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ResearchBlogging.orgThe title of this post is a somewhat obscure reference to an episode of the Nineties Sci-Fi show “Sliders“.  The premise of the show was based on the Multiverse theory in physics, a favourite trope in science fiction.

In “Sliders” a small group of individuals are accidentally set adrift in the multiverse, travelling from Earth to Earth in the hopes of getting home again. The show gave a unique opportunity to explore interesting historical counter factual situations, you know, of the “What if Hitler won the war” variety.

This was handled a little unevenly throughout the 5 season run of the show and some episodes were definitely more plausible than others. One of the less plausible ones sprang to mind when I read this press release a couple of months ago*.

In this episode the intrepid inter-dimensional explorers find themselves on a world where a fat-loss pill turns it’s users into mindless fat craving monsters – coincidentally resembling movie zombies. Cool huh?

Okay, so that isn’t likely to happen. But in a world where approximately a fifth of the population is overweight and a majority of the world populace has more to fear from over rather than under-eating the focus on obesity and methods to combat it is only going to grow. The solutions to obesity likely will need to be multi-pronged, each facet adding an incremental advantage. With this in mind medical solutions have their place alongside education, social and legislative approaches.

One of the medically based avenues open to us is to regulate the activity and/or amount of brown fat in our bodies.

Brief biology lesson: Humans (and other animals) have two main types of fat cell; brown and white. White fat is the regular old fat that we think of, know, and loath. It contributes to unsightly cellulite, increases our risk of various diseases that kill us and is generally something that you want to only have in moderation.

Brown fat on the other hand is a slightly different beast. Like white fat it is a repository of energy, but unlike white fat it is not simply a passive receptacle for these lipids1. Brown fat gets it’s colour (and hence name) from the high density of mitochondria in the cells. The presence of such high numbers of mitochondria allows the cells to channel the force, oh wait that’s a different organelle, sorry. They mean that the cells can burn energy and contribute to thermal regulation, what’s known as Non-shivering thermogenesis.

This type of heat regulation is most important to infants and it was thought that as we grew and matured the brown fat disappeared. This is now known not to be the case, further, manipulation of brown fat in adults may give us a means to burn extra calories and hence reduce our white fat.

Another paper released last year attempts to give a detailed background of the possibility of manipulating brown fat for the purpose of weight regulation. It also notes the potential benefits and drawbacks of this approach and is a very interesting read. Essentially though the idea with utilising brown fat is to increase the body’s basal metabolic rate (the amount of energy you consume while at rest), by doing this we can increase the total number of calories used by the body and effectively burn up the excess calories consumed.

The press released that sparked this post is related to a paper presented at The Endocrine Society’s 93rd Annual Meeting in Boston. It details an investigation into the location of brown fat in the adult body and the mechanisms involved in the creation of brown fat from undifferentiated progenitor fibroblast cells. The fat tends to be deep within the adipose tissue of the neck and chest as well as mixed in with white fat, hence the thinking that we lost it as we age – it’s not easy to find. This incremental step in understanding gives us another tool that may be used to increase our proportion of brown fat cells and thus increase our metabolic capability.

Previous work by the same lead author has correlated amount of brown fat with BMI, finding an inverse relationship. The implication here is that a larger amount of brown fat does contribute to a higher metabolic rate and there for allows some individuals to avoid long term accumulation of fat, confirming that this is a potentially viable approach to weightloss. The numbers of this study were pretty low though and I’m not sure how clinically relevant this finding is.

The authors caution however that benefits may be modest, the lead author is quoted:

“As powerful as brown fat could be at burning calories, we can easily out-eat the benefit.”

So don’t be looking at this as a panacea for obesity, as noted above we will likely have to tackle this problem from multiple sides. Those who view our increasing dependence on drugs and medical interventions with suspicion may not be happy with treating obesity in this fashion2, but it is such a growing problem we should use every tactic at our disposal to reduce the risks associated with this threat to our health.

So, bring on the human experimentation and lets hope the reducing of people to vacant fat-starved cannibals is kept to a minimum.

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Cypess, A., Lehman, S., Williams, G., Tal, I., Rodman, D., Goldfine, A., Kuo, F., Palmer, E., Tseng, Y., Doria, A., Kolodny, G., & Kahn, C. (2009). Identification and Importance of Brown Adipose Tissue in Adult Humans New England Journal of Medicine, 360 (15), 1509-1517 DOI: 10.1056/NEJMoa0810780

Tseng, Y., Cypess, A., & Kahn, C. (2010). Cellular bioenergetics as a target for obesity therapy Nature Reviews Drug Discovery, 9 (6), 465-482 DOI: 10.1038/nrd3138

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* Yes, I really am that lazy.

1. Yes again, I know that’s a gross over simplification. White fat does stuff too.

2. I have no evidence of this but I’m sure they’re out there.

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Suicide is a sensitive subject, by it’s very nature it seems we are obliged to treat it with kid gloves. In public it is virtually taboo to even mention suicide, in news media euphemisms are employed in order to avoid explicit use of the “S” word. Attitudes are beginning to change, with more vocal discussion about mental illness and euthanasia in both this country and abroad.

One of the key issues is whether a person is capable of deciding to end their own life or if such a decision automatically excludes them from the definition of mentally competent. I found myself pondering these things as I attempted to come up with a way to introduce the research that is ostensibly the focus of this post.

Regardless of your moral position on the subject of suicide I think we can mostly agree that identifying persons at risk of suicidal tendencies would be helpful in alleviating the pain that accompanies this choice (if indeed it can be described as such). This is where a paper published recently in PLoSONE comes in. The study authors point out in the introduction that previous work has been able to correlate increased blood brain barrier permeability with suicide in patients with prior mental disorder.

Perhaps at this point I should take a step back and provide a little more information on what we are discussing here. The blood brain barrier (BBB) is a system of control that restricts what can and cannot pass between the normal circulatory system and the cerebrospinal fluid (CSF) or the bath that your brain sits in.

In practical terms this means tight connections between the cells of your capillaries to prevent leaks and transport systems to get nutrients back and forth across the barrier. Imagine a dam made of tightly packed stones with channels for the controlled movement of water and you have the basic idea.

Anyway, if the BBB becomes more permeable then it is reasonable to suppose that proteins found in the CSF would be found in higher concentrations in the blood than would normally be expected. If the permeability of the BBB is also correlated with suicidal behaviour then the presence of these proteins become an indirect test for suicidal tendencies.

This is the hypothesis that the research then tested, ie. does the presence of proteins in the blood normally found in the CFS correlate with suicidal tendencies? This study looked specifically at a protein known as S100B, primarily associated with certain cells in the brain and spinal cord. Included in the study were 64 adolescents (average age ~14.5 yrs) diagnosed with either psychosis or mood disorders and 20 healthy control subjects.

The subjects were evaluated and their suicidality was ranked from 1-7*, Blood tests then determined the levels of S100B. The findings showed that levels of S100B significantly correlated with suicidality in the subjects. Looking at the data accompanying the study it seems there is a wide margin of uncertainty on these readings. With a relatively small number of subjects I’m not particularly surprised by this but I would be looking to see more investigation into this approach to determine it’s reliability.

Obviously this technique will not replace psychiatric evaluation, it may prove useful though in helping identify those that are most at risk of suicidal behaviour. If I may return to the broader issues I raised at the start of this post, I would also find it interesting if this test (once extensively validated) could separate those who wish to end their lives due to illness into groups consisting of those with suicidal thoughts because of mood disorders and those who are otherwise of sound mind.

Something to think about.

* 1-no suicidality is present, 2-very mild (thoughts when angry), 3-mild (occasional thoughts), 4-moderate (thoughts present in the last week), 5-moderately-severe (recurrent thoughts present almost daily), 6-severe (current suicidal plan), 7-extremely severe (patient attempted suicide within the last week)

Falcone T, Fazio V, Lee C, Simon B, Franco K, Marchi N, & Janigro D (2010). Serum S100B: a potential biomarker for suicidality in adolescents? PloS one, 5 (6) PMID: 20559426

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ResearchBlogging.org

We like to think of ourselves as rational actors when it comes to making decisions, we take in information, process it and choose the path that we think will lead to a desirable outcome (if we aren’t deep-seated masochists I suppose). Regular readers of this blog and others that espouse a sceptical viewpoint will know that this isn’t really the case. We are influenced by a large number of factors from implicit biases, to environmental factors, and errors of thinking. The hope is that if we are aware of these factors we can go some way toward mitigating their effects and making choices that are both rational and lead to improving our lives.

Well, here’s another one for you. You may have guessed by the title of this post that it involves food and risk taking behaviour. A paper published last month in PLoS ONE out of the University College London looked at how hunger and food intake affected choices that had a monetary reward. The actual experimental design ran something like this, subjects fasted for 14 hours they then performed tasks that in effect were an idealised lottery, the tasks were performed before, directly after and an hour after a standardised meal. Over this time the subjects also had blood samples taken to measure hormones that correlate with hunger and energy reserves.

The task subjects had to perform consisted of choosing one of a pair of “lotteries” where there was a 25% chance of receiving one of four monetary amounts. Each pairing was designed so that there was always a difference in risk between the two  (see the picture it’s hard to explain).

Paired Lottery doi:10.1371/journal.pone.0011090.g002

How the subjects performed on the tasks was measured to determine the amount of risk aversion. In other words, humans have a tendency to normally prefer less risky choices. The effect of of hunger and especially immediate satiation (right after eating the meal) is to decrease this risk aversion and to make the subjects more risk neutral.

This way of referring to the subject matter is a little counter intuitive and can take a bit of getting used to, the bottom line is that the researchers looked for the point at which the subjects were equally likely to choose the “safe” bet which promised an certain average reward, and a “risky” bet that may lead to a higher average pay off but a lower chance of receiving it. Thus risk aversion has been reduced. By varying the reward amounts the researchers can measure the degree of risk aversion in each subject as the trial proceeds.

Actually the correlation is more complex than I would have thought, not only is the fact that calories are received taken into account but also the amount of calories. It seems that the size of the meal (in terms of calorific intake) is assessed to determine if it meets the rate of food intake required to meet baseline energy requirements. If it does risk aversion is increased (less risky behaviour) if not the risk aversion is decreased.

In hormonal terms this meant that a greater drop in the hormone associated with hunger was correlated with greater risk aversion but a smaller drop meant an increase in risk taking behaviour. The study authors also note that the adiposity of an individual (eg higher BMI) correlated with the size of the hormonal decrease after eating with higher BMI subjects experiencing a smaller drop and a corresponding greater increase in risk taking behaviour.

In effect we not only look at the reward in terms of the gain we will receive compared to our external resources (cash in the bank, say) but also in relation to our internal resources (metabolic requirements for example). This makes sense if we consider that for most of our history true advantage was not measured in abstract accumulation of “wealth” which we would recognise today but in available energy, including that within our bodies. That’s just a speculation of course, I’m no expert in this area.

What is the take home message of this research then? Well first off we should be careful to realise that risk taking behaviour is not limited to single domains in our lives. If you take away from this that only financial decisions are affected then that is too narrow an interpretation. In the final analysis though, no matter our eating habits or body size, we should endeavour to think over important decisions carefully and be aware of the changeable nature of our biology and it’s effects on our thinking.

Symmonds M, Emmanuel JJ, Drew ME, Batterham RL, & Dolan RJ (2010). Metabolic state alters economic decision making under risk in humans. PloS one, 5 (6) PMID: 20585383

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ResearchBlogging.orgAt the same time as we were learning that Vegetarians and Vegans might be more empathic than Omnivores we were also discovering the nature of empathy in Ravens. Published in PLoS One recently was a paper called “Do Ravens Show Consolation? Responses to Distressed Others” looking at the behaviour of Ravens and the implications for the emotional lives of these birds.

I’m always interested in these sorts of studies as they show that each facet of human capability is not unique and the variation seen between humans and the rest of the animal kingdom is usually only a matter of degree. For some reason I find this immensely satisfying, an emotional connection with the rest of the life on this planet that I rarely encounter in the suburban environment that I inhabit.

So how do you determine empathy among Ravens?

Well, it’s tricky. Essentially you have to determine a particular behaviour that occurs under particular circumstances indicating that an element of recognition of stress in one bird triggers behaviour to reduce that stress in another bird. Follow that? I’m not sure I did. What I’m saying is that definitions matter, if you want to infer a mental state from behaviour you have to be very clear on what that behaviour is to protect against confounding factors.

In this case the behaviour investigated consisted of monitoring the interactions of the birds for ten minutes after conflicts (either chase-flight, hitting [high intensity]  or forced retreats [low intensity]) and determining whether the interactions occurred more quickly than in the corresponding ten minute time frame on a following day. In this way normal interactions could be controlled for and allow interpretation of the post-conflict interactions.

One other ingredient was also required. In order to assign significance to an interaction the so-called “value” of the relationship between interacting birds has to be known. Explicitly assigning value to a relationship is a bit of unusual concept in day-to-day life but, for example, friends and family would be classed as more valuable relationships than colleagues and acquaintances. So basically the researchers were attempting to determine who the birds friends were.

What was found was that birds who were the recipients of high intensity conflict (eg hitting) were more likely to receive interactions with high value bystanders. In other words, when birds got into a serious fight their friends came over afterwards. The correlation with conflict intensity implies that the “friends” knew when the victim would be more distressed and would need to be calmed. This insight further implies some level of empathy.

Further research might investigate what (if anything) the “friends” get out of comforting the victim. Perhaps the “friend” also becomes distressed and such interactions work to lower the stress of both the victim and the “friend”.

If such experiments seem dry compared to our experiences of empathic emotion remember that teasing out the mental states of humans is just as difficult by looking at behaviour. Consoling behaviour in humans may not indicate genuine empathy but a savvy use of circumstance to increase political control. Examinations of behaviour alone might not reveal the difference. Still, it’s nice to know that birds have friends too.


Fraser, O., & Bugnyar, T. (2010). Do Ravens Show Consolation? Responses to Distressed Others PLoS ONE, 5 (5) DOI: 10.1371/journal.pone.0010605

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ResearchBlogging.orgLast week I posted about the effects of alcohol availability on the amount of violence in an area and mentioned that disorder in the area might also contribute to this. I thought this needed expanding upon, are we really so shallow as a species that we allow the environment that we may be in only briefly to dictate how we behave?

This approach to behaviour is referred to as the Broken Windows Theory and states that signs of disorderly behaviour will beget more disorderly behaviour. These signs might be graffiti, littering or the observation that legitimate signage requesting a particular behaviour is being ignored. We are a species that learns by watching others, it is reasonable to conclude that we don’t only pick up good and productive behaviours in this way but potentially antisocial or destructive behaviours as well.

Acting on this theory cities around the world have embarked on projects to clean up urban areas in order to reduce the instance of petty crime. Trouble was that there was no conclusive evidence to back this theory up. A paper that goes some way towards rectifying this was published in late 2008. It looked at the effects of manipulating the environment on the propensity for people to break either social norms, police enforced ordinances or requests by companies.

The paper hypothesised that people were not merely copying behaviours but that indications of social or legal norms not being followed in an area allowed other personal goals to override our normal instincts to act in socially acceptable ways. To investigate this the researchers set up conditions to see if the breaking of one rule lead to the breaking of a different rule e.g. graffiti leading to littering or litter leading to stealing.

In all 6 studies were performed, in the first an ally where bicycles were commonly parked was set up to have either clean or graffiti covered walls. The effect of this environment on littering was then observed by attaching a useless flyer onto the bicycle handlebars and counting instances of littering compared to those that took the flyer with them (there were no bins in the ally). In the clean wall condition 33% of those collecting bikes littered, compared with 69% in the graffiti condition.

In the second study the conditions were whether an injunction to not lock bicycles to a fence would affect whether or not people would take a police sanctioned detour. Two signs were placed along the fence of a car-park, the first prohibited locking bicycles to the fence while the second advised that the closest entrance to the car-park was closed and that a second entrance 200 metres further along had to be used. The entrance was closed with a temporary fence but a gap left that could be used. Bicycles were then conspicuously left either locked or not locked to the fence. When the bicycles were not locked to the fence 73% of people entering the car-park took the detour compared with only 18% when the bikes were seen violating the sign.

I think we can see a pattern emerging. I’m going to skip the third and forth studies that are variations on the littering theme and to go straight for the fifth and sixth. These two studies concerned stealing and had very similar set-ups, an envelope visibly containing a €5 note was set-up hanging out of a mail collection box. The box was then either clean and the area around it tidy or the box was graffitied or there was litter around the box. Taking or opening the envelope were both counted as stealing. The clean and tidy condition resulted in 13% of passers-by stealing the envelope, whereas the graffiti and litter conditions resulted in 27% and 25% of people stealing respectively.

What does this tell us about human behaviour? First off I see it as very positive, social conventions are a powerful factor for encouraging acceptable behaviour, on balance people prefer to act responsibly in the absence of cues that suggest irresponsible behaviour is tolerated. This suggests that policing general behaviour may be achieved in a subtle fashion by re-enforcing social conventions rather than with actual shows of force and punishment. That said the authors of the paper take a slightly more pessimistic view of areas that have already succumbed to spreading disorder, concluding with this thought:

“.. once disorder has spread, merely fixing the broken windows or removing the graffiti may not be sufficient anymore. An effective intervention should now address the goal to act appropriately on all fronts.”

The trick then is prevention rather than clean-up, at least in areas where behaviours have become entrenched. I think this is good news over all.


Keizer, K., Lindenberg, S., & Steg, L. (2008). The Spreading of Disorder Science, 322 (5908), 1681-1685 DOI: 10.1126/science.1161405

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Are you Right, Left or mix-handed? Haven’t heard of mix-handedness? Current thinking in neurology and psychology seems to be leaning towards describing handedness as a function of the degree of preference for one hand or the other. For some tasks you may use your right hand, others your left, it is the amount or preference you show that will determine what handedness you are. Not sure now? This page has a simple test that aims to determine hand preference by asking about simple tasks and which hand you prefer to use.

The test involves thinking about tasks (such as writing and drawing) and deciding which hand you prefer to use.Each answer is given a score for each hand your handedness is then given a score using the formula: (Right – Left) / (Right + Left). A pure Left hander will score -1.0, conversely +1.0 indicates pure right handedness, intermediate scores show mix handedness with a preference one way or the other. One thing to note here though, a score of 0 does not necessarily indicate ambidexterity.

This approach may indicate how well the two hemispheres of your brain communicate with strong handedness correlating with less communication and mix handedness with more. So how well are your hemispheres getting along?

This concept of communication between hemispheres is also being implicated in more abstract capabilities such as creativity. A recent study (very well summarised Here and Scientific American’s 60 Second Science podcast) looked at whether creativity can be increased in individuals who performed an exercise designed to increase cross-hemisphere communication. The exercise involved having the study participants move their eyes back and forth horizontally for 30 seconds. This activity likely increases the amount of hemisphere cross talk due to the fact that for each eye the right side of the visual field is processed on the right side of the brain and the left field on the left, this is represented diagrammatically Here (this can lead to a fascinating pathology called Hemispatial Neglect where a patient acts as if the left side of the world simply does not exist, not relevant here but too interesting not to include).

So moving your eyes back and forth means that each side must communicate a little more while forming a coherent whole for the visual field. This extra communication may then carry over to other tasks, that was the hypothesis. The measuring of creativity would seem to be a tough call, in this case participants were asked to come up with as many different uses for mundane objects (like bricks) as they could, participants were regarded as more creative when they came up with more categories of use and uses not thought of by other participants (originality).

The study found that the exercise did have an effect but that the strength of the effect was determined by strong handed or mix handedness. Strong handers had a creativity boost for 6-9 minutes (depending on the type of creativity, originality or more categories of use). If you are a mix hander then there is no benefit from the exercise, but don’t be worried, you are more creative than the strong handers in the first place. The increase of the strong handers performance really only seems to bring them up to the mix handers level.

Perhaps then, if you favour one hand much more than the other and you need a quick increase in creativity, you could do worse than this simple eye exercise. For once science has come up with an easy answer.

It is an accepted fact of life that alcohol and good decision making have only loose a acquaintance  with one another. Like ships passing in the night, they may meet or they may not. This is true for the momentarily intoxicated but does that propensity for poor choices follow us even after the libations cease? Adolescents who drink alcohol from an early age appear to suffer from impaired decision making skills later in life but the connection is not clear cut as to whether the alcohol lead to that ill advised life choice or if the bad decisions lead to the alcohol.

In an effort to tease out those threads researchers used rats to model behaviour. In this case to entice the rats to consume the alcohol they provided it as part of a “palatable gel matrix” or in common parlance, jelloshots. This allowed the researchers to promote high levels of voluntary alcohol consumption among the adolescent rats. Now to measure the effect of this alcohol on the rats decision making abilities they weren’t able to offer the rats stock market options or the choice of marrying Tony Veitch. To substitute for these sorts of things the rats were give a choice between low risk certain rewards and large but uncertain risky rewards.

Rats that had consumed large amounts of alcohol were biased towards the high risk behaviour even after 3 months without alcohol, or well into maturity. Whereas the control rats displayed behaviour that assessed the risk against the pay-off and went for the more certain rewards. Unfortunately the full study is locked behind a pay wall* so I can’t determine how the study was controlled, how reliable these results are and what they actually tell us about the link between early alcohol abuse and risk taking behaviour later in  life. If anyone has access to this info I’d appreciate it. In the absence of this information it seems as if the alcohol is a significant predictor of risk seeking behaviour independent of the innate predilections of the individual. Or to put it another way:

AlcoholStupidThings

*Why is the best stuff hidden away? Universal Open Access, your day will come!

I’ve said it before and no doubt I’ll say it again but we know science works because it makes predictions that we can then measure against the universe and determine if the models we have created to describe it are accurate or not. One of the more successful models is the theory of evolution by natural selection. A criticism levelled against the theory of evolution by detractors is the claim that new information can not be introduced into the system, only taken away. This is actually false but lets consider how we might tackle this question scientifically

First, the underlying assumption here isn’t unreasonable, let’s explore it. The accepted mechanism of introducing change in an organism, change that natural selection can then act upon, is mutation. Mutations involve a mistake in the copying of an organism’s DNA, this might consist of a change in a single base of a gene (an insertion of an extra base, deletion of an existing base or swapping one base for another) or it might involve large stretches of DNA. The basic principle that is relevant here is the same, a change is made to the blueprints of life in our cells.

As you might expect there are many more ways of being wrong than there are of being right, any random change is more likely to introduce a defect in the complicated machinery of life than it is to create an improvement (bearing in mind that “improvement” is a value judgement that really cannot be applied here but don’t focus on the wrong part of the story). So on the surface it would seem that random change is very definitely a bad thing, mutations would likely lead to loss of gene function, and by extension, loss of information and specifically death of the individual.

How might evolution get around such a problem? One solution would be to make copies of critical genes, this way is one copy is damaged through mutation the other can still function and produce a viable organism. The “spare” gene would then be free to mutate and the resulting gene may be selected for or against by natural selection (or human breeders).

If you have been reading closely you will have picked up on our prediction, the genomes of organisms should contain copies of various genes that allow mutations to occur without harming the individual that accumulates them. It turns out this is exactly what we find.  A recent study found a significant amount of redundancy in the genome of Zebrafish which allows mutations to occur in genes critical to development without lethal consequences to the fish.

The researchers intentionally gave mutagens to populations of Zebrafish and looked for changes in fish morphology indicative of mutations. In particular they created a mutation that lead to the loss of most of the fish’s scales, similar to that of Mirror Carp. The mutation was traced to a gene critical to normal development, further investigation revealed that the gene existed as a redundant pair, only one of which being required for normal development.

It is tempting to talk about this phenomenon in terms of intention, the gene was duplicated so that it could mutate and provide raw material for evolution. This is a mistake however, evolution can not move towards any putative desired future state. the genes that are duplicated in this way will be random and the mutations that affect the genes will be equally random, there are likely many genes in the Zebrafish that are not duplicated and would cause death to the individual if they were to change. This does not detract from the fact that a proposed mechanism for introducing new information into an organisms genome has proven correct.

Science is Awesome.

The ability to recognise the emotional states of those around us is a very useful tool which allows us to act appropriately in social situations. If this ability is impaired then it could lead to inappropriate reactions when dealing with others, this in turn could land us in hot water. An impairment like this has been suggested to explain the behaviour of delinquents, though it is unlikely to be a sole cause of antisocial behaviour.

A study published recently lends support to this hypothesis, published last month in the journal of  Child and Adolescent Psychiatry and Mental Health (or CAPMH for short, catchy) the study looked at 24 Japanese young adults that were serving time in correction facilities (in Japan). Simply put the researchers compared these so-called delinquents with a control batch of young people (matched for age and gender), in the ability to correctly match an emotion to a facial expression. Six basic emotions were represented with 8 different pictures each, so participants had to match a total of 48 pictures.

The emotions covered were anger, disgust, fear, happiness, sadness, and surprise, the prediction was that the incarcerated subjects would have difficulty interpreting some facial expressions and that this difficulty would skew the subjects towards misidentifying expressions as anger. This in fact did happen, the delinquent subjects actually identified disgust as anger more than the control group.

This interesting result is lessened in it’s impact somewhat due to the fact that the control group also made this mistake a large percentage of the time. This predilection in the delinquents however is an insight into how certain personalities might perceive some social situations as being more hostile than they really are. These personalities are also marked by being quick to anger and experiencing more intense anger than others so recognising how this occurs can be useful information in diffusing these situations and possibly diagnosis of individuals who might otherwise be labelled as simply “difficult”.

Tim Roth from the TV show <a href=

I have to say I cringe every time I see an advertisement for some magnet based item that promises health benefits. I’ve ragged on these Magnet Therapies before but today I’d like to cover one of the ways that magnets are legitimately being used to treat medical problems. A couple of months ago a study was published in the The Journal of the American College of Cardiology: Cardiovascular Interventions (a mouthful huh?) that detailed the use of magnetic nanoparticles and an externally applied magnet in guiding cells inside the body to a site of injury.

Specifically the study attempted to tag a particular type of stem cell, Endothelial Progenitor Cells (EPCs), with iron oxide superparamagnetic* nanoparticles. This was rather simply achieved by the addition of the particles to the growth medium of the cells. The cells then took up the particles via endocytosis. Once this was done they injected the cells into rats whose carotid artery had been damaged by angioplasty. A magnet was then applied to the outside of the rat to attract the tagged cells to the site of the damage. This technique showed a 5-fold increase in cells attaching to the damaged area compared to not using the magnet.

The difficulty of getting the cells to the right place without the magnet is due to the rapid blood flow past the injury. Imaging being swept down a fast flowing river with the goal of grabbing onto the river bank at a particular spot, not that easy, if there are thousands of you doing it some will manage but most will be carried right past. The addition of the magnet is like throwing a rope out to the hapless swimmers, once they get that helping hand they can then clamber onto the bank on their own. The EPCs will naturally attach themselves to places where damage is evident but under the high flow rates in arteries this process is inefficient.

This technique is specifically tailored to helping repair damage caused by angioplasty and it is hoped that it’s use might reduce the occurrence of Restenosis, or the re-narrowing of arteries after they have been widened by the angioplasty procedure. Even so, the guidance of the cells by magnetic field has obvious applications for other types of stem cell therapies as well as targeting drugs and gene therapies to specific organs of areas of the body.

Magnets are awesome.

*This sounds like a good name for a cheesy super hero, Superparamagnetic Powers Activate!.

It is virtually taken for granted nowadays that multi-tasking is a must. The demands on our time seem to be coming ever faster and in more complicated ways than we ever had to deal with before. Most of us are resigned to the fact that we are expected to be able to type up emails while on the phone and organise our calendar at the same time. If you’re a teenager (or ultra-hip oldie), throw in txting friends, updating your Facebook status and keeping a running commentary on pointless activities on Twitter. Previous studies on multi-tasking have shown that switching rapidly between tasks incurs a cost in time but what is actually happening when we do two (or more) things at once?

It certainly seems when we perform two tasks we are familiar with that we drop into “autopilot” where we might do one task without conscious thought while we focus our attention on another task, say driving while talking to a passenger. While we are deep in discussion it seems as though we are allowing the actions required for driving to be  handled by a “lower” part of our brain while we actively think about appropriate responses to the conversation. Anyone who has accidentally “driven to work” while meaning to go somewhere else would swear this interpretation is true.

Recent work published in the July16th issue of Neuron however disputes this interpretation of how our brain works. The study seems to show that instead of tasks becoming automatic and thus not requiring oversight by the pre-frontal cortex (responsible for conscious control), this area actually works more efficiently and switches tasks faster. In other words we are still only doing one thing at a time but swapping between tasks fast enough that it gives the appearance of multi-tasking. In the words of the researchers:

“The effect of training is to speed up information processing through this pre-frontal bottleneck, thereby reducing temporal processing overlap of the sensory-motor tasks in this brain region”

So, next time you boast of being a multi-tasking maven you can add that this actually means your brain works faster than those lounging in non-multitasking mediocrity. On the other hand, no need to inspire unnecessary ire among your peers unless you can handle the multiple tasks of running away and dodging projectiles.

A few weeks ago my wife went out dancing with friends, when she came back the one thing that had stood out for her in the evening was how similarly certain groups of people had been dressed. As the youngsters dancing around her left and were replaced each new batch had it’s own discernible style, this type of clothing with that kind of jewelry. Of course there were variations within each group but the similarities, at least to her, were far more striking. We all know of people around us that seem to slavishly follow the crowd, who wear the popular clothes, style their hair the popular way, listen to to popular music or in other ways agree with the popular opinion. We are certainly not as easily influenced as them, we are individuals.

There does seem to be this tendency to be able to recognize conformist behaviour in those around us while simultaneously denying such influences in ourselves. Our peers follow the pack while we make reasoned and informed choices. This effect is the focus of a study performed by Stanford and Princeton Universities. Students were subjected to a number of different surveys and situations designed to show how much they deemed their own choices were dictated by social influences versus their peer group. From university policy decisions to political party positions, driving behaviour  and why they bought an iPod respondents consistently followed popular behaviour themselves while ascribing to their fellows more susceptibility to such influences.

This pattern seemed to hold whether or not such conformity was described as positive or negative behaviour. In other words even when making the same choices as their peers was set up as being desirable they still denied that it was a factor in their own choices. As discussed in the final paragraphs of the study this difference in perception of other’s behaviour compared to our own is likely to contribute to exacerbation conflict and misunderstandings when dealing with those whose views disagree with our own. In such circumstances if we regard ourselves as rational and others as blindly following the crowd (and vice versa) then this makes finding common ground more difficult and demonising the enemy easier. So it may be more constructive not to wonder why are they behave the way they do but to step back and consider why do I think the way I do?

* Obviously this title is ironic, I am of course trying to show people that they are following the pack even while admitting that I must do so myself.

I think it’s safe to say that in recent years the push to “Become Healthier” has become much stronger than it was previously. Statistics like 1/4 of New Zealand adults are obese and New Zealand being the “3rd Fattest” country in the world are used to promote a lifestyle that is aimed at making us healthier. Many of us have taken this message to heart (pun intended) and attempted to shape up but sometimes it’s not clear exactly what is healthy. The primary action people are urged to take is exercise and it’s a good one. There are many recognised benefits to regular exercise including reducing risk of Type II diabetes and possibly even reversing the condition.

Another item that is also touted as a general health promoter is antioxidants. Here’s where things start to get tricky, in order to reap the benefits of excersise there has to be some way that the fact that you are exerting yourself is communicated to the cells of your body. A promising candidate for this signal is ROS, or Reactive Oxygen Species. In other words – Oxidants. This brings up an interesting question, if you are taking antioxidants and exercising in your attempt to be healthy – what happens? A study released early this year suggests that the antioxidants reduce the beneficial effects of excersise in the body.

Researchers looked at two markers of insulin sensitivity: Glucose infusion rates and plasma adiponectin levels (high Glucose infusion rate and high adiponectin levels correlates with high insulin sensitivity = no diabetes for you). They found that taking two antioxidants (Vitamins C and E) while engaging in exercise (not literally, friends don’t let friends jog and pill-pop) actually reduced the before and after exercise difference in these markers. This result strengthens the evidence that ROS are involved in signalling changes in cells and that taking antioxidants interferes with this process.

The drawback of this study is that the participant numbers were quite small. The intial group was made up of forty men, 20 that had athletic backgrounds and 20 that didn’t. These where then split into two goups either recieving supplements or not. So the end was 4 groups of ten, not exactly a significant cross-section of the population. Even so the results are compelling and should be investigated further.

I think the moral still holds, beware of taking too many suplements, you don’t always know what the side effects will be.

I don’t think the observation that cancer contributes to depression would win any awards for profundity, it’s likely such news would put a crimp in anyone’s day. Indeed, the very fact that the news of cancer itself can influence our emotions  makes it difficult to examine the contributing factors toward depression in those suffering from cancer. Our ability to foresee our own possible demise and react emotionally to it confounds attempts to tease out the strands of cause and effect. Approximately 10% of cancer sufferers are diagnosed with clinical depression and up-to two thirds experience some sort of mood disorder.

In order to separate out the effect of conscious knowledge of the disease from the psychological symptoms researchers have to turn to rats. How do you tell if a rat is depressed? To find out the scientists monitored the rat’s Twitter and Facebook pages for negative statements, no actually the rats are subjected to a swimming test, the longer the rats floated in the water without trying to escape the more depressed the animal is. The researchers found that rats with cancer showed signs of depression but not other behaviours normally associated with sickness, implying the rats were not simply feeling unwell.

Analysis of the rats tumours, blood and brain showed an increase in specific cytokines that have been linked to behavioural changes. In other words the presence of the tumour triggers changes in the brain that influence behaviour. This means that depression could be considered another symptom of cancer and not merely a by-product of knowledge of the cancer. This could have implications for how we treat depression in cancer patients and help them deal with the side-effects, simply knowing that being depressed is not something under their own control might itself be helpful.

Man Flu, scourge of modern Manly life. Struck down by this dreaded disease men are reduced to a shadow of their former glory, unable to maintain the meager level of household responsibility they usually get away with or even care for their own well being. Reduced to mewling invalids, men afflicted with Man Flu have little recourse beyond bed rest and watching daytime television while a significant other tends to their every need. After being ridiculed by wives and girlfriends for decades science has come to the rescue and vindicated us, the Man Flu exists!*
*The preceding is a work of fiction and any resemblance to real people or events is coincidental.
Despite what the media would have us believe recent advances in scientific research has not in fact established that Man Flu is a real phenomena beyond simply showing our inability to deal with sickness effectively. The real science behind the hype, as usual, is much more modest in it’s scope and consequences.

So what was actually studied? The research was carried out by McGill University in Canada and looked at the effects of a certain protein, caspase-12. The study involved investigating how the activity of this protein affects immune response against Listeria monocytogenes bacteria, a microbe that can cause serious food poisoning, in mice. Part of the study also investigated the effect of gender on the activity of the protien and whether any difference was mediated by the hormone oestrogen. To do this researchers infected mice with the bacteria and looked at spleen and liver bacteria levels in male and female mice with and without the gene for the protein and male mice with the gene and being treated with estrogen. 

The interesting thing is that this gene did have a different effect on how sick the mice got depending on the presence or absence of estrogen. Those male mice with the gene were more susceptible to the infection than females or males recieving hormone treatment, but the gene is inactive in most humans. Only about 20% of native Africans have a working version of the gene, so this research has virtually no applicability to general differences in flu severity between men and women. I guess Man Flu remains a myth, for now.

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