Psychology Research

New Scientist has got a nice feature online where they explain seven touch illusions you can try yourself, with the explanations for how they’re tricking your brain. My favourite is probably the most simple, the ‘Aristotle illusion’: One of the oldest tactile illusions is the Aristotle illusion. It is easy to perform. Cross your fingers, then touch a small spherical object such as a dried pea, and it feels like you are touching two peas. This also works if you touch your nose. This is an example of what is called “perceptual disjunction”. It arises because your brain has failed to take into account that you have crossed your fingers. Because the pea (or nose) touches the outside of both fingers at the same time – something that rarely happens – your brain interprets it as two separate objects. It’s a fantastic little collection and it follows on from NewSci’s recent collection of five auditory you can check out online. Link to NewSci seven tactile illusions.

Philosopher A.C. Grayling has a just-released opinion piece on the New Scientist site arguing that we should regulate armed military robots before they are responsible for, presumably, what would otherwise be classified as war crimes. As we reported in 2007, a military robot has already malfunctioned and ended up killing nine people with gunfire. Grayling notes that military robots are already deployed on ‘active duty’ and that we need to regulate the consequences of an increasingly mechanised military that relies on artificial intelligence technology to engage its firepower. Robot sentries patrol the borders of South Korea and Israel. Remote-controlled aircraft mount missile attacks on enemy positions. Other military robots are already in service, and not just for defusing bombs or detecting landmines: a coming generation of autonomous combat robots capable of deep penetration into enemy territory raises questions about whether they will be able to discriminate between soldiers and innocent civilians… In the next decades, completely autonomous robots might be involved in many military, policing, transport and even caring roles. What if they malfunction? What if a programming glitch makes them kill, electrocute, demolish, drown and explode, or fail at the crucial moment? Whose insurance will pay for damage to furniture, other traffic or the baby, when things go wrong? The software company, the manufacturer, the owner? Most thinking about the implications of robotics tends to take sci-fi forms: robots enslave humankind, or beautifully sculpted humanoid machines have sex with their owners and then post-coitally tidy the room and make coffee. But the real concern lies in the areas to which the money already flows: the military and the police. Link to NewSci piece by A.C. Grayling (via David Dobbs ).

New Scientist has a fascinating article on sleep and mental illness. While it’s long been known that mental illness can disrupt sleep the article discusses the much less explored connection where loss of sleep might trigger symptoms of mental illness in some. Until recently, however, the assumption that poor sleep was a symptom rather than a cause of mental illness was so strong that nobody questioned it. “It was just so easy to say about a patient, well, he’s depressed or schizophrenic, of course he’s not sleeping well – and never to ask whether there could be a causal relationship the other way,” says Robert Stickgold, a sleep researcher at Harvard University. Even when studies did seem to point in the other direction, the findings were largely overlooked, he says. Scientifically, sleep and mental illness have been long linked. Theories of bipolar disorder as a disruption to circadian rhythms have been kicking round for years and treatments that reduce disruption to sleep routines are known to have a therapeutic effect. The NewSci article reviews various studies that suggest sleep problems can increase risk for mental illness, but it doesn’t mention an equally interesting link. We also know that sleep deprivation can help otherwise untreatable mood disorders. For example, missing a night’s sleep can be used as a treatment in depression. Link to article ‘Are bad sleeping habits driving us mad?’.

I was just reading an interesting paper on the interaction between antipsychotic drugs, caffeine and smoking and I found this interesting snippet on how smokers need to take in three to four times more caffeine than non-smokers to get the same effect, owing to the fact that by products of increases enzymes in the liver which break-down caffeine. Byproducts of tobacco smoking, particularly the polycyclic aromatic hydrocarbons, are metabolic inducers. These byproducts are inducers of the [liver enzyme] cytochrome P450 isoenzyme 1A2 ( CYP1A2 ) and of the less understood UDP-glucuronosyltransferases (UGTs).The metabolic inductive effects are not specific to tobacco smoking; they can also be expected from marijuana smoking. Because inducers require the synthesis of new enzymes, several weeks are usually needed before the maximum effects of inducers are seen. Inducers’ effects may take a few weeks to disappear as well…. Additional pharmacologic support of the relevance of smoking’s inductive effects comes from caffeine intake studies. Caffeine, a drug that is more than 90 percent dependent on CYP1A2 for its metabolism and that is widely used in the United States, can exemplify smoking’s effects on drug metabolism. The C/D [concentration-dose ratio] of caffeine appears to be threefold to fourfold as high among nonsmokers compared with smokers. This higher ratio means that smokers need three to four times the caffeine “dosage” as nonsmokers on average to get the same plasma caffeine levels. It turns out that two antipsychotic drugs, olanzapine and clozapine, are also broken down by the same enzyme, so smoking will reduce the effect of these drugs. Hence smokers need larger doses to have the same effect, and patients on these drugs who give up smoking might find a sudden increase in side effects if the dose isn’t dropped. We tend to think of the effect of psychotropic drugs as happening in the brain but drug metabolism happens all over the body with the liver and kidneys being particularly important and having a profound impact on the effect of the compound. Link to ‘Atypical Antipsychotic Dosing: The Effect of Smoking and Caffeine’.

The latest edition of Neuron has a fantastic tribute to the recently departed amnesic Patient HM , “probably the best known single patient in the history of neuroscience”, covering the scientific work he participated in and what it has told us about the structure of memory. The piece is by respected memory researcher Larry Squire and he tackles HM’s personal history while also reviewing his contributions to science through numerous landmark studies. It can be said that the early descriptions of H.M. inaugurated the modern era of memory research. Before H.M., due particularly to the influence of Karl Lashley, memory functions were thought to be widely distributed in the cortex and to be integrated with intellectual and perceptual functions. The findings from H.M. established the fundamental principle that memory is a distinct cerebral function, separable from other perceptual and cognitive abilities, and identified the medial aspect of the temporal lobe as important for memory. The implication was that the brain has to some extent separated its perceptual and intellectual functions from its capacity to lay down in memory the records that ordinarily result from engaging in perceptual and intellectual work. The article is fascinating not least because it dispels a few common myths about HM – such as the original study showed the hippocampus was necessary for memory when HM also had the amygdala and parahippocampal gyrus removed and so it wasn’t possible to say which were most important. It also notes that the original studies over-stated how much brain was removed owing to the basic knowledge of neuroanatomy that existed at the time. Link to ‘The Legacy of Patient H.M. for Neuroscience’. Link to PubMed entry for same.

Folks, it has been a really rough time for Sheril–she may or may not tell the full story herself, but suffice it to say that she has been hospitalized for several days and has only recently been allowed to come home, and this unfortunate turn of events has prevented her from attending the AAAS meeting in Chicago, where she was set to headline at the high profile “Science of Kissing” panel on Valentine’s Day. That’s a very sad missed opportunity; but luckily, Sheril has also done a freelance article for New Scientist about the same subject, which has just come out and which you can read here . A brief excerpt: As natural as kissing seems, it also means swapping mucus, bacteria and who knows what else, so how and why would such a behaviour evolve? Science has been seeking answers for decades. Neuroscientists point to the way it unleashes a flood of neurotransmitters and hormones associated with social bonding and sex. Anthropologists explain it as a relic of mouth-to-mouth feeding from mothers to infants. Others have suggested that kissing conveys important information about prospective mates and so evolved as a guide to mate selection. It has even been passed off as a purely cultural phenomenon since some groups refrain from it entirely…. It’s a fairly brief piece, but it marks her move into real science journalism–and that’s something I want to applaud. I hope you’ll join me–and enjoy the article . Read the comments on this post…

Just a random Casual Friday survey this week. Click here to take survey . As usual, the survey is brief, and should take only a minute or two to complete. You have until Thursday, February 19 to respond. There is no limit on the number of responses. Don’t forget to come back next Friday for the results. Read the comments on this post…

I love when I can talk about science while using words like “testicles” and “cocks”. I really should have gone into something like urology, only then I know people would probably be all serious about it. And where’s the fun in that? Anyway, today’s Weird Science comes to you courtesy of Monica, an awesome reader of the blog at Purdue. Monica found this study courtesy of Dr. John Anderson’s Endocrinology class (Bio 559) at Purdue, which she says was amazingly awesome. I personally think any class devoted entirely to endocrinology would be pretty awesome, and when you add in a paper about testicle transplants in cocks? Heh. Heh. I would have LOVED to take that class. (Side note: should anyone come across a paper that they happen to think is gloriously weird, do drop me a line! I’d love to hear it and it may end up on the blog! I’m always looking for new material.) Berthold, A. “The transplantation of testes” Bulletin of the History of Medicine, 1944. Read the rest of this post… | Read the comments on this post…

Alzheimer’s research is an ongoing field. Although we know a lot more than we used to, we still don’t entirely understand why the accumulation of proteins in Alzheimer’s disease kills neurons or renders them non-functional. One intriguing part of the explanation may be offered by Varvel et al. who show that the active proteins in Alzheimer’s disease (more on this in a second) cause neurons to re-enter the cell cycle in a mouse model of the disease. Read the rest of this post… | Read the comments on this post…

One of the perverse pleasures of spending too much time in airports is getting to people watch. I put on my “anthropologist from Mars” glasses and pass the time by staring at strangers, watching what they eat, read and how they struggle to nap in uncomfortable positions. This morning, while waiting on a very delayed plane in the Portland airport, I watched a woman perform yoga by the gate. But if I really were an anthropologist from Mars I’d be most puzzled by something else that people in airports do: drink lots of diet soda. I write this in the San Francisco airport, where I’m sitting on a bench with five other people, all of whom are sipping some sort of beverage with artificial sweetener in it, from Diet Snapple to Pepsi One. This is a bizarre ritual, no? We’re deliberating duping our tongue, enjoying the illusion of sweetness without the thing that the sweetness is supposed to represent: metabolic energy. What I find most ironic about these diet colas is that there’s good evidence that fake sugar actually leads to weight gain. Consider this recent paper in Behavioral Neuroscience, which found that rats fed artificial sweeteners gained more weight than rats fed actual sugar: Animals may use sweet taste to predict the caloric contents of food. Eating sweet noncaloric substances may degrade this predictive relationship, leading to positive energy balance through increased food intake and/or diminished energy expenditure. Adult male Sprague-Dawley rats were given differential experience with a sweet taste that either predicted increased caloric content (glucose) or did not predict increased calories (saccharin). We found that reducing the correlation between sweet taste and the caloric content of foods using artificial sweeteners in rats resulted in increased caloric intake, increased body weight, and increased adiposity, as well as diminished caloric compensation and blunted thermic responses to sweet-tasting diets. These results suggest that consumption of products containing artificial sweeteners may lead to increased body weight and obesity by interfering with fundamental homeostatic, physiological processes. There’s also some tentative evidence of the same effect in humans: Splenda is not satisfying–at least according to the brain. A new study found that even when the palate cannot distinguish between the artificial sweetener and sugar, our brain knows the difference. At the University of California, San Diego, 12 women underwent functional MRI while sipping water sweetened with either real sugar (sucrose) or Splenda (sucralose). Sweeteners, real or artificial, bind to and stimulate receptors on the taste buds, which then signal the brain via the cranial nerve. Although both sugar and Splenda initiate the same taste and pleasure pathways in the brain–and the subjects could not tell the solutions apart–the sugar activated pleasure-related brain regions more extensively than the Splenda did. In particular, “the real thing, the sugar, elicits a much greater response in the insula,” says the study’s lead author, psych ia trist Guido Frank, now at the Univer sity of Colorado at Denver. The insula, involved with taste, also plays a role in enjoyment by connecting regions in the reward system that encode the sensation of pleasantness. The essential lesson is that the brain doesn’t like being tricked. When you give us sweetness without the caloric energy, we end up craving calories more than ever. Read the comments on this post…