously done autism research).  As someone who has both the autism research and gaming experience, I’m able to draw on a really unique mix of skills and expertise. Game design is a much different process than the traditional approach to making computer-based interventions. Most existing interventions tend to stick the reward piece from games onto existing tasks that are boring and repetitive, but they don’t really have a plot and storyline. Imagine an intervention task where you have to identify what people in the computer task are looking at. You complete one of these trials and identify that the person is looking at a cup, and you receive your reward (“Good job! You earned 10 points! The girl was looking at a cup!”). This “game” may involve 20 to 100 trials of doing the same thing. The computer says: “Good job! You earned 1000 points! The girl was looking at a plate!” and by the end of 100 trials, you are probably thinking, “Who cares if she’s looking at a plate or a cup? Are we done yet?”). However, good game design isn’t just about rewarding you with points for doing something boring. Good game design is about building intrinsic motivation, so that you want to do the task because you enjoy being part of something that feels “epic”. For example, the quests in World of Warcraft that people enjoy the most are ones that have very strong ties to the storyline and plot in the game. You don’t care about collecting fifty fish heads. You care about slaying the dragon and saving the world, or stopping a plague from killing the town. So, imagine now that the same eye gaze training task is now a detective-themed game providing a storyline and plot for essentially the same task of identifying what object people are looking at. In this case, correctly identifying the cup item logs this into evidence as clues to solve a bank robbery (there is a fingerprint on the cup, likely that of the bank robber!) and the reward for identifying 10 clues was arresting the robber (Congratulations! John Doe, leader of the biker gang is now locked up in prison and can’t terrorize the banks of the city anymore!). Once you have arrested 10 criminals, you are promoted from a cop to a detective. This second “game” draws on really important elements of game design that aren’t obvious unless you have played games such as World of Warcraft and have an understanding of what drives people to spend seven or more years of their life playing this type of role-playing game.

I really appreciate Elisabeth taking the time out to talk to me about her research, it sounds incredibly exciting, and I wish her the best of luck with it. I can't wait to see the results!

Well, it's not. Not according to the press release on which the story is based, anyway - it doesn't mention children once. The only data in the story are from a commercial report from Childwise last year (all yours for the princely sum of £1800), and that doesn't mention cancer anywhere. The Mirror manages to further bungle information from the report - we're told that "With the sort of technology now available, children are spending more time in front of a screen than ever", alongside a graphic that, actually, shows pretty much no increase in the average time watching TV, spent online or spent on a console between 2002 and 2012. Even more strangely, the graphic that the Mirror chose to use online shows a drop in the amount of time spent online per day between 2002 and 2012, compared to the one in the print version. Or is that time spent watching TV? Who knows?

Online version (top), print version (bottom)

Annoying niggles aside, the story is basically a misinterpretation of some quite sensible information from the World Cancer Research Fund. Their original press release highlights the very real link between sedentary behaviour and its association with obesity, type-2 diabetes and heart disease. In turn, obesity increases the risk of developing cancer. It's not just an issue for children - anyone at any age who engages in too much sedentary behaviour is at risk. And that's a problem for many adults today, who spend a good proportion of the day working at a desk, or sitting at home watching TV in the evening. The WCRF press release offers a bit of advice on how to break up long periods of doing nothing, such as getting up to speak to co-workers or to get a drink every so often, and basically not turning into a couch potato as soon as you get home. For more sensible advice, check out the Cancer Research UK website here.

The press release is fairly straightforward and unambiguous in the message it's trying to get across. So how did the Mirror manage to mess it up so badly? Enter Professor Mitch Blair, Officer for Health Promotion at the Royal College of Paediatrics and Child Health. "Whether it's mobile phones, games consoles, TVs or laptops, advances in technology mean children are exposed to screens for longer amounts of time than ever before" says Blair (er, see above graphics)."We would also advise restricting prolonged periods of screen time and recommend less than two hours a day in total", he goes on to say.

Screen time. 2 hours a day. RCPCH. If any of these are ringing any bells, that's because they were all in the news last year, when Aric Sigman gave a guest lecture at the RCPCH's annual conference in Glasgow. I wrote about it at the time, and again a few months later when Sigman had an opinion piece published in the Archives of Disease in Childhood (the RCPCH's flagship journal). The recommendation that children spend no more than 2 hours a day comes from that piece, and is based on guidelines being issued in other countries on the matter. As I mentioned in my blog, this ignores research suggesting that guidelines that are issued for one geographical location won't necessarily work all that effectively in another.

Now, to be fair to Blair, he doesn't mention a link between cancer and watching TV or using computers. But why the RCPCH is involved in this piece is absolutely beyond me.  More worrying is this continuing trend for the RCPCH to apparently want to be associated with sensationalist headlines, cherry-picked information and misinterpretation of data. Are all of these stunts calculated, or are they simply spectacular PR fails? Either way, it seems like someone at the RCPCH needs to start asking serious questions about why this is happening. If it's deliberate, then shame on them. As Ben Goldacre so eloquently puts it, integrity is easy to spend on a few minutes of fame, but much harder to earn back.

"We recently came across a new book, Pole Positions - The Polar Regions and the Future of the Planet, by Daniel Snowman. Then, a couple of weeks later, we received a copy of London Under London - A Subterranean Guide, one of the authors of which is Richard Trench. So it was interesting to see Jen Hunt of the University of Manchester stating in the October issue of The Psychologist: "Authors gravitate to the area of research which fits their surname." Hunt's example is an article on incontinence in the British Journal of Urology (vol 49, pp 173-176, 1977) by A. J. Splatt and D. Weedon."

So over the past year, I've been collecting the finest examples of nominative determinism that I could find from the academic literature. Here are some of the ones I liked the most:

• "Childhood proactive and reactive aggression: Differential risk for substance use?" by Fite et al. Aggression and Violent Behaviour.
• "High-performance polymer solar cells with a conjugated zwitterion by solution processing or thermal deposition as the electron-collection interlayer" by Sun et al. Journal of Materials Chemistry.
• "The evolving epidemiology of HIV/AIDS" by Doctor de Cock et al. AIDS.
• "Heat transfer to foods: ensuring safety and food microstructure" by Fryer et al. Journal of Heat Transfer.
• "Passive resting state and history of antagonist muscle activity shape active extensions in an insect limb" by Ache et al. Journal of Neurophysiology.
• "Why we need to be righteous" by Haidt et al. New Scientist.
• "Does anonymity increase the reporting of mental health symptoms?" by Fear et al. Journal of Epidemiology and Community Health.
• "A solid base to build on" by Water. Nursing Standard.
• " The effect of dry cow antibiotic with and without an internal teat sealant on udder health" by Failing et al. Journal of Dairy Research.

And probably my favourite:

• "Reflections on sixty years of solid state chemistry" by Goodenough. Journal of Inorganic and General Chemistry.

Have a wonderful Christmas and New Year. See you in 2013.

You may have heard that the world is ending this Friday. We don't know how, or when precisely - those damn dirty scientists know, but they're not telling us. But we do know that it's all because of the Mayans. As everyone knows from high school history, the Mayans were a group of people who lived about 20,000 years ago in what is now known as Sheffield, and had amazing powers over life, the universe and everything. They were responsible for a lot of innovations that we simply couldn't live without today: things like chocolate, paper, suitcases, and Jonathan Ross. They also invented the calendar, but I think they got tired of generating new dates after getting to December 21, 2012, so they stopped. And that's why the world's ending. Way to go Mayans.

Now, some of you may be asking "Pete, how do I survive the end of the world??!" Well, you can't - the clue's in the name. But that doesn't mean that we can't prepare ourselves as much as possible! Here are some handy tips and hints to help make your last few days before the apocalypse as easy and as stress free as possible:

1. PANIC

It's the END OF THE WORLD, you idiot! Why are you not panicking?!

2. Stock up

Ahem, sorry about that last one, but I needed to get it out of my system. Right, as in any disaster, it makes sense to be prepared. For the end of the world, that means you need to BUY ALL THE THINGS. Seriously, buy everything. For food, you're going to want to buy as much fresh fruit and veg as you can find, because it's tasty and nutritious. But don't forget the other things - sure, you want toilet paper (lots) and toothpaste, but don't forget things like cheese graters (which double up as elbow protectors) or mobile phone cases too (everything needs protection!). If you buy anything online, remember to order it for next day delivery - we can't be sure the postal service will be functioning noticeably differently come Saturday.

While we're at it, have you done your Christmas shopping yet? If you haven't, don't worry! Why not stick it to the apocalypse and have Christmas early this year? Here's my handy list of Christmas stocking fillers to help your loved ones survive the end times:

1. Plasters: Chances are, someone's going to have a boo-boo on Friday. You'll need some plasters to fix them up.

2. Zippo lighter: For holding up at the inevitable U2 benefit concert we'll see in the aftermath.

3. Something to read: There's not going to be much to do after the world ends. Buy them Ben Goldacre's new book, Bad Pharma, so they can comfort themselves in the knowledge that all of those evil drug companies have been destroyed by the Mayans.

4. Bear Grylls: He'd be useful in an apocalypse, and I'm sure he'd fit in a stocking. Be sure to give him some breathing holes (not too many though, he might get out of one of them).

3. Stop buying Mayan products

We might still be able to stave off the end times - all we need to do is economically ruin the Mayans before it's too late. According to this website I just read, the Mayans traded in all sorts of things - fish, squash, potatoes, corn, honey, toys, jewellery, and so on. Don't buy any of that stuff. Apparently they also traded chocolate too, so stop opening your advent calendars and stick it to the Man! Er, Mayan. Toys are a bit of a bummer though, but the kids are going to have to learn how to compromise. Apparently the Mayans also had an important service sector which included mathematicians, so we need to either stop adding things up, or solve all of the equations we've not figured out, AND FAST. Thankfully, Simon Singh's already on the case, so go get his book too.

4. Get another calendar

This is it. I've cracked it. The Mayans weren't the only ones to make calendars, you know. We've been making new ones for literally years! Go out and buy a new calendar before it's too late - preferably one that has dates after the 21st December in it. We can do it if we all work together! Stuck for suggestions? Go and buy the ScienceGrrl one. If you do, you might just save us all.