The race between science and new doping techniques

With the Olympics being held in London later this year, and the controversial abolishment of lifetime banning for athletes caught using illegal performance enhancing drugs, there has never been a better time to try and cheat your way to the top. The desire to be the best in your field is what drives professional athletes to be at the top of their game. When this desire gets too much, it can push athletes to use illegal drugs and other performance-enhancing methods.

With rapid progress in the field of sports science, the ways by which athletes enhance their performance are evolving rapidly. New methods are emerging that threaten to undermine the efforts of those who try to win honestly.

Recent research has shown that drinking large amounts of green or white tea is enough to mask the illegal use of testosterone in deceptive athletes. The use of testosterone by athletes is currently illegal since it is known to increases muscle mass. Unfortunately it is extremely hard to detect athletes who are using testosterone since the hormone occurs naturally in both men and women. However, some tests are capable of detecting increased levels of testosterone. These rely on looking at the ratio between testosterone and another hormone found in urine, epitestosterone.  A study at Kingston University London has found that tea contains unusually high levels of anti-oxidants called catechins. These inhibit an enzyme required for testosterone to be excreted in urine, meaning that athletes drinking large volumes of tea will secrete less testosterone, so can evade detection by current doping tests. Therefore green tea can effectively help ‘fool’ scientists into thinking that an athlete is clean. Who knew the quintessentially British ‘cup of tea’ could benefit dishonest athletes, pulling the wool over the world’s eyes!

Another potential ‘game-changer’ facing the World Anti-Doping Agency (WADA) is the concept of using doping genes to improve an athlete’s performance. Research at the International Centre of Genetic Engineering and Bio-technology in Italy has found that injecting certain growth genes into mice causes  them to develop significantly more muscle mass than non-treated animals. A virus, acting as a carrier, is used to implant the gene for Insulin-Like Growth Factor 1 (IGF-1) into muscle cells in the mice. Mice injected with the gene are able to swim for three times as long as normal animals. Along with increased endurance, the IGF-1 gene also triggers production of 10 times more protein than is seen in normal muscles and an increase in genes controlling energy production, muscle contraction and respiration – all vital for a ‘super-human’ sportsman (or woman)!

When testing for indications of this in blood and urine samples from treated mice, there was no trace of any of the implanted gene, protein or virus. This may make it possible for doping cheats to get around the laws! Biopsies of athletes’ muscles would show up differences between the structure of the muscles of a trained athlete and a cheat, however, there are ethical concerns over subjecting athletes to such tests.

At a recent conference held in London, aptly called Tackling Doping in Sport, it emerged that new blood and urine tests were currently under development that could potentially expose ‘DNA doping’. If all else fails, authorities could expose cheats using this method of performance enhancement by creating a biological passport for each professional athlete. This file would regularly record the profiles of an athlete and would indicate when a dramatic change in their fitness is observed.

The idea of a biological passport is considered by some to be controversial. This could mean that honest athletes, who train and compete well within the laws of their sport, may end up being severely penalised because of corrupt athletes who want to cheat their way to the top. It is easy to argue that athletes join the profession knowing they are required to provide fluid samples if requested. However, muscle biopsies and biological passports may be considered a step too far!

Although regulating bodies have identified gene doping as an imminent threat to the sporting community, no athlete has yet been caught using this method.   Due to the growing potential of gene doping, WADA is taking a proactive stance to ensure that athletes attempting to use this method will be identified, and that structures will be in place to test for such cases.

The world of sport is being flooded with novel ways in which athletes can illegally improve their performance. This field is evolving from one where hormones in the body are elevated to improve performance, to a field where athletes could potentially use viruses to interfere with their DNA. The exact nature of how athletes will try to dodge drug tests in the future is not clear, although we can be certain that some will try their hardest! It will be interesting to observe the evolution of ways to test for illegal drugs in sport, to reflect novel performance enhancement ideas. Whatever happened to putting in the hard work yourself, and reaping the benefits?

Post by: Samantha Lawrence

Blame it on the brain: can you be held legally responsible for your brain?

Earlier this year, Edwin Hart Turner (38) was executed by lethal injection after being convicted of murdering Eddie Brooks and Everett Curry in a robbing spree near Mississippi. Shortly before the murders, Turner had been admitted at a mental hospital for depression after an attempted suicide. The defence attorneys’ main argument against Turner’s execution was his unstable state of mental health. Guilty or not guilty, Turner’s lawyers argued that a mentally ill person should be exempt from state execution.

Charles Whitman was a sporty, popular man who became increasingly aggressive and violent, while complaining of ‘tremendous headaches’. In 1966 he shot 13 people dead and wounded 32 others at the University of Texas in Austin before committing suicide. His autopsy discovered a cancerous tumour the size of a walnut invading his amygdala – a part of the brain important in regulating fear and rage.

Currently, the trial of Norwegian Anders Behring Breivik is dividing both social and professional opinion. Breivik, led by his far right-wing views, killed 8 people with a car bomb in Oslo and 69 more on the island of Utoya, a camp for the youth wing of the Norwegian Labour Party. Breivik maintains that he is not legally insane and that he should be held fully culpable for his acts. Legally this would mean the difference between him being sectioned in a mental hospital, possibly indefinitely, or being incarcerated for a very long time. Professional opinions of Breivik’s mental health vary from him being ‘lucid but lonely’, to having personality disorders, including extreme narcissism; paranoid schizophrenia or psychosis; being both suicidal and homicidal; to having ‘a rare form of Asperger’s and Tourette’s syndrome’.

Admittedly, cases such as these aren’t exactly common. However, with further advances in our understanding of mental illness these stories are increasingly relevant, necessitating a level of crossover between neuroscience and legal ethics. This crossover poses a major dilemma for society, the question of how much personal control we have over our own brains and whether or not we can be held entirely responsible for our actions? Must all mass-murderers be, to some extent, mentally ill since they fall so far outside a ‘normal’ moral spectrum? Are we less accountable for our actions and decisions since our brains’ functions are a product of our biology and social influences?

These more general philosophical questions lead us to specific practical questions about how society should act. Should all criminals be psychologically and neurologically tested when being trialled? Should brain scans be used as evidence in a court of law? How should we treat people who have committed terrible crimes but are psychologically or neurologically unwell and should there be a distinction between the two?

At the end of 2011 The Royal Society published a report stating that in the USA, neurological or behavioural genetics were used as evidence for 722 legal defences between 2005 and 2009. In Italy, a woman had her sentence for murdering her sister reduced after the defence lawyers presented genetic and imaging evidence that her brain’s anatomy was different to that of 10 normal women. On the other hand, in 2008 an Indian woman was convicted of poisoning her husband when a scan of brain activity allegedly revealed that she had knowledge of events surrounding her spouses death which could only have been gained through experience. Neuroscientists are now often called upon as expert witnesses and so should have a understanding of the legal and ethical implications of their testimonies.

Following this, there has been a lot of research investigating how people perceive neurological or psychological evidence. In this research, mock-jurors were asked to decide whether a virtual defendant was guilty or ‘not guilty by reason of insanity’ (NGRI). The virtual defendants had different levels of neurological or psychological evidence to support their claim of insanity. For example, in some cases medical evidence was provided proving the defendant had suffered brain damage, whilst in other cases the results of psychological analysis was given showing various types of personality disorder. This research found that around 50% of mock-jurors will find the defendant NGRI on the basis of evidence suggesting the defendant has suffered physical brain injury or neurological disease, especially if this is backed up by a brain scan. However, only about 10-12% of mock-jurors find virtual defendants with a personality disorder or psychopathy to be NGRI.

So what does this mean in real life? Today, it is estimated that 90% of UK prisoners have a diagnosable mental illness or substance abuse problem (Office for national statistics). About 1 in 7 of all prisoners in the UK are thought to have four concurrent mental health problems, often not simply associated with the time spent in prison. Also more than half the reported prisoners who commit suicide in prison exhibit symptoms of mental health problems on entering prison. Whether or not these mental health issues preceded or even contributed to their crime is unknown (and I can’t say how one would ever prove that beyond reasonable doubt), but I think that this has huge implications for the prison system. Seeing as people outside prison with mental illnesses are treated as patients rather than criminals, I think the government should focus on treating and rehabilitating, rather than punishing, prisoners who have been incarcerated on their brain’s behalf.

Post by: Natasha Bray

The Flow-Chart of Science

Next time you’re perusing your favourite newspaper or news website, it’s quite likely you’ll come across a headline announcing a new scientific discovery, perhaps saying something like “New drug found to reduce tumour growth in lung cancer patients”. This headline seems simple enough, but don’t be fooled, in order to generate it several scientists, several years and a whole lot of blood, sweat and tears (sometimes literally) will have been involved. What makes it all so complicated you may ask? Well to answer this question I have created, for your entertainment and enjoyment, some (very generalised) flow-charts of a scientist’s life, which I hope will provide you with a small window on our world:

#1 Experimentation:


All research starts out with a hypothesis (an idea). Normally, after months of reading around a topic, you build on existing knowledge by proposing your own question. This question may stem from something someone else has discovered, or perhaps a hunch or suspicion you have based on your own previous research. For example, you may propose that “daily intake of a new experimental drug will significantly reduce growth of tumours in lung cancer patients”. The difficult part is working out how to prove this! You must find the best way to design an experiment to answer the question, preferably in the quickest and cheapest way possible.

Designing the experiment is arguably the trickiest part of scientific research. It is important that you can prove, beyond reasonable doubt, that the factor you are testing is the sole cause of the effect you are seeing. Taking our cancer-drug hypothesis above, you will need to prove that the experimental drug is the main factor which is causing the reduction in tumour growth. In order to prove this, you need to find a relevant ‘control’ for your experiments. A control experiment largely mimics the actual experiment with the exception of the factor you are testing. To test that a new experimental drug works against lung cancer, you will need to use two groups of individuals (humans, or perhaps experimental animals depending on what stage of development the drug is in) with the same type of lung cancer. The first group will have the experimental drug given to them and the effect it has on the size of their tumours will be monitored. This group is the “experimental group”. However, the data from this group cannot stand alone; you need something to compare it to. This is where your control group (also known in human trials as the “placebo group”) comes in. The placebo group will usually also receive a pill, but it will be inactive, such as a sugar pill. You can then compare the rate of tumour shrinkage between the experimental and placebo groups. If the placebo group also experiences a reduction of tumour growth, then it shows that the effect is not due to your drug, but rather something else.

The selection of the experimental and placebo group is immensely important; you must ensure that the only real difference between the groups is whether or not they receive the drug. For example, if your experimental group are all females but your control group are males, you will not be able to say whether it was the drug or the effect of gender which caused your results. This is much easier to achieve in laboratory settings than in clinical studies (carried out with human subjects) since in a lab you can easily control for factors such as diet and lifestyle in both groups.

Ensuring your experiment works and is properly controlled can often be a serious headache and can take up a significant amount of time. However, once you’ve got your experiment working, then it’s time to get the results. If you’re lucky, the results will prove your hypothesis and you can move on to the next stage. However, there’s also a chance it’ll disprove your hypothesis. This means that you’ll need to generate a new hypothesis and start the whole process again.

So you’ve got your experiment to work, it’s well controlled and it proves your hypothesis. Now you’re good to go, right? Actually, no. Science rarely gives a definitive answer, and what’s more likely is that getting the answer to your original question will produce more questions which need further investigation. You may have noticed several infinite loops in the flow charts (if you follow the “no” answers anyway) – it is sometimes arbitrary when you decide to break the loop and publish your data in a ‘journal’ for the rest of the scientific community to see.

#2 Publishing:

There are several hundred different journals covering all specialities, from general science (maths, physics, biology, chemistry, engineering etc.) to incredibly specific areas such as Alzheimer’s disease. These journals publish “papers” which have been submitted by a group of scientists detailing their research, any relevant data required to back up their claims and explanations of how their work is relevant to the wider community. The important thing about publishing data is that you have a coherent story which is interesting to other people, especially fellow scientists.

So what happens when you finally decide to publish? Firstly, there is a significant advantage in having positive data (results which prove your original hypothesis). A big problem with scientific research is that negative data (results which disprove a hypothesis) are much harder to publish. A positive result is generally regarded as more interesting and a journal is more likely to accept it.

Another thing about publishing is that the data you present has to be of the highest quality. This may mean repeating experiments until the data produced is both convincing and aesthetically pleasing. This could take months to do well. Once you’ve got your data, then you can write your paper, in the style of your intended journal. This again can be a lengthy process.

So you’ve got convincing positive data which you’ve written up as a paper but now what do you do? Well, It depends on which journal you submit to but generally the paper will first be scrutinised by the journal’s editors. This is where they decide whether it’s interesting enough to publish. This can depend on the journal – top-level publications (also known as “high impact journals”), will only accept the highest quality most interesting stories and are quite likely to reject research if it’s not interesting enough. If your work not deemed good enough for your chosen journal the paper is ‘bounced back’ to you and you’ll have to rewrite it for another journal with a lower “impact factor”, or perform more experiments to help back up or round off your story.

If the editors accept your data, they’ll send it for review. This means giving it to (usually) three other scientists who work in a similar field. They thoroughly check the data and ensure that it makes sense. At this point, they may give the green light to publish, but they could also ask for additional experiments or data to add to the story. However, they could also decide that it isn’t interesting or convincing enough to be published in this particular journal. You can then attempt to submit it to a different journal, or you may have to scrap your whole idea and come up with a new hypothesis.

The pay off for all of this time and frustration is finally having your work published and available to the wider scientific community. Fellow scientists around the world will now be able to see what you’ve been doing and what you’ve achieved, making all the blood, sweat and tears worth it. Hopefully your work will make a recognisable contribution towards your field – even small or seemly insignificant discoveries can turn out to be very important later on.

So you’ve published … now what? You guessed it: time for a new hypothesis. Prepare to re-enter the loop and start the whole business over again.

Post by: Louise Walker

Blurring the line between man and machine

In the last few years a small piece of science-fiction has become science-fact. In a recent study a woman, paralysed from the neck down, was able to move a robotic arm using only the power of her mind. Through this robotic appendage she was able to do something she hadn’t done for many years: pick up a cup of coffee and drink from it out without help.
This life changing feat was achieved through the surgical implantation of a computer chip within her motor cortex (the area of your brain which activates when you initiate a movement). The chip detected activity within this region of the brain, forming what is known as a ‘neural interface’. This chip was then connected to a computer which controlled the robotic arm. After some practice, the participant’s brain adapted to the neural interface allowing her to control the arm. What makes this amazing is that despite being paralysed for 15 years, only 20 minutes of adaptation was needed to manipulate the arm adequately.

Coffee served by a robotic arm: almost as expensive as Starbucks (Original work by: Hochberg et al., 2012).

This research is the latest in a long line of studies showing how machines or devices linked directly to the brain (so called “neuroprostheses”) can be controlled by thoughts alone. First pioneered in rodents and monkeys, this technology is now showing promise for improving the lives of many handicapped people. Potentially, anyone suffering from paralysis in the future will be able to regain a degree of independence and control over their surroundings.

These interfaces also have scope beyond treatment of paralysis, they have in fact been applied to the treatment of many different disorders. A few examples include: Locked-in syndrome, a state where a person is completely unable to move or signify that they are conscious. These patients are unable to speak or in some cases even blink. Trapped in a prison of their own body, patients have gone years before anyone has known that they are conscious. Thankfully, neural interfaces have been developed that allow direct control of a cursor on a computer screen and control of text selection systems for communication. For these people, neural interfaces will provide an outlet through which they can communicate with and interact with the outside world. Similarly, a neural interface in the visual cortex connected to a camera has enabled blind subjects to regain some of their sight. Although sight is only restored to a level that allows them to perceive the outline of shapes and to read, this is still an amazing breakthrough.

Right: Stephen Hawking uses a text selection system using input from moving his cheek to communicate. However for someone with locked-in syndrome even this would not be possible. Left: Jens Neumann, who regained his vision with a neural implant.

Taking the research further, the ‘Holy Grail’ would involve a neural interface coupled with muscle stimulation (a therapy already in use). This would give the patient direct control over their own limbs; providing what could be described as a substitute nervous system which could bypass the injury causing the initial paralysis. Although such complex limb control is still just an ambitious long term goal, more basic control is already within reach and is currently being implemented.

And what about amputees? There are already advanced mechanical prosthetic limbs that can be controlled by muscle movements. One example is shown below:

However, whilst the control and range of motion of these hands is already sophisticated, a direct neural implant would provide numerous advantages in the complexity of movement as well as the ability to perceive touch, temperature and position. Were all of these incorporated into a neural interface, a prosthetic limb would feel more like a new arm or leg rather than simply a mechanical appendage.

Of course in fiction, people with neuroprosthetic implants are often depicted as psychotic transhuman abominations bent upon the destruction or corruption of normal society. But, given the brain’s incredible ability to adapt, what sort of non-therapeutic implants should we realistically consider? What if instead of recovering some form of lost function, neural interfaces were instead used by healthy people to gain some new function? For example, what about a new sense? Birds can navigate thousands of miles across featureless ocean by intrinsically perceiving the earth’s magnetic field. If there was a compass in your head that was always on and as easy to interpret as your sense of hearing, you might never get lost again. What if a neuroprosthetic implant allowed you to perceive sounds beyond the normal range of human hearing, like a supercharged hearing aid? Or perceive light beyond the normal range of human vision in conjunction with eye augmentation? You then quite literally would have x-ray vision.

Precisely how neural implants will develop in the next few decades is difficult to predict. Significant technical challenges exist in the long term function of these devices and their ability to resist problems such as tissue deterioration, movement and the body’s own immune response. Despite these issues, they undoubtedly will play a huge role in the lives of people with debilitating injuries, but how much of a role will they play in the lives of the rest of us? We will simply have to wait and see.

Post by: Chris Logie

We are not alone: How the bugs in our gut influence our eating habits.

Your gut is literally teeming with microorganisms, the majority of which are bacteria. Indeed, the single celled squatters residing in our gut are estimated to outnumber our own cells 10:1 (this means that your body contains ten intestinal microorganisms for every one of its own cells!). Although these figures may make you feel uncomfortable, there is nothing sinister about our resident bacterial tenants; in fact scientists believe that the relationship we have with most these bacteria is actually beneficial. These bacteria or ‘microbiota’ help us absorb important nutrients from our food whilst also boosting the guts immune system, making them pretty much indispensable.

However, not all gut bacteria are alike. We know that, just as everyone expresses their own individual compliment of DNA , each individual also houses his or her own host of gut microorganisms. The specific compliment of bacteria resident in your gut depends heavily on environmental factors such as diet and is also liable to change throughout the course of a lifetime. Interestingly, as with DNA, different compliments of bacteria confer different properties to the host, some less favourable than others.

Work with mice suggests that certain types of gut microbiota may make an individual more prone to weight gain. This idea stems from work with three separate groups of mice: fat mice, lean mice and germ-free mice (mice with no detectable gut microorganisms). Scientists found that, unlike normal mice, germ-free animals did not gain weight when fed a high fat ‘Western’ diet. In fact, these mice needed to eat more than normal animals just to maintain a healthy weight. This is presumably because their lack of intestinal bacteria made it harder for them to absorb nutrients from their food. The researchers then moved on to investigate how these germ-free animals responded to infection from different compliments of gut microbes. They infected two separate groups of germ-free animals with gut microorganisms taken from either fat or lean mice. Both infected groups gained weight, however, only animals infected with gut microbes from the fat mice became overweight. These findings indicate that the fat mice may carry a specific array of microbes which promote excessive weight gain.

This research raises the question of how bacteria living in our guts can influence the amount of food we eat and the amount of weight we gain? Findings suggest that by-products generated by gut bacteria can influence both the amount of nutrition absorbed from food and the way the gut signals to the brain telling us to stop or start eating. Since different groups of bacteria will influence these systems in different ways, it has been suggested that the type of bacteria you house could influence both your eating habits and the nutrients gained from the food you eat.

So how do these findings fit with what we already know about weight control and the gut’s microbiome? Although the overall picture emerging from this research area is complicated, there are a few things we can be quite sure of: Firstly we know that our gut microbiota are generally more beneficial than they are harmful (note that although germ-free mice seem resistant to weight gain, they are also much more susceptible to infection and do not live as long as normal animals). We now also know that not all bacteria are equal, with some appearing more beneficial than others. Finally it is widely accepted that the role bacteria play in weight control is just one part of a much larger picture involving genetics, diet and exercise. Therefore, although I don’t think we know enough to claim that ‘good bacteria’ can offer a miracle solution to weight loss, the possibilities for further research into this area are exciting, especially since the gut’s microbiome is easily altered by changes in diet and the use of pro and prebiotics.

Post by: Sarah Fox