Manchester mathematicians give us all a chance to play the Imitation Game.

Let’s get the shameless plug out of the way first…

cumberbatch1 Manchester mathematicians give us all a chance to play the Imitation Game.On November 14th, `The Imitation Game’ – a biopic about the codebreaker, mathematician and computer scientist Alan Turing, and starring Benedict Cumberbatch in the lead role – is released in cinemas.  To promote the film, StudioCanal together with the School of Mathematics at the University of Manchester are running a cryptography competition based on Alan Turing and set around Bletchley Park. Prizes include film posters signed by the principal cast, soundtracks, DVD bundles, day passes to Bletchley Park, etc.  The competition, which runs until November 28th, is open to everybody and can be found here.

Ok, advert over, so let’s talk about how and why we got involved in this…

Starting in 2012, the School of Mathematics at the University of Manchester has been running `The Alan Turing Cryptography Competition’.  Unlike the Imitation Game competition, this is open only to schoolchildren in Year 11 or below.  We’re aware that many children are turned off mathematics at a young age as they equate it with `doing hard sums’ and often don’t get to see that it’s actually about creative problem solving and logical thought.  The competition is a way of addressing this.  In fact, we deliberately make sure that the codes in the competition can be solved bare-handed (without recourse to computer programming or even GCSE-level mathematics) – provided that you can `think-outside-the-box’!

Each year the competition is themed either around some aspect of Turing’s life and work or the University, often incorporating perhaps less-well-known facts.  One example (and one which we rutherford1 211x300 Manchester mathematicians give us all a chance to play the Imitation Game.revisited for the Imitation Game competition) is that, in 1940, whilst Turing was working on cracking the Kreigsmarine Enigma machine at Bletchley Park, he was worried that if the Germans invaded the British Isles then sterling would become worthless.  He converted his life-savings into silver ingots and buried them somewhere near Bletchley. Unfortunately, he subsequently forget where – and they are (presumably) still there, likely buried under a housing estate in Milton Keynes!

We also incorporate some classical ideas or other stories relating to cryptography into the competition.  One code involved solving crosswords.  This was inspired by the fact that, in 1941, the Telegraph (at the behest of the War Office) organised a cryptic crossword competition; those who did well were recruited as codebreakers at Bletchley Park.  Another code mimicked a `numbers station’ (a numbers station is a shortwave radio broadcast often consisting solely of a computer-generated voice reading out sequences
of numbers; they are believed to be broadcasts from governments to spies in the field).

hieroglyphics1 232x300 Manchester mathematicians give us all a chance to play the Imitation Game.One reason I believe that the competition has been so successful is that cryptography is a great way to bring mathematics alive.  The abstract thought processes that are needed to crack a code are very reminiscent of the skills needed to be a professional mathematician. It’s also easy to relate cryptography to the real world: from codebreakers in the 1940s slaving away late at night to crack the Enigma machine so as to defend Britain, through Turing’s own tortured personal life, to how cryptography is used by all of us whenever we send secure information (credit card details, for example) across the internet.

The Imitation Game Cryptography Competition runs until Nov 28th.  Next year’s Alan Turing Cryptography Competition starts in Jan 2015,

Post by Dr. Charles Walkden

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Winter: a SAD time for some

 Winter: a SAD time for someWe all feel a little ‘blue’ over the winter period. With the days getting shorter and cold setting in, it’s no wonder we find it harder to be our usual ‘perky’ selves. But for some people, this feeling is far more extreme. For those with seasonal affective disorder (or SAD for short), the winter months each year mean a period of significant depression, fatigue and a loss of interest in the activities they would usually enjoy.

Despite some ongoing cynicism, SAD is classified as a medical condition by the American Psychiatric Association – though the individual must already be diagnosed with a major depressive or bipolar disorder and should have experienced SAD symptoms for at least two consecutive years [1,2]. What is interesting about SAD, however, is that in contrast to the typical symptoms of depression, individuals with SAD often experience hypersomnia (an increased desire to sleep) rather than insomnia and a heightened rather than reduced appetite, resulting in weight gain [1,2].

So far there is no consensus as such on the causes of SAD but it is generally agreed that seasonal changes, primarily shorter light periods and lower levels of environmental light available, play a significant part. This is supported by the use of light therapy to successfully treat up to 70% of individuals with SAD [1]. But how does a lack of light translate into SAD?

 Winter: a SAD time for someOne of the major theories relating light to SAD involves our circadian system, known more anecdotally as our ‘biological clock’. This system controls our daily (and seasonal) cycle, dictating when we feel alert and sleepy, when we get hungry, and being responsible for the onset of hibernation in certain (some may argue more sensible) animals. Our circadian system responds to environmental cues, principally light, using these signals to sync our body clocks to the outside world through the release of chemicals which indicate when it is most appropriate to eat, be active or sleep [3]. In individuals with SAD, this delicate and complex system is believed to be disrupted, leading these people to become ‘out of phase’ with their environment, upsetting their sleep and eating patterns and causing them to become depressed.

Much of the research behind the circadian theory to date has focused on melatonin, one of the key components of our circadian systems and the chemical responsible for making us sleepy. Under normal circumstances, our bodies release melatonin at night and stop in the morning in response to light. This allows us to sleep when it is most appropriate. In some people with SAD, however, this cycle appears to be out of sync, with melatonin being released either earlier or later than usual [4]. By normalising this release pattern using either light therapy or the administration of melatonin itself, it may be possible to relieve the symptoms of SAD, and a number of studies have been carried out which support this hypothesis [3,4].

A second theory linking light and SAD looks at the eyes, or more specifically the retinas, of people with SAD, suggesting a lower sensitivity of these structures to light. Under normal circumstances, our retinas increase their sensitivity in response to low light conditions, i.e. dark winter days. In individuals with SAD, however, this may not happen [2]. Studies designed to test retinal function by measuring the electrical response of the retina to light have found that the retinas of some people with SAD are less responsive to light in the winter compared to the summer and in relation to healthy controls, lending support to this theory [3,4].

 Winter: a SAD time for someThe third and final theory we’ll discuss in this article involves a family of signalling chemicals found in our brains, known as monoamine neurotransmitters. Members of this family, namely serotonin and noradrenaline, are known to affect our mood, eating and sleeping habits, making it logical to suggest they may be involved in the biological basis of SAD [1]. They also appear to respond to light availability and time of year. Our serotonin levels, for instance, are higher in summer than winter [3,4]. In some people with SAD, levels of serotonin and noradrenaline seem to be lower than in healthy controls. Increasing these back to the norm using either light therapy or drugs which promote serotonin or norepinephrine production has been shown to improve mood in these individuals and relieve their SAD symptoms [3,4].

As is so often the case with medical conditions, particularly those involving our mental health, our understanding of the causes behind SAD is still somewhat hazy. However, irregular responses to low-light environments found in SAD sufferers, whether it be through abnormal melatonin production disturbing their circadian systems, less sensitive retinas, or atypical levels of neurotransmitters, does seem to be a major factor. Both time and further investigation are needed to understand fully the biological causes of SAD and improve therapy options. Nevertheless, for those suffering with this condition, rest assured there is light at the end of the tunnel (do excuse the pun).

Post by: Megan Barrett

Gupta A, Sharma P, Garg V, et al. Role of serotonin in seasonal affective disorder. Eur Med Pharmacol Sci 2013; 17: 49–55.
Roecklein K & Wong P. Seasonal affective disorder. In: Gellman M & Turner J (eds.). Encyclopedia of behavioural medicine. New York: Springer; 2013. p1722–4.
Danilenko K & Levitan R. Seasonal affective disorder. In: Schlaepfer T & Nemeroff (eds.). Handbook of Clinical Neurology, Vol. 106: Neurobiology of psychiatric disorders. 3rd series. Amsterdam: Elsevier; 2012. p279–90.
Rohan K, Roechlein K, Haaga K, et al. Biological and psychological mechanisms of seasonal affective disorder: a review and integration. Curr Psychiatry Rev 2009; 5: 37–47.

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Bovine tuberculosis in the UK- the bigger picture

Bovine tuberculosis (bTB) is a disease that seems to gather a lot of attention in the popular press, especially the highly controversial badger culling trials in England and Wales. But what is this disease, and why is it so important in this country?

The disease 

Bovine TB is caused by the bacterium Mycobacterium bovis (M. bovis), a very close relative of the principle cause of human TB, M. tuberculosis. It predominantly infects cattle, but perhaps not surprisingly can also be transmitted to, and cause disease in, people making it a zoonosis (a disease which can be transmitted readily between humans and animals). In both cases the resulting disease is very serious; symptoms include persistent cough, weight loss and fever of increasing severity over weeks and months, ultimately leading to death if no intervention is applied.

Mycobacteria Bovine tuberculosis in the UK  the bigger picture

A high magnification image of mycobacteria captured using an electron microscope (CDC)

Historically, human infection with bTB has been a very serious problem in the UK; records from the 1930s suggest it accounted for at least 16,000 deaths in that decade alone! The major route of transmission at the time was through people drinking the milk of infected animals. Widespread implementation of pasteurisation (the process of heat-treating milk to kill disease causing bugs) from the late 1930s onwards, combined with the routine testing of cattle for the disease and meat hygiene inspection, virtually eliminated M. bovis as a causative agent of human TB in the UK. However, in many other parts of the world, particularly developing countries (where such measures are sometimes harder to implement) human infection with bTB remains a very serious issue, with millions of people still at risk across the globe, as demonstrated by figures published by the WHO on human TB; it is estimated that in the 1990s, TB accounted for 30 million deaths worldwide, of which M. bovis is believed to have been the causative agent between 10 and 50% of cases in developing countries, the areas where TB is a particular problem1.

bTB in cattle: an ongoing saga 

M. bovis is a very slow growing bug, with disease taking several months to become obvious physically. Unfortunately, during this time infected animals may remain within their herds, potentially spreading the disease with other individuals. The slow growing nature of the bacteria also makes it incredibly difficult to kill. As a consequence in the UK, and many other countries where bTB is a problem, the treatment of infected animals is not considered an option. Instead a “test and cull” policy is employed, whereby animals are tested for the disease and immediately slaughtered if found to be positive.

The test used in cattle is very similar to that used to detect TB in people (some of you may remember having this procedure as a child). It works by injecting a small amount of material taken from the M. bovis bacteria (called the “antigen”) into the skin of the cow. Animals that are actively fighting infection will react strongly to this material resulting in a large swelling in the area; this inflammation indicates that they are bTB-positive. At present all cattle in England and Wales are tested at regular intervals, typically every 1-4 years depending upon the current level of disease in the area. Farms where positive animals are found are placed under restrictions, whereby no animals may be moved off the premises until the farm’s ‘TB-free’ status is restored, in an attempt to stop the disease being spread through the movement of infected cattle to other farms.

MooCow Bovine tuberculosis in the UK  the bigger picture

Courtesy of Rachael Evans

Testing was originally introduced in the mid 1930s on a voluntary basis, but became compulsory from the 1950s across the entire country. There was initially a rapid reduction in disease prevalence, and throughout the 1960s and 70s it was all-but eradicated. However, from the mid-1980s onwards, and for reasons which are still not fully understood, the disease underwent a resurgence and the situation today in parts of the UK is as bad as it ever has been; between 2000 and 2010 over 250,000 cattle were slaughtered as a result of these strict measures at an estimated cost to the UK taxpayer of     £500million. Currently Scotland is the only part of the country considered to be free of the disease, and while the most recent government figures suggest disease prevalence is slowly decreasing, whether this trend will continue, as hoped, remains to be seen2

Completing the picture

One reason that bTB has continued to be an issue after so many decades is that there are a great deal of unanswered questions in connection with its resurgence and transmission. As with many diseases, more discoveries simply raise more questions- none more contentious than the issue of badgers.

It is known that badgers can act as a “reservoir host”, meaning that they are able to carry M. bovis and transmit it back to cattle. What is less clear is the significance badgers play in spreading the disease, and whether or not controlling badger populations would help in controlling bTB in cattle.

In the autumn of 2013, badger-culling trials were commenced in 2 areas of England in an experimental effort to quantify whether any benefit is afforded through a reduction of the disease in cattle. However, these trials were abandoned early in 2014, since it was not possible to achieve the target of culling 70% of the badger population; the minimum figure believed to be necessary to reduce overall disease prevalence. This is a hugely disappointing outcome, as it means that badgers have been culled for no beneficial reason, and the trial has therefore provided no new information as to whether culling badgers helps control disease in cattle- a situation neither pro nor anti-badger culling campaigners can possibly be happy with.

In addition to the link with badgers, there are many other aspects to bTB biology that are not fully understood. Two notable examples of this include the recent and rather startling news that domestic cats have infected their owners with M. bovis. This not only underlines the issue of public health surrounding bTB, but also demonstrates the variety of species which are capable of carrying infection, potentially further muddying the waters as regards reservoir host species and disease control3. A second example is that of recent research from the Department of Infection Biology, at the University of Liverpool, which has shown a new experimental link between bTB and liver fluke, a common parasitic worm that infects livestock across the UK. In this study researchers found that liver fluke were capable of ‘modulating’ a cow’s immune system, meaning they can in effect ‘turn down’ the immune response in an effort to avoid being killed by it. This appears to have knock-on consequences for the cow, since it also reduces the animal’s ability to fight off other infections like bTB. Additionally, dampening of immune responses has been shown to reduce the sensitivity of the bTB test, meaning that in areas where there is a lot of liver fluke, bTB may go un-diagnosed for long periods. This could help explain in part why certain areas of the country remain in the clutches of bTB despite our best efforts4.

Clearly then, there is a much more to bTB than the press would have you believe. The next time you see or read an article in the news about the rights and wrongs of badger culling, remember this is only one small part of a much bigger picture. For example, would the public feel differently if the government was pursuing the control of feral cat populations in an attempt to reduce the risk of TB infection in people?

SSA 150x150 Bovine tuberculosis in the UK  the bigger pictureThis post, by author John-Graham Brown, was kindly donated by the Scouse Science Alliance and the original text can be found here.


1. Statistics worldwide:
2. Statistics for bTB in the UK:
3. M. bovis in cats:
4. Liverpool liver fluke research and bTB:

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The Science of Fear

Haloween1 300x224 The Science of FearThink of Halloween and FEAR comes to mind. From the scary horrors of the darkest of our imagination to just the thought of pestering children knocking on your door! We’ve all been there. Facing our worst nightmares. Heart starts racing. Palms sweating. Stomach turning. But what is fear?

Fear has been with us since the dawn of time. Promoting survival, fear allows the animal kingdom to handle threats through the well-known fight-or-flight response. Faced with danger we either attack and escape or freeze- whatever is best for our survival. So, through evolution, those who feared the “best” survived, reproduced and passed their fears on to their children.

Haloween2 205x300 The Science of FearSo does being a scared-y cat makes you a dream catch?

Not quite. Over the course of time, fear began to evolve in human society. Alongside our rooted survival-fears, we began to develop our own personal fears. Our personal experiences unconsciously shape what we fear, meaning we now have the potential of being scared of anything – from bananas to zebras.

So, with so many potential fears surrounding us, the body’s response to these possible fearful stimuli must be controlled.

Our brains translate information about a fearful scenario – i.e. ghosts, ghouls, upcoming deadlines- and decide the right course of action. The resulting hormonal responses in the body leads to the standard fearful feelings we all know and loath.

Haloween3 300x245 The Science of FearAdvancements in imaging, such as magnetic resonance imaging (MRI) and positron emission tomography (PET), have helped show the key areas of the brain involved – identifying the Amygdala as fear central. This evolutionarily conserved, almond-shaped group of neurons, located deep within the brain is essential for emotion, decision-making and memory – all crucial features of fear.

The amygdala can be activated by a variety of stimuli that entices any of our senses. As the hub of fear, it is believed to process information about the threat, assesses the level of fear, bringing about an appropriate response. Many studies have confirmed the role of the amygdala in fear using visual stimuli.

Haloween41 232x300 The Science of Fear

Amygdala activation shown using MRI

Conscious fear responses provoked by images of common phobias like snakes and spiders occurs alongside amygdala activation. Interestingly, in the absence of conscious stimuli, the amygdala still becomes activated. In these experiments, subjects were again shown the images but only momentarily so they never actually became aware of the threat. However they still suffered impeding fear alongside enhanced amygdala activity.

So with the amygdala being incredibly crucial for fear on all levels of our consciousness, what would life be like without the amygdala?

Well we are actually able to see. A few years ago a case came to light of a 44 year-old woman who was essentially fearless.

Referred to as “SM”, the woman suffered from an incredibly rare, less then 300 cases ever reported, genetic disorder called Urbach-Wiethe Disease. The disorder affects the extracellular matrix, the cells scaffold, meaning the symptoms vary drastically between cases. Usually the disease causes hardening of the brain and, in the case of SM, progressive degeneration of the amygdala.

The case of SM proved to be a unique way to continue exploring the amygdala. SM’s response to situations, from exposure to her once personal fears, a visit to the world’s scariest house to endless viewing of horror films, shown she failed to experience any sort of fear.

Haloween5 300x199 The Science of FearWhile this may seem wonderful, we need to remember fear is essential for survival. Never the attacker, SM has found herself as the victim of numerous crimes in her lifetime, including being threatened at knife point and being involved in an abusive relationship. During these horrific ordeals, while feeling emotions like anger, she has never felt fear. Without amygdala function, SM is vulnerable, unable to sense looming threats

So this Halloween, when you feel fear trickling down your spine, remember the most terrifying fear is not being able to feel fear itself!

Haloween6 The Science of Fear

Post by: Claire Wilson

Some references to sink your fangs into over Halloween

  • Feinstein, J.S., et al., The Human Amygdala and the Induction and Experience of Fear. Current Biology, 2011. 21(1): p. 34-38.
  • Ohman, A., The role of the amygdala in human fear: automatic detection of threat. Psychoneuroendocrinology, 2005. 30(10): p. 953-8.[1]
  • Ohman, A., et al., On the unconscious subcortical origin of human fear. Physiol Behav, 2007. 92(1-2): p. 180-5.
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3378813599 64d9006e0f z 225x300 PredictionHave you ever wondered what you would do if you could see in to the future? It’s right up there with invisibility, flight and super-strength as the super-power that people would love to possess.

I don’t mean the type of prediction you get from suspect clairvoyants who read palms or tea leaves. I mean prediction with certainty, every time, guaranteed. The obvious thing would be to predict the winning lottery numbers and watch with knowing satisfaction as each ball drops into place.

Or perhaps, if sport is your thing, you could predict the Grand National winner or the football scores – just like Marty McFly in the Back to the Future films.

After enjoying the rewards for personal gain, maybe you could use your new superpower for good, like Bill Murray in Groundhog Day, saving kids from dangerous falls and helping stranded old ladies.

Or maybe you could simply use your predictive powers to plan that camping trip to coincide with sunshine for a change. This might even be the most spectacular achievement given the Great British weather and the infamous difficulty in predicting it.

This is clearly the stuff of fantasy but scientists look into the future all the time using mathematical models. The predictions are best guesses of what might happen. Predictions are useful for all kinds of things from students’ predicted A-level grades to the state of the economy.

The problems with predictions is that the further into the future we go, the more uncertain we are of what might happen. If you want to buy a season ticket for your local football team, you can be fairly sure how much it’ll cost in the coming season but who knows how much it’ll cost in ten years’ time?

With the recent cabinet reshuffle bringing more women to the fore, I wondered not just about the positions held by men and women but about equal pay. Research done in 2011 by the Chartered Management Institute predicts that men and women will not be earning equal pay until 2109 if current trends continue. In the 12 month period leading up to the results, a 2.1% and 2.4% increase in salaries was observed for men and women respectively.

How certain should we be about these predictions?

3064351634 2985f244c7 z 300x200 PredictionA comparison was made between the £10,546 gender pay gap in 2011 and £10,031 from the same study the previous year. However, if we work backwards and reduce the current wages by the 2.1% and 2.4% growth rates to get an estimate of last year’s pay gap, this doesn’t match up. By this method, the estimated previous pay gap is about £10,421- giving a smaller absolute difference between the two years. As there is an inconsistency between the current and the previous year, so how can the predictions using the same growth rates be taken seriously out to 2109?

To emphasise this point further a similar report in 2008 about equal pay for women being ‘several generations away’, found that women’s pay increased by 6.8% over the year, compared with 6.6% for the men. The associated statistics then show that women will not receive equal pay equal pay until 2195

This very simple comparison highlights one of the problems with predictions: they are just a guess. In the case of using the same salary rates to predict way into the future, it should be made clear that these figures are uncertain at best and at worst, simply a fantasy- just like having superpowers.

Post by: Nathan Green

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The Fractal Factor: Patterns in Nature – The Building of the MegaMenger at this year’s Manchester Science Festival

Aristotle once said “In all things of nature there is something of the marvellous.” Living in a world brimming with technology, it is easy to forget the beauty and wonder of the world around us -unless it is accompanied by an Instagram filter, of course.

Despite the glorious diversity of the world we live in, we commonly see naturally occurring image12 300x187 The Fractal Factor: Patterns in Nature   The Building of the MegaMenger at this year’s Manchester Science Festivalpatterns. While early Greek philosophers were the first to investigate these shapes, the science behind these patterns still draws curiosity now in the 21st century. At the upcoming Manchester Science Festival an attempt to build the world’s largest fractal (the mathematical model behind some these patterns in nature) is taking place in the hope of enthusing and exciting the public about the wonders of maths.

What is a fractal?

How do trees grow? A single root divides into two branches which in turn each divide into two and so on and so forth. In the end the pattern made by a single twig is the same as the complex branches of a giant oak. So no matter at which scale you look at it, the patterns made by the branches are similar, and this self-similarity is mathematically termed a fractal.

image3 300x214 The Fractal Factor: Patterns in Nature   The Building of the MegaMenger at this year’s Manchester Science FestivalThese self-similar patterns are not only seen in trees, but also rivers and clouds, the cardiovascular system, broccoli – the list is endless. Since the 17th century the mathematics concept underlying these shapes has been investigated, with the mathematician Benoit Mandelbrot coining the term fractal in 1975. He defined a fractal as “a rough or fragmented geometric shape that can be split into parts, each of which is image21 300x241 The Fractal Factor: Patterns in Nature   The Building of the MegaMenger at this year’s Manchester Science Festival(at least approximately) a reduced-size copy of the whole”.

So – in a nutshell – fractals are infinite patterns made by repeating the same process over and over again to form structures which appear the same no matter which scale you look at them. They also happen to be an important and commonly occurring part of the world we live in!

The MegaMenger Project

The 8th annual Manchester Science Festival is set to run from 23rd October to 2nd
November. Showcasing a wide range of playful and imaginative projects to enthuse the public, one of this year’s star attraction events is the building of the MegaMenger. Scatted across twenty cities worldwide, a series of Menger Sponges will be displayed which will hopefully form the world’s largest 3D fractal – the MegaMenger!

How are Menger Sponges made?

Menger Sponges are fractal cubes named after their inventor Karl Menger. To form a Menger Sponge, you begin with a cube and divide it into 27 smaller cubes. Then you remove the smaller cube in the middle of each face and in the very centre of the cube. This is a level-1 Menger Sponge. By simply repeating the process of dividing each of these small cubes and removing central cubes, level-2, level-3 and so on cubes are formed.

 The Fractal Factor: Patterns in Nature   The Building of the MegaMenger at this year’s Manchester Science Festival

In the MegaMenger project, each city will build a level-3 cube. These 3D fractals will be made of 20 cubes, each made of 20 smaller cubes that -you guessed it- are made of another 20 smaller cubes. The smallest cubes are simply made of 6 business cards. Using over a million business cards, the twenty level-3 Menger Sponges will form a distributed level-4 sponge – the largest ever made out of business cards.

How to get involved?

For a week starting from 20th October these fractals will begin to take shape across the world. Here at Manchester Science Festival on the Saturday and Sunday, 24th and 25th October, drop-in sessions are taking place at the Museum of Science & Industry so you can pop by to witness the build in action and find out more about the magic of fractals!

By visiting you can get more information about the enormous world record attempt and print off Menger cards so you can make your own 3D fractal.

Happy building!!!!

Useful links

• Manchester Science Festival.

• More about Fractals.

October these fractals will begin to take shape across the world. Here and 25th October, drop-in sessions

Post by: Claire Wilson

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Exercise and brain power: how does physical activity help us think?

We might believe that the best way to improve grades at school is to spend more time studying, even at the cost of physical activity. According to research however, we might be wrong. In fact, girls and boys with high level of cardiovascular fitness do better in subjects such as English, science and maths than those less active. A healthy set of heart and lungs appear to have more influence on grades than factors such as self-esteem, parents’ income, weight at birth, prenatal smoking and your subjective academic ability.

Exercise improveimage11 Exercise and brain power: how does physical activity help us think? s goal-directed activity. This includes selecting, planning and coordinating actions, as well as ignoring distracters and managing several pieces of information at once allowing inhibition and flexible thinking. The cognitive control involved is supported by the frontal parts of the brain, which continue to develop well into our twenties. Furthermore, compared to their sedentary peers, physically active adolescents also show better memory – a function supported by the temporal region of the brain (behind the temples).

What might be more important for those of us well past our adolescent years is that exercise helps to maintain mental abilities in old age. Physical fitness at midlife reduces the risk of dementia, and in those with dementia physical activity can attenuate its progress. This is because physically active seniors tend to have larger volumes of the brain in areas that typically shrink in dementia, such as the hippocampus.

But how exactly can sport increase our academic performance and thinking power? One way is by reducing children’s disrupting behaviour and increasing their ability to attend to the task in class. Also physical activity goes in hand with better brain structure, with a larger volume of some areas. Such beneficial effect of exercise on the brain could be related to the change in the levels of the substances that stimulate the growth of brain cells. It seems that when sedentary people undertake exercise, they produce more of these growth factors immediately following activity.

In those, however, who exercise regularly, the mechanism might be slightly different. Instead of producing more of the growth substance, the brain becomes more sensitive to it. Related to thinking prowess, exercising can also make us feel more lively and energetic, allowing us to think better. This is because physical activity enhances levels of certain chemical messengers in the brain, e.g. acetylcholine. These messengers activate areas of the brain supporting cognition, emotion and arousal. Finally, in older adults exercise seems to help to recruit compensatory brain areas, which help in completing the tasks.

image2 Exercise and brain power: how does physical activity help us think?

Li et al. (2014) Acute Aerobic Exercise Increased Cortical Activity during Working Memory: A Functional MRI Study in Female College Students. PLoS One 9(6): e99222. Published online Jun 9, 2014. doi:  10.1371/journal.pone.0099222

How much should we exercise then and what sort of exercise would be best? Opinions are mixed, but it seems that moderate aerobic activity might be optimal, although strengthening exercise also brings cognitive benefits in seniors. Before undertaking physical activity we also need to remember that exercise carries risk and that it might be worth asking our doctor for advice. One thing is certain though, the human body is a machine designed to move!

Post by: Jadwiga Nazimek

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