This Christmas remember: Wash your hands not your turkey!

2169185215_c80cc1d607_zWith Christmas fast approaching, many of us will be stocking up ready for a festive feast – the centrepiece of which is usually a nice plump goose or turkey. But this year, alongside preparations to ensure your bird is moist and mouthwatering, it’s important to also keep in mind the dangers associated with putting your turkey under the tap!

Raw poultry provides a home for Campylobacter and Salmonella – the most common causes of food poisoning in the UK. In fact, in 2014 it was found that approximately 7 in 10 chickens sold in British supermarkets were contaminated by Campylobacter. But don’t fret, as a rule, good kitchen hygiene and thorough cooking are usually enough to avoid infection.

However, there is one important aspect of kitchen hygiene which seems to be regularly overlooked, this being the importance of not washing your bird before cooking. Placing a turkey under the tap causes an invisible storm of bacteria to spray from your meat, settling on anything within range (from clean utensils to previously sterile working surfaces). This cross contamination significantly increases the risk of infection to yourself and your family.

2187298129_ea44b55d86_zLast year almost 900 people took part in a national survey carried out by researchers at the Universities of Manchester and Liverpool which found that around 50% of participants always or usually washed their turkeys under the tap before cooking. This means that, despite warnings from the food standards agency, the message is still not getting across.

This year the Brain Bank wants to add our voice to this campaign and keep our readers healthy over the festive period. So, this Christmas make sure to treat your favorite bird correctly and remember – Wash your hands not your turkey!

Wishing wish you all a happy and healthy holiday!

Post by: Sarah Fox

Heretic to hero: Sir Harold Ridley and his sight-saving invention

It’s a strange phenomenon that some of the most revolutionarily successful people are initially rejected, scorned or unappreciated. Galileo, van Gogh, Darwin, Lovelace, Mendel and Austen were all vastly unpopular in their time, yet now we all take their scientific and creative contributions for granted. Sir Harold Ridley, the inventor of the intraocular lens, is another example of these late-sung heroes. His work saves the eyesight of millions of people across the world every year, but at first his idea of placing a plastic lens onto the surface of the eye was thought by peers to be impossible, laughable and even dangerous.

Cataract in a human eye. The pupil looks milky or cloudy. Image from Rajesh Ahuja, MD, Wikicommons.

The eyeball acts like a camera: light from the outside travels through the pupil and the lens to focus on the back of the eye, where the light is translated into images by light-sensitive cells that are located there. Due to age, trauma, toxic chemicals or certain diseases such as rubella or diabetes, the proteins that make up the lens denature and become opaque which prevents light from entering the eye and causes cataracts. People with cataracts suffer from very poor vision or blindness (see the image comparison); over half the world’s blindness (around 20 million people) is caused by age-related cataracts alone.

Normal vision. Image from National Eye Institute, NIH, Wikicommons.
Sight with cataracts: the image is blurry or out of focus, . Image from National Eye Institute, NIH, Wikicommons.

 

 

 

 

 

 

 

Over the course of history, several gory approaches to treating cataracts have been trialled. Somewhere between 2000-600BC, a procedure called ‘couching’ was used. This procedure involved using a sharp instrument, or just blunt pressure, to detach the cataract-riddled lens from where it normally resides into the back of the eye. Not surprisingly, this procedure was usually massively unsuccessful: patients usually suffered pain (as this was before a lot of modern anaesthetics were available), inflammation, infection and even blindness as a result. Even if the procedure and aftercare went smoothly, the patient was still left with inadequate eyesight. Unfortunately, couching is still performed in some developing countries where access to healthcare is often restricted.

As general surgical practice improved over the centuries, better tools and instruments were developed that allowed the opaque lens to be either removed, or broken up into small, more easily absorbable pieces. More often than not, patients were still left with poor eyesight and had to wear cumbersome, thick glasses to compensate for the missing lens.

Gordon Cleaver flew a Hurricane, the windshield of which was made from Perspex. Image from Tony Hisget, Wikicommons

Dr Harold Ridley, a recently trained medical doctor who specialised in ophthalmology, worked in the south of England during the Second World War. In August 1940, Flight Lieutenant Gordon ‘Mouse’ Cleaver forgot to put on his flight goggles before going out in his plane for what was to be Adlertag (Eagle Day) – the first day of Luftwaffe’s mission to eliminate the Royal Air Force from the sky. On returning to base, a bullet went through the side of Cleaver’s cockpit and shattered the Perspex window, a small fragment of which entered his eye. Cleaver had many operations on his face to treat the damage, but Dr Harold Ridley’s operation was to change medical history.

When Ridley removed the Perspex from Cleaver’s eye, he observed that there was no inflammation: the body hadn’t recognised the material as ‘foreign’ and so hadn’t initiated an immune response against it (as it usually does against materials like wood or metal). Ridley started thinking: if you could take the Perspex out of eye and there was no inflammation, then there would surely be no biological reason why you couldn’t put it back in.

A modern intracoular lens. The two arms help to fix the lens in place within the eye. Image from Wikicommons.

With this in mind, Ridley developed the first intraocular lens (IOL) – a small disc made from Perspex – and in 1949 placed it into the eye of his patient after first removing her cataract. With further modifications to improve the IOL’s power (that is, the ability of the lens to bend light, as glasses do), some of his first patients even attained 20/20 vision. Initially, Ridley sought to keep his patients’ implants a secret from the academic community until he could confirm from follow-up checks that there were no adverse effects, but a patient accidentally let slip the secret. So, in 1951 Ridley published his results and took two of his patients to be inspected by the Oxford Ophthalmological Congress. His work was rejected by other eye experts and deemed heretic. As a result, Ridley became a professional pariah and sank into depression.

Actor Robert Young had an IOL implanted that allowed him to carry on working. Image from Wikicommons

But not everyone was so sceptical about the IOL. Foreign eye doctors saw the promise of the invention and in 1974  – 25 years after the first IOL implant – a Club was started with the aim of discussing the use of IOLs in cataract surgery. Robert Young, a famous American actor, underwent the procedure and sang its praises to the press. Only years after he retired in 1971 was Harold Ridley officially recognised by the ophthalmic societies and institutions. In 2000 he was knighted by Queen Elizabeth, but he passed away in 2001.

The long-unappreciated work of Harold Ridley is now recognised as not just an invaluable contribution to ophthalmic medicine, but also one of the first ever feats of bioengineering. Applying a scientific strategy such as using materials that are foreign to the body to fix a medical problem was previously unheard of, yet today we benefit from IOLs, dental implants and pacemakers to name just a few. Increasingly, bioengineering takes advantage of 3D printing and other advancing technologies and materials in the production of tissue grafts and implants that, like IOLs, will make such a huge difference to peoples’ lives.

A plaque commemorating Sir Harold Ridley’s achievement at St. Thomas’ Hospital, London. Image from Wikicommons.

Post by Natasha Bray

 

Can a brain scan reveal your true age?

TWOFor as long as carnivals and funfairs have been around, there have been people who try to guess your age; a trick that often goes hand-in-hand with horror at the response. With our ageing population, which is most likely due to advances in medicines, treatments and our understanding of diseases, age is quite topical.

A recent study has shown that observing  the anatomy of your brain may be able to uncover your true age. A set of biological markers has been shown to accurately predict the age of a young person’s brain. So, if you have ever told a white lie about your age at the cinema to get a child’s ticket, or if you ever tried to trick shop owners into thinking you were 18 so that you could be served alcohol or cigarettes then this could soon be a thing of the past!

Previous studies have tried to observe aspects of brain structure and function with the aim of identifying whether there are common patterns and timings during the development of our brains. Although many studies have been unsuccessful in trying to show this, a study carried out by Timothy Brown at the University of California combined a range of parameters regarding the structure of the brain in order to assess its age. Using 885 subjects aged between 3 and 20 years, individuals were selected from a diverse range of races, educational backgrounds and economic statuses.

Children can develop – in terms of mental capability and maturity – unpredictably, but what is not known is the extent to which these differences are based on physical features of their brain, and or are due to psychology or environment.

Magnetic resonance imaging (MRI) was performed on each of the subjects to look at the internal structure of brains, of which 231 features were studied, including certain structures, the connectivity between different regions, and thickness or volume of different areas of the brain.

oNELarge variations in many of the measurements were observed that corresponded to the ages of the subjects. By combining the data from each of the measurements using a complex mathematical equation, an accurate ‘snap-shot’ of how the brain appears at each age during development was formed.  Although there were slight differences during development between brains of a similar age, the equation was able to correctly predict the age of a child to within a year, with an accuracy of 92%.

These findings indicate the presence of a developmental clock within our brain that produces a precisely timed development of brain structures throughout childhood.

Although these findings are incredibly interesting, aside from giving us insight into how our brains work you may be wondering what the relevance of these findings are. Whether we would be able to use the same technique to reliably determine the age of an adult by looking at the structure of their brain is another question. To be able to identify the true age of an individual has many advantages, but one of the most important clinical applications of this would be in observing whether a child’s brain is developing at a rate that is comparable to others of a similar age. It would also be useful in observing brain structures in individuals with autism, and other developmentally related disorders.

There are also non-clinical applications for this technique, such as cases where border staff need to be able to accurately determine the age of an individual without documents to be able to make a decision on whether to grant asylum. In the Olympic Games in Beijing in 2008, controversy arose when officials were unable to decide whether some of the competing athletes had entered the games illegally by lying about their age in order to compete.

To further this work, the study should address whether the anatomy of the brain is able to reliably predict age in subjects that have reached adulthood. If biomarkers are able to accurately predict our age even after development, then this could lead to rapid advances in the development of medicines for age and development-related illnesses.

Study: Neuroanatomical assessment of biological maturity – Timothy Brown et al. – Current Biology, September 2012.

Post by  Sam Lawrence

Pint of Science 3 day festival comes to Manchester!

Pint-of-Science-logo-with-glasses-528x746What better way to enjoy a sprinkle of scientific banter than down your local pub complete with pint in hand! For three days only, this summer we have enticed some of Manchester’s finest academic researchers out of the lab and into the pub to talk to you about their work. Events are taking place across Manchester on the 19th to the 21st of May and cover a wide range of topics, with enough variety to keep even the pickiest scientific dabbler satisfied. So have a look at our line-up and pick your favourite night, if you’re lucky you may even spot a brainbanker or two, but be quick tickets are selling fast.


Matters of the mind @ The Albert Club in West Didsbury – Click here for tickets

Monday the 19th: Mental health: breaking the stigma

1We’ve all experienced the feeling of being unwell with the accompanying trips to the GP, time off work and medication. Coughs and colds are common and well understood, but what happens when our minds become unwell? One in four of us will be affected by mental illness, the effects of this are no less real than a bout of the flu, but are often much harder to understand. Despite the extent of mental health problems, those affected still experience stigma and discrimination – a burden which can be even worse than the symptoms themselves. This evening, join Dr Rebecca Elliott and mental health experts from the University of Manchester for an evening of discussion where we hope to break down barriers and challenge stigma.

Tuesday the 20th : Understanding stroke.

2With around 152,000 strokes occurring in the UK every year, it’s never been more important for us to understand the ins and outs of this devastating condition. As part of the Stroke Association’s Action on Stroke Month, speakers from the University of Manchester and the Stroke Association will give us a window into the brain and the lives of stroke survivors. Professor Stuart Allan will introduce the workings of the brain, how strokes occur and what makes them so destructive, including how targeting inflammation could offer a brighter future for survivors. A real highlight will be provided by stroke survivor and nurse Christine Halford and her daughter Natalie who will offer moving first-hand accounts of what happens when a carer becomes the cared for. We will have an interactive activity provided by the wonderful artist Amanda McCrann to bring together a fascinating night of information and discovery.

Wednesday the 21st : The ups and downs of sleep and circadian biology (sold out)

3Have you ever wondered why it’s so hard to function when you just wake up or what really drives us to spend almost a third of our lives tucked up in bed? This evening we will address these questions and more as we explore the ups and downs of circadian biology. Join Professor Andrew Loudon and Dr Penny Lewis from the University of Manchester as they take us on a journey through the mysterious landscape of circadian rhythms and sleep. We will explore what makes our biological clocks tick, how our hectic 24-hour lifestyle affects our internal rhythms, how snoozing is vital to our memories and uncover the difference between morning larks, night owls and the indecisive humming bird with a live science experiment!


Understanding our bodies @ Solomon Grundy in Withington – Click here for tickets

Monday the 19th : Unlocking the Sense of Smell – The Scent of A Maggot

4Professor Matt Cobb’s lab studies how the sense of smell works. To do this they use a rather unusual animal – a maggot. You and I have about 4 million smell cells in our noses. A maggot has just 21, and by using genetics they can make a maggot with just a single smell cell. By studying the behaviour of these animals, and the electrical activity of their smell cells, we can understand how smells are processed in the nose and in the brain. Not only does a maggot have a brain, but the bits of its brain that process smells are also wired up just like ours. So by studying something as simple as a maggot we hope to understand how the sense of smell works in all animals, including humans.

Tuesday the 20th : Nanotechnology & the Role of graphene

5Manchester is leading the way in graphene research, with a nobel prize being given to two of its researchers in 2010. The material has some exceptional properties: tougher than diamond, stretchier than rubber, and better able to conduct electricity than anything else. It also has a myriad of possible uses: bendy touchscreens for mobiles, super-light batteries, artificial retinas, more effective drug delivery … and that’s just for starters. Graphene could become as much a part of our daily lives as plastic, and its implications will be huge!

Wednesday the 21st : Personalised medicine and the future of cancer treatment

6This talk will provide a fascinating introduction to personalised medicine, and the future of cancer treatment. No two cancers are the same. So, even patients with the same ‘type’ of cancer will respond differently to treatment. Personalised medicine aims to understand each person’s individual cancer at a molecular level, so doctors can match patients with the treatments that will work best for them. This aim of treating every patient as an individual is still some way off, but Professor Caroline Dive, from the Manchester Cancer Research Centre, will discuss how scientists in Manchester are playing a pivotal role in bringing forward this era of personalised medicine.


Chemistry and Physics @ The English Lounge in the Northern Quarter – Click here for tickets

Monday the 19th : Ocean circulation – the awkward bits

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The heat capacity of the ocean is around one thousand times that of the atmosphere, and the ocean circulation plays a crucial role in climate change. For long term model simulations one needs to average over space and time to make the computations feasible, but important processes happen over relatively small time and length scales. In this talk, Dr Gregory Lane-Serff will explain some of these processes, including mixed-later deepening, flow over sills and through straits, and flows of dense water into the deep ocean. He will show results from observations, and explain how insights from laboratory models can help our understanding – with some experiments for the audience to do!

Tuesday the 20th : A sonic wonderland

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What are the sonic wonders of the world? Trevor Cox, a renowned professor who engineers concert halls, has made a career out of eradicating bizarre and unwanted sounds. But after an epiphany in the London sewers, Trevor now revels in exotic noises – creaking glaciers, whispering galleries, stalactite organs, musical roads, humming dunes, seals that sound like alien angels, and a Mayan pyramid that chirps like a bird. Join him and discover what insights these remarkable effects give us into how sound is made, altered by the environment and perceived by listeners.

Wednesday the 21st : Waste not, want not – A Radioactive Reality

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Radioactive waste can be one of the most sensitive issues regarding the production of nuclear energy. However, are we too quick to jump to conclusions without considering all the evidence? Matt will talking about the preconceptions that most people have when they hear about radioactive waste and the scale of the problem in the UK. He’ll also talk about what we’re trying to do to solve the problem, while binding all these topics together with some anecdotes about his experiences regarding the topic.


Planet Earth @ Odder bar on Oxford Road – Click here for tickets

Monday the 19th : Unlocking ancient DNA

10Michael is a Royal Society University Research Fellow based in the Faculty of Life Sciences, University of Manchester. His main research interests are in the recovery of genetic information from extinct animals. Due to the age and environmental conditions of the remains of the more poorly understood species, this usually takes the form of cutting-edge techniques in proteomics. In this talk he highlights some of the key areas that ‘palaeoproteomics’ has helped improve our understanding of mammal evolution.

Hunting dinosaurs in the 21st Century…

Dr Philip Manning

Phil is Reader in Palaeobiology and Head of the Palaeontology Research Group at the University of Manchester. He is also an STFC Science in Society Fellow, a Research Associate at the American Museum of Natural History (USA) and a Visiting Scholar at the University of Pennsylvania (USA). In 2014 Phil was elected a Fellow of the Explorer’s Club (New York). His research is both broad and interdisciplinary with active research topics from biomechanics of dinosaurs to the synchrotron-based imaging of both extant and extinct organisms. He and his team have worked extensively in the Hell Creek Formation of South Dakota and Montana, but their field program also includes sites in South America, Europe, Asia, Africa and Australia.

Tuesday the 20th : Taking volcanoes to the IMAX

11Kate Dobson is a geologist who applies the latest cutting edge 3D and 4D imaging techniques across a wide range of geological research, to capture and quantify the spatially and temporally variable processes that control how our planet works. She has been at the University of Manchester since 2011.

From Core to Crust: A journey through the interior of the Earth

Michael Ward Broadley

Michael Ward Broadley is a PhD student at the University of Manchester, and his research revolves around the use of noble gases and halogens as tracers of volatile movement between the Earth’s geological reservoirs. Studying magmas erupted from deep within the Earth’s mantle, by means of analysing their unique geochemical signatures rich in primordial noble gases, it is possible to understand how the Earth obtained its volatiles. The theories that are being put to the test include impacts with primitive meteorites and solar wind influence, among other fascinating mechanisms. Michael is also a regular contributor to his research group’s outreach program.

Wednesday the 21st : Secrets of the Moon

13Katherine Joy is a senior research fellow at the University of Manchester SEAES. Her research focuses on studying the geological history of the Moon throughout lunar samples returned by the Apollo astronauts, and lunar meteorites that are found here on Earth. She analyses these samples in the laboratory to investigate their chemistry, mineralogy and age. With the contribution of data collected by satellites orbiting the Moon it’s possible to reveal its fascinating geological evolution, as well as explore the wider history of the Solar System. Her work may one day help guide people planning to send astronauts back to the lunar surface.

Cooking Up A Comet – Francesca McDonald

Francesca is a first year PhD student and her research concerns determining and comparing the volatile budgets of the lunar and terrestrial mantles. This will make us understand the volatile behaviour during the formation and evolution of Earth-Moon system. The rock samples she studies are Apollo lunar basalts and terrestrial komatiites. She also partakes in outreach work where she talk about comets whilst having her glamorous assistant Alex Clarke cook her up a comet.

Hope you see you there!

the Brain Bank Team.

Battle of the brain’s sex differences…or not really?

Why some people are surprised at the very idea of there being differences between male and female brains I don’t understand. But, what really confuses me is when journalists misinterpret research findings and overextrapolate speculative comments to fit cliched gender stereotypes.

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“Brain networks show increased connectivity from front to back and within one hemisphere in males (upper) and left to right in females (lower).”
Credit: Ragini Verma, Ph.D., Proceedings of National Academy of Sciences, from press release.

Whenever I ask my (less sciencey) friends what they’d like to read on The Brain Bank, there is a perennially raised topic. At least one, usually single, hopeful will ask desperately for a guide on how men and women’s brains differ – and why they might work in different ways, scientifically speaking. Efforts to crack the mental codes of the opposite sex started as far back as Aristotle, who claimed that women were “more mischievous,  … more easily moved to tears[,] more apt to scold and to strike[,] … more void of shame or self-respect,…of more retentive memory” (History of Animals).

White matter tracts, as imaged using diffusion tensor imaging. Author: Xavier Gigandet et al., source here.

Earlier this month, a research paper from the University of Pennsylvania used a fancy imaging technique called diffusion tensor imaging (DTI) to solve the mystery behind the different ways guys and gals think. DTI basically gives you a picture of where the white matter tracts – the wiring between different brain areas – lie between various processing parts of the brain.

The technique works by looking at how water travels within the brain: water ‘prefers’ moving along bundles of fibres, such as white matter tracts. In this way, DTI examines the strength of ‘connectivity’ between various parts of the brain.

Researchers, led by Prof Ragini Verma, scanned the brains of 949 youths aged 8-22. They found that, in general, the connecting pathways within each half of the brain were stronger in guys, but that in girls, the wiring between the two halves was stronger. In other words, connectivity in girls tended to be more ‘left-right’, whereas in boys, ‘front-back’ connectivity was stronger.

The researchers also reported that the girls performed better on tests involving attention; word and face memory; and social cognition, whereas boys fared better on spatial processing and sensorimotor speed tasks.

NOT REALLY. Author: Miz Mura.

This paper and its associated press release rallied some…OK, a lot, of interest from the press. But then something strange happened. Something was lost in translation between the original paper and the resulting newspapers reports, claiming that ‘hardwired’ differences between men and women’s brains might explain ‘why men are better at map reading’ and women are more ‘emotionally intelligent’…

OH dear…

Seriously, NOT REALLY. Author: Miz Mura

…Then there was a knee-jerk reaction against the potentially neurosexist connotations of this ‘kind of science’, and not just because the research was published in PNAS (hehe). In my opinion, if a conclusion is based on valid and reliable science, you shouldn’t really argue unless you have definitely read the research. If, on the other hand, the offending ‘conclusions’ are the result of a bizarre ‘Chinese Whispers’ scenario where no one has actually read the original research, then no,  it’s probably not worth listening – but then, mistranslation isn’t based on science anyway…I digress.

While we all know that there are some obvious – and other more subtle – distinctions between men and women. This research article doesn’t actually claim to explain anything besides the physical connections between different parts of the brain. Just to clarify, here are some of the problems with treating this particular research paper as the Holy Grail of sex differences:-

1. There’s no saying whether there’s a big difference or not. The authors present (undeniably) a very striking diagram, with the statistically significant bits indicated in gender-relevant colours. However, just because a difference is statistically significant, doesn’t mean the effect of being male, or female is a big deal. In fact, as the study uses such a large sample (949 youths), even very small differences between male and female brains may prove significant.

2. Less wiring doesn’t necessarily mean lower ability. The authors don’t actually indicate anywhere in the paper that the ‘wiring’ is associated with men and women’s differing abilities on the tests – though Prof Verma has been quoted speculating on the possibility. Instead, the authors have pointed out the brain’s physical differences and then separately comment on behavioural differences without saying whether the two correlate.

If the hypothesis is that men or women with mega-strong connectivity left-to-right, or front-back are respectively better at, say, language, or football, you could easily find that out with a bunch of correlations. Not that correlation would imply causation anyway. In fact, the strengthening or weakening of physical connections could even suggest that women and men’s brains change to compensate for innate differences!

3. Size/proportions might matter. It’s pretty well-known that men have larger brains than women – the situation is pretty complicated though, as women reportedly have more grey matter, less white matter and a thicker cortex than men. However – please correct me if I’m wrong – the authors don’t correct for brain sizes (either front-back, left-right, total volume or any other measure), which could be very important. Especially considering the people being imaged are aged between 8 and 22, when brains grow a lot anyway. Not to mention that girls and boys grow at different rates too. Oh well.

Social media word clouds for females (top) and males (bottom). Size = strength of the correlation; color = relative frequency of usage. Underscores (_) connect words in phrases. Words and phrases in center; topics surround. Author: H. Andrew Schwartz et al.; Source. Apologies for the bad language!

4. There are many more potential mechanisms than meets the eye. Yes, it’s very possible that exposure to sex hormones could change the brain’s connectivity. But, there’s a whole host of other possible influences on a child going through puberty that can’t be ruled out, because the brain is notoriously/amazingly plastic. Environmental influences, influences that can’t ever be controlled for, such as parents, peers, teachers and the media – could just as easily alter the physical structures of the brain, or the brain’s abilities. In fact, hearing in the news that ‘men are better at map reading’ because it’s ‘hardwired’ in their brains is conceivably rather likely to make guys feel a bit more confident navigating, while discouraging women from taking that responsibility instead.

This piece of research is not the first and certainly won’t be the last to be accidentally misinterpreted or overhyped. Research into the differences between men and women will continue to fascinate us because, for whatever reasons – social, biological or otherwise – people of different sexes tend to look, sound and act differently. More seriously (and the authors of the paper explain the motivation of their research), sex differences are linked to brain disorders like autism and depression, so the differences between ‘Martians’ and ‘Venetians’ should be properly understood, and carefully reported.

For further examination of this topic, here’s another blog article and a BuzzFeed piece with a few more reasons why it should all be taken with a pinch of salt.

Post by Natasha Bray

Gambler’s mind: The thrill of almost winning

Taken from Sescousse et al 2013
Taken from Sescousse et al 2013

Almost three quarters of the British population participate in gambling of some form, despite the fact that we know the odds are so heavily stacked against us.  So why do we gamble despite the massive risk?

The answer to this question lies in the biology of our brains; exactly how does the brain change during addiction? Circuits known as the ‘reward system’ connect to regions of the brain involved in memory, pleasure and motivation. When we enjoy something these neurons release dopamine, a chemical neurotransmitter that makes us feel happy, a feel-good chemical that makes us satisfied and encourages us to continue our habits. This is similar to what happens in the brains of drug addicts.

A collaboration between Drs Luke Clark from the University of Cambridge and Henrietta Bowden-Jones from the only NHS clinic for gambling addicts is trying to address what makes some of us so hooked on gambling and what happens in our brains. We know that there are both external and internal factors that influence our gambling habits such as our personality type, neurobiological and neurochemical make-up, as well as the different features of the games themselves.

Using a number of control and ‘gambler’ subjects, behavioural tests looked at impulsivity, compulsivity and dopamine levels. As suspected, gamblers were more impulsive than controls; something which is mirrored in drug addicts and alcoholics. Brain imaging studies have shown that near-misses recruit areas of the brain that are associated with winning. The ‘near-miss’ phenomenon is the theory that losing a game acts as an aversive stimulus- it actually puts us off gambling. But, coming close to winning acts to fuel our desire to gamble. The fact that the same areas are activated when we almost win, and when we actually do win may encourage us to gamble – and this is something that can be exploited by game manufacturers.

Is the degree of brain activation during winning related to gambling severity? Subjects were asked to play on a slot machine whilst an fMRI machine measured brain activity in response to the game (functional magnetic resonance imaging- looking at the level of blood flow to areas of the brain in response to stimuli). Results found that those subjects with severe gambling addictions had the greatest activity in their midbrain in response to near-misses, but the activity to a real-win did not differ with gambling severity.  This brain region is of interest because dopamine is produced here, and is implicated in other addictive behaviours such as alcoholism.

This leads us to ask if there is a chemical basis to gambling addiction.  Well, scientists know that there are a decreased number of dopamine receptors in the brains of drug addicts, but is this mirrored in the brains of gambling addicts? Surprisingly, although there were no differences overall in the amount of dopamine receptors in gamblers compared to controls, gamblers that were more impulsive did have a lower number of dopamine receptors. Strikingly, when they studied the gambling behaviour of patients who had suffered a brain injury, the ‘near-miss’ response observed in gambling addicts was not seen in patients that had damage to their insula. The insula may be central to the distorted thinking patterns seen in gamblers.

Compulsive gamblers are not necessarily greedier than the rest of us, but their brains may be wired differently. Gamblers are more likely to prioritise money over other basic needs such as food and social interactions. Perhaps there are changes in a gamblers brain that render them hyper-sensitive to the ‘rush’ of winning. On the flip-side, it is possible that pathological gamblers are less sensitive to the things that the rest of us would find rewarding, such as alcohol or sex.

Brain 2
Taken from Ted Murphy

Healthy controls and pathological gamblers were put into an fMRI scanner to record brain activity during a task where they had to press a button in response to money-based or sexual images. The faster the button was pressed, the more motivated the subject was to get the reward.  Despite stating that they found both money and sex equally rewarding, results found that gamblers pressed the button 4% faster when viewing money-related images than sexual images. Indicating that gamblers attributed a higher value to money than sex. The gambling cohort had increased blood flow to the ventral striatum (part of the brain involved in reward processing) in response to monetary images, more than to sex. In contrast, no difference was found in the controls. Interestingly, they found altered activity in the orbito-frontal cortex of gamblers, which is also involved in reward processing. Past studies have shown that different parts of the orbito-frontal cortex are activated in healthy individuals in response to money and erotic images- which is thought to reflect the dissociation between rewards that are vital to survival such as food and sex, and secondary rewards such as money and power. In gambling addicts, the same region of the orbito-frontal cortex was activated in response to sex and money, suggesting that they have an altered perception of money as a more primal reward.

A large proportion of future work will focus on uncovering the precise role of the insula in addiction by observing how its activity changes whilst gambling. Another area of interest is looking at relatives of gambling addicts, and trying to identify if differences exist in both their brain activity and also in their behaviours when gambling. This may be of huge importance as therapies and treatments may be able to focus on targeting affected areas of gamblers’ brains.

For more information:

Clark L, Lawrence AJ, Astley-Jones F, Gray N. Gambling near-misses enhance motivation to gamble and recruit win-related brain circuitry. Neuron. 2009; 61(3):481-90.

Sescousse G, Barbalat G, Domenech P, Dreher JC. Imbalance in the sensitivity to different types of rewards in pathological gambling. Brain. 2013

Image taken from Ted Murphy, Flikr

Post by Samantha Lawrence

 

 

 

Why are all the bees dying?

Photo by Erik Hooymans

Bees are great. They have an amazing social hierarchy, they provide medical care for their sick, they have ruthless security ‘bouncer-bees’ and each bee travels huge distances to gather about one twelfth of a teaspoonful of honey. For us humans, the benefits of bees don’t stop at honey. About a third of our crops – approximately $220 billion-worth globally – are inadvertently pollinated by foraging bees and, from what I’ve heard, we really don’t want to have to start doing that ourselves.

The problem is that bees are dying at an alarming rate. As it happens, my father is a budding bee-keeper and has just received a letter from the Food and Environment Research Agency that reports a halving of honey production in South-East England in the last six years alone. This problem is, however, happening all over the world. Imaginatively dubbed ‘colony collapse disorder’ (CCD), a mystery disease is wiping out huge numbers of bees yet no one can pin down exactly what the cause is. There are several theories, so I’ve taken the liberty of making a list akin to a ‘Top Six Most Wanted Villains’ of the bee world.

A varroa mite feeding on a honeybee (Wikicommons)

Varroa mites: Affectionately known as ‘vampire’ mites, these teeny-weeny bugs are big trouble. They suck hemolymph (the bee’s version of blood) from honeybees and, in so doing, weaken the bee and may even transmit deadly viruses (more later).

Neonicotinoids and other pesticides – Neonicotinoids (NNs) are chemicals designed to kill insects that feed on farmed crops. They bind to acetylcholine receptors on the cells of the insect’s nervous system, eventually blocking their normal use, causing paralysis and death. In the past couple of years, various research groups have shown that these chemicals get into bee hives at dangerous, though not lethal concentrations. Not only that, but a paper published in Nature showed that a cocktail of these chemicals may lead to CCD by affecting bee behaviour, presumably through their effects on the bees’ brains. Bees affected by these chemicals tend to forget where they are in relation to the hive, and produce less food. Other research has shown that NNs may affect the way that bees metabolise their food to produce energy. Scientists have even shown that exposure to NNs affects an important immune defence pathway, which may make bees more vulnerable to parasites and viruses.

Viruses: Viruses such as Israeli acute paralysis virus, deformed wing virus and acute bee paralysis virus are spread by varroa mites and have all been identified as possible causes of CCD. Deformed wing virus is particularly tragic; if pupae are infected and develop wing deformities, they are kicked out of the colony, and the number of healthy bees dwindles. Israeli acute paralysis virus has been shown to interfere with the bees’ cellular machinery that produce proteins.

Nosema – this is a fungus that causes intense diarrhoea when swallowed by a bee, leading to worker bees pulling a sickie, which means less food for the hive. To add insult to injury, the queen bee becomes infertile and the colony stops producing young.

Malnutrition – Bees that collect their food from a variety of sources tend to be more hardy and resistant to infection than those that rely on only one or two types of flowering plant. In the US where farms cultivating one or two crops such as wheat or corn are vast, bees may become malnourished and more susceptible to disease.

Female phorid fly laying eggs into a worker honey bee. Core A, Runckel C, Ivers J, Quock C, Siapno T, et al. (2012).

Parasitic phorid fly – Last year, a researcher found a phorid fly larva in a test tube containing a honeybee that had died from suspected CCD. Phorid flies (which apparently scuttle more than they fly) lay eggs on the bee’s abdomen, which then hatch and feed on the bee. Weirdly, bees that carry this parasite end up acting more like moths than bees (foraging at night, buzzing around bright lights) before abandoning the hive.

What’s most likely is that CCD is caused by a mixture of two or more of the culprits mentioned above working in tandem. For example, varroa mites weaken bees and give them viruses. While a colony may be able to withstand either the mites or the virus, the two knocks together could be lethal. This interplay between several different factors makes it all the more difficult for scientists and beekeepers to research and prevent CCD.

So what’s being done to stop all the bees dying? Aside from all the tried and tested treatments for the parasites and viruses known, there are new efforts to save the bees via various industrial collaborations. Earlier this year, Monsanto set up its own Honey Bee Advisory Council including scientists, beekeepers, industrial and governmental representatives to try and tackle the issue. In 2011, Monsanto also bought Beeologics, a company in Israel that researches possible solutions to CCD. One strategy used by Beeologics against bad viruses is to deliberately infect bees with a special artificial ‘good’ virus. In turn, this good virus infects any varroa mites feeding on the bee. Amazingly, this good virus acts to prevent the mites from being able to pass on bad viruses to the bee. This treatment is currently passing through regulatory tests, but it will hopefully represent the start of a new approach to keeping bees alive for the benefit of humanity – and not just for the honey.

Post by Natasha Bray

A pill to cure Alzheimer’s!?: Why science stories should be reported more carefully

On October 10th 2013, there were headlines on the front pages of several British papers claiming that “A simple pill may cure Alzheimer’s”. These papers included the Times (£) and the Independent, who both put the stories on their front pages, the BBC website and breakfast show. The story was also tweeted by these outlets as well as America’s Fox News:

As a scientist who has worked on Alzheimer’s disease, headlines like this always provoke my cynical side. I’ve seen stories proclaiming a cure many times before, yet no cure is forthcoming. My cynicism was somewhat rewarded when I researched the story further. The study did indeed find that a pill, which inhibits a protein called PERK, was able to prevent brain cell death in mice which showed symptoms of disease. However, the disease the mice had was not Alzheimer’s; they had a prion disease.

In order to understand the research, here’s a quick explanation. Prions are misfolded, infectious proteins which are linked to neurodegenerative diseases such as BSE (or “mad cow disease” as it was known in the 80s) and CJD in humans. Alzheimer’s is also caused at least in part by a misfolded protein, called amyloid-beta (Aβ). Both prions and Aβ are affected by something called the Unfolded Protein Response (UPR) in cells. The UPR detects the misfolded protein and stops the brain cell making any new proteins. This means that the cell cannot make proteins which are essential to its survival and so will eventually die, leading to neurodegeneration.

Don’t get me wrong, the results from the study are promising. However, the newspaper headlines are incredibly misleading. There are some key problems with interpreting the research as a “cure for Alzheimer’s”:

mouse

    • This study only theoretically applies to Alzheimer’s disease as the authors note that Aβ is subjected to the same UPR as prions. The effects of the drug will need to be tested on Aβ before any definitive conclusion can be made about its effectiveness in treating Alzheimer’s. Furthermore, Alzheimer’s disease has other contributory destructive mechanisms not related to the UPR which also need to be assessed. The same is true before a link can be made to the other neurodegenerative diseases mentioned in the paper, such as Parkinson’s or ALS.
    • The research was conducted in mice rather than humans and there is no guarantee that the drug will be usable in humans. It may not have the same effects or the side effects may render the drug unusable.
    • The drug causes potentially serious side effects in mice such as mild diabetes and weight loss. This would have to be rectified before the drug can be administered to humans which could take a significant amount of time.
    • The weight loss side effect in mice means that they could not be used for a long time and it is unknown what the long term effects of the drug are. Something which targets both the brain and an essential cellular process such as the UPR may have detrimental effects if used over a long period of time.
    • The pill does not “cure” memory loss. The mice that were treated with the drug did not regain memories which were already lost. However, treating these mice did prevent the disease from progressing further. This pill will not help people who already suffer from mid to late-stage dementia.
  • Even if the drug is suitable for use in humans, it will have to go through clinical trials before being put to regular use. This will take years, possibly even decades.

Most of the newspapers covering this story did mention some of these problems. The Independent in particular made it very clear the study was in mice and a cure is “a long way off”. (However, in their tweet (above) they say that, “This breakthrough in treatment for Alzheimer’s could very soon pave the way for a simple pill to cure the disease.” showing the differences in these types of news communication). The Express, on the other hand, took seven lines to even mention that the study was in mice. Unfortunately, in this day and age, many people don’t read further than the headline, sub-heading and possibly the first two or three paragraphs.  Many people therefore may well get the impression that a cure for Alzheimer’s is imminent and misunderstand the point of the study.

Later on in the day when things had calmed down a bit many newspapers did write editorials (for example in the Independent and the Guardian). These mostly highlighted some of the points above and clarifying that there is still a long way to go in curing Alzheimer’s.  But this is after the damage had been done, the headlines had been seen and the tweets had been sent. The point is that the story should never have been given so much prominence in the first place.

It’s quite easy to assess how people are reacting to a story by use of Twitter. A quick search of “Alzheimer’s” on the day the story broke showed a lot of people re-tweeting the story from various news sources, some with a link, some without. The misleading nature of the headline can be seen by the nature of some of these tweets, including one which said “They’ve found a cure for Alzheimer’s. This is big”. One of the big tweeters was the comedian Jimmy Carr, who tweeted this (rather lame) joke:

With no link to the story, how are people supposed to know where he got the information from? Another problem with today’s microblogging news delivery system is that there isn’t a lot of room for details and so the story can easily get mutated.

There were some expressing cynicism. The Alzheimer’s Society stated “This is a promising development as it shows this biological pathway is a potential target for new treatments.  However, it is important to note that this study was carried out on mice with prion disease and so it is not clear how applicable it is to humans with diseases such as Alzheimer’s.”

But it’s not the users of Twitter who I am concerned about. The problem with misleading story reporting like this is the effect it has on sufferers of the disease or their relatives. The reason this particular story has got me angry is because I have seen the effects that this sort of reporting can have. Long-term readers will be aware that my grandmother suffered from Alzheimer’s Disease, which took a huge toll on my grandfather.

I still clearly remember a day when a national tabloid newspaper carried the headline “Vaccine for Alzheimer’s Disease!” My grandfather read the headline, turned to me and said “Does this mean they’ll be able to cure your grandmother?” My cynicism piqued, I read the article and had to gently tell him no. That story held many of the same points as this one; it was a study done in mice and no human trials had been conducted. It is five years later and there is no news on that subject; whether it failed at clinical trials or is still being tested I don’t know. But the false hope it gave to my grandfather, and the countless others who read these headlines and think their disease may be cured soon, is a sad and dangerous thing.

newspaperWho is to blame for this misinformation spreading? It’s probably a subtle combination of the scientists who wrote the paper, the journal who published it and the reporters who wrote the newspaper stories. For scientists, having work published in national newspapers is a huge coup; national reports result in interest in your work and so you’re more likely to secure funding  to continue with your groundbreaking research. Unfortunately, newspapers and by extension their readers will mostly respond to “interesting” stories, which translates to “treating a disease that people have heard of”.

Alzheimer’s is big news now, as it is predicted to affect 1 million people by 2021. Therefore, the scientists probably put Alzheimer’s as the key point of the findings to increase interest in their research. This is a common practise amongst researchers desperate to secure funding from a dwindling pot. I noted when researching this post that every single headline said the more evocative “Alzheimer’s” rather than “Parkinson’s Disease” or “ALS” which were also mentioned in the research paper as potential beneficiaries of the drug. Curiously, CJD isn’t even mentioned by the researchers as a disease which can benefit from the treatment despite being the best-studied prion disease in humans. However, CJD is much rarer than Alzheimer’s (causing 1 death per 1-2 million of the population) and the media storm that happened around it in the 90’s has died down. It is not a “sexy” enough disease to sell research or newspapers on such a grand scale.

How is this problem going to be solved? Is it possible to make research interesting if it’s not linked to a disease? I would like to think it would, but them I’m biased. It’s a real bugbear for me as a biologist that an “interesting” story about biological research has to be about curing a disease. Research which just explains how a system works can be fascinating.

Certainly taking out a small, speculative point and blowing it up to the key part of the story doesn’t work.  However an accurate headline such as “There’s a drug which prevents brain cell death in mice that have something similar to Alzheimer’s disease; won’t be used in humans for a decade or so” is hardly catchy. But it should be made crystal clear in the very first reading points of the article exactly what has been found and its relationship to the disease; the authors and journalists at least owe that to the people affected. As a reader, it’s probably best to take headlines involving the words “cure” and a deadly disease with a pinch of salt until you’ve read the full article. Unless they involve the words “repeated successful human trials” then it’s probably best to treat the information with caution.

Post by: Louise Walker (in rant mode)

Body disorders that you never knew existed- Part 1

Welcome to the world of the weird and wonderful. You will be taken on a run down through five of the most unusual, rare, fascinating and possibly unthinkable disorders that we know exist.

1.  Hypertrichosis- ‘Werewolf syndrome’

HypertrichosisImagine having a body covered in so much hair that people mistake you for a werewolf. This is something that sufferers of hypertrichosis have to deal with on a daily basis. Hair growth isn’t restricted to the areas of the body that we consider ‘normal’, instead spreading to areas over their body and face in men, women and children alike. The disorder is extremely rare with fewer than 100 known cases worldwide. But how does this unusual condition come about? Scientists think that there are two causes; one of a genetic nature, and the other developing due to certain external factors. Researchers in China tested the DNA of two unrelated patients with the condition and found that there were extra genes present in the same region of the X chromosome. This extra DNA sits near to a gene involved in hair growth (SOX3) and is thought to switch on this gene, stimulating mass hair production. Next time you have a moan about having to shave or wax to get rid of your unwanted hair, spare a thought for hypertrichosis sufferers.

2. Foreign Accent Syndrome

Speech_2Whilst this sounds like something from a very strange medical drama, foreign accent syndrome really does exist. Usually occurring as a result of severe brain injury such as stroke or trauma, the patient ends up speaking with an accent distinct from the one they had before. One of the most recent cases occurred after a women suffered from a severe migraine. She woke up in hospital to find that she was speaking with a Chinese accent despite never having visited China. What is to blame for this sudden change in dialect? Scientists have found that damage to the parts of the brain required for speech and movement of muscles during speaking affects how we pronounce words. This changes the timing and rhythm of our speaking. As our tongue forms words in a different way, it sounds as if we are speaking with an accent.

3. Congenital pain insensitivity

SplinterA condition where you are unable to feel any pain sounds like an absolute blessing. No headaches, no pain when you’ve broken a bone, or when you whack your knee on the side of a table. But now think about it seriously, imagine not being able to tell if you’ve pushed your body too far exercising or cut your finger whilst chopping up a carrot. Pain is one of our body’s most protective mechanisms, alerting us that something is wrong and needs our attention. Without this basic mechanism we would have no way of knowing when something has gone wrong.  Individuals born with this condition have what we call a loss of sensory perception: they are unable to feel pain but can feel pressure and touch. A mutation affecting how the nerve cells form during development is thought to cause the improper functioning of these nerves in response to pain. Sadly, this is likely to occur with other deficits such as mental retardation and in some cases the ability to regulate body temperature. Not being able to feel pain would be extremely advantageous-…if you are a superhero that is. For us mere mortals, not so helpful.

4) Fibrodysplasia Ossificans Progressiva- ‘Stone man syndrome’

FOPStone man syndrome does what it says on the tin. Cue an image of The Thing from the Fantastic Four- a body essentially made of rock. Slowly over time, sufferers of this excruciatingly painful disorder start turning to bone. Due to a malfunction of the bodies repair mechanism, the gene that is responsible for ossification (bone growing) during development remains active. This gene is usually switched off after the development of bones in the fetus. In time, muscles, tendons and ligaments slowly begin to harden and turn to bone. As the degree of ossification worsens, everyday tasks such as tying your shoelaces or walking to the shop become an impossible task. Would surgery provide suitable relief? In short, no. Surgery is not considered an option as this type of trauma causes the body to attempt to repair the damaged area – creating more bone and more damage than before. Although there are around 700 confirmed cases of FOP worldwide, there is very little known about how to treat it. Remember next time your body feels stiff and uncomfortable that what you are experiencing couldn’t even scratch the surface of what these people of made of stone are subjected to.

5) Trimethylaminuria- ‘Fish odour syndrome’

FishTrimethylaminuria is a rare metabolic condition that can be embarrassing for individuals suffering from it. An enzyme (FM03) that is needed to breakdown trimethylamine (TMO) into a substance called trimethylamineoxide is absent from the body. TMO gradually builds up without the enzyme to break it down, and so has to be removed from the body through other outlets such as the skin, urine and breath.  Whilst sweating out toxins isn’t unusual, it is the strong fish-like odour that comes partnered with it that is considered abhorrent. The condition is more common in women, possibly irritated by female hormones. Despite the putrid odour, there are no other symptoms associated with it.

Acne bacteria to blame for back pain?

What do acne and chronic back pain have in common? Well, as it turns out, more than people once thought.  A group at the University of Southern Denmark have found that the same bacteria that gives people spots might be to blame for up to 40% of patients with lower back pain. What’s more, these infections can be treated with antibiotics.

Slipped disc popping out from in between the evenly grey vertebrae

Your backbone is a column of alternating vertebrae (bones) and intervertebral discs (cushions). The bones provide the strength and support, while the cushion discs allow movement and flexibility. Occasionally, thanks to a mix of age and awkward movement, the disc can bulge out from between the bones. In some cases the jelly-like goo in the disc’s centre, called the nucleus, can even ooze out – a bit like thick jam leaking out of a doughnut. If the nuclear material or the disc itself puts pressure on nerves coming in and out of the spine, it can be even more painful.

Slipping a disc is, by all accounts, excruciating, but it usually starts to heal by 6-8 weeks. However, someone can be diagnosed with chronic back pain (CBP) when the pain doesn’t subside after three months. Trouble is, this happens all too often, with an estimated 4 million people in the UK suffering from CBP at some point in their lives. The cost of CBP to the NHS is about £1 billion per annum. This doesn’t even cover lost working hours or the loss of livelihood suffered. Treatment usually focuses on relieving pain, preventing inflammation and more recently, cognitive behavioural therapy to treat the patient’s psychology, especially if the organic, physical cause of the pain is no longer obvious.

Recently, scientists in Denmark found a really important link between the bacteria responsible for acne, known as Propionibacterium acnes (P. acnes) and bad backs. The researchers found that in about half of their patients with slipped discs, the disc itself was infected, usually with P. acnes. A year later, 80% of the infected patients – compared to 43% of the uninfected patients – had dodgier bones either side of the slipped disc than 12 months before. The affected bones had developed tiny fractures and the bone marrow was replaced with serum, the liquid found in blisters.

Acne is not to blame for bad teenage hairstyle choices.

So how did the discs get infected? Bacteria like P. acnes get into our bloodstream all the time, particularly when we brush our teeth or squeeze spots. P. acnes and other similar bacteria don’t like oxygen-rich environments and so don’t normally grow inside us. The spinal disc doesn’t have a lot of oxygen around, providing a perfect home for the bacteria. If the disc is damaged – say, after popping out from the spinal column – tiny blood vessels sprout into it, letting the bacteria move in and settle down.

There, the bacteria grow and, rather than spread anywhere else, they spit out inflammatory chemicals and acid. The acid corrodes the bone next to the disc and causes more swelling and pain around the area. This discovery is ground-breaking, since before this research it was thought that discs couldn’t get infected except in a few exceptional cases.

The Danish researchers then conducted a second study, testing whether simple antibiotics could get rid of these bacteria and therefore treat chronic lower back pain. Patients that already had the characteristic signs of bone inflammation (tiny fractures and swelling) were given a 100-day course of antibiotics. The patients were reassessed a year after the trial began. Patients treated with antibiotics reported less pain, less ‘bothersomeness’ (yes!), took fewer days off work, made fewer visits to the doctor and, crucially, their bones looked in much better nick than the patients given a placebo.

Considering the huge numbers of people who are affected by chronic back pain, and the cost of treatments like surgery versus a course of antibiotics, this discovery has been glorified as the stuff of Nobel prizes. The revelation that bacteria may be to blame for some cases of this mysteriously untreatable condition rings familiar. It has been likened to the discovery of the culprit bacteria behind stomach-ulcers, Helicobacter pylori. Like back pain today, stomach ulcers were dismissed for years to be a disease of the mind, endemic among stressed-out melodramatics or people who ate too much spicy food. (And yes, Barry Marshall did get a Nobel Prize for swallowing a Petri-dishful of H. pylori.) It would be fantastic if, instead of resorting to surgery, half a million CBP patients could be effectively cured within 100 days or less!

The bacteria in the plate on the right have become resistant to many of the antibiotic white spots and so are more widespread.
Photo by Dr. Graham Beards

Unfortunately, there is a downside. Antibiotics have long been the magical cure-all, but just like fossil fuels, housing and talent on TV, we’re running out. Bacteria are becoming resistant to antibiotics faster than we can create new, effective ones. It’s an arms race and we’re losing, very quickly. What’s worse is that because of the recent negativity surrounding over-prescription, there are now restrictions on giving patients broad spectrum antibiotics. Since antibiotics can’t be used as much as they were 30 years ago, pharmaceutical companies can’t make any profit from developing new ones. And so, to further compound the problem of antibiotic resistance, there are fewer and fewer antibiotics being created every year.

In 2000 alone, UK doctors made 2.6 million prescriptions of antibiotics for acne. One study by a group in Leeds looked at the number of acne patients who were infected with P.acnes and were resistant to at least one type of anti-acne antibiotic. Between 1991 and 2000, the fraction of acne patients with antibiotic-resistant bacteria rose from about a third to more than a half.

The discovery that acne bacteria might be to blame for so many cases of debilitating back pain is hugely important. However, it also highlights how dependent we are on our dangerously dwindling supply of effective antibiotics, and how we might be wasting antibiotic effectiveness on comparatively trivial conditions such as spots.

Post by: Natasha Bray