Denying the evidence – Why do people stick to their beliefs in the face of so much evidence? Emma Hazelwood

It has been accepted in the scientific community that climate change is a result of human activity for almost twenty years. However, a study in 2016 found that less than half of U.S. adults believed that global climate change is due to human activity. In 2012, Trump tweeted that “The concept of global warming was created by and for the Chinese in order to make U.S. manufacturing non-competitive”. In a world with overwhelming evidence to the contrary, how can people continue to believe that global warming doesn’t exist?

Once people believe an argument, it is very hard to persuade them otherwise, even if they are told that the information they based their opinion on is incorrect. In a study conducted at Stanford University, two groups of students were given information about a firefighter named Frank. One group were told that Frank was a good firefighter; the other that Frank was a poor firefighter. Participants were then told that the information they’d been given was fake. Afterwards, they were asked to give their own opinion on how Frank would respond to a high-risk situation. Those who had initially been told that Frank was a good firefighter thought that he would stay away from risks, but those who had been told that he was a poor firefighter thought that he would take risks. This study shows that, even though they were then told it was fabricated, the initial information influenced participants’ opinions.

Confirmation bias is when people are more likely to believe facts which support an opinion they already had, rather than evidence to the contrary. A study in Stanford in 1979 involved two groups of students. One group was for capital punishment, the other against. Both groups were shown two fabricated articles. One contained data that supported capital punishment, the other data that opposed it (the statistics were designed to be equally strong in each article). Both groups stated that the source which supported their argument was more reliable. Furthermore, when asked to express their opinions on capital punishment after the study, both groups supported their standpoint even more than before. This demonstrates human nature to selectively believe what we want to be true.

It is believed that humans act this way because it was beneficial in early hunter-gatherer societies. Confirmation bias not only encouraged humans in societies to collaborate, but it was also important for social status to be considered correct. One theory for why seemingly rational humans continue to think irrationally is that we get a rush of dopamine when we see evidence which validates our opinion.

However, early human societies were not teeming with “fake news” and fabricated studies as we are now. It is increasingly clear how having a public swayed by confirmation bias can be dangerous to modern society.

We live in an illusion, where we think we know more than we actually do. For instance, one study found that when people were told about the new (fictitious) discovery of a rock that glowed, if they were told that the scientists who discovered it did not know why it glowed, participants did not claim to know as much about the rock as those who were told that scientists understood how it works (even though the subjects were not given any information on why the rock glowed). This phenomenon of people thinking they understand more than they do is common, and has actually been advantageous in terms of scientific progress. As scientists, we do not need to understand every scientific discovery there has ever been – we rely on the knowledge of our ancestors and those around us.

Humans are programmed to be influenced by information which they are then told is fake, and to think of sources which support their pre-existing opinion as more reliable than those which question it. However, this can be dangerous in areas such as politics. For example, if people around an individual claim to know why Brexit would be economically beneficial to the country, then even when presented with evidence to the contrary the individual is less likely to believe it. Likewise, if a person believes that global warming is a conspiracy, they are more likely to believe Trump when he says it was created by the Chinese than ecologists who say we are pushing our planet to critical levels. In a world where we are bombarded with clickbait and fake news, it is more important than ever to think rationally and critically about every piece of information.

The Teenage Brain – Charlie Delilkan

We’ve all been there. “I’m leaving home and I’m never coming back!” “It’s not just a phase, Mum.” Slammed doors. Smashed plates. My Chemical Romance t-shirts and “bold” eyeliner. If you haven’t guessed already, I’m referring to those golden teenage years. Whilst we may have given our parents a hard time, we may not be completely responsible for that increased phone bill.

When we’re born, our brains aren’t fully formed so the first few years of our existence involve an expansion of connections – synapses – between cells. Approximately 10,000 different connections are made between the hundred billion brain cells you were born with by the time you are six-years-old!

But during our teenage years, these numerous connections are trimmed down; the brain decides which connections are important enough to keep, and which can be let go, depending on how frequently each neural link is used. This process is called synaptic pruning. This process actually continues well after we stop calling people “teenagers” – some researchers believe this only ceases in our mid twenties, sometimes later! But sometimes this process can go wrong, leading to important connections being lost which could lead to psychiatric disorders such as schizophrenia.

The synapses that are kept are then subjected to a process called myelination, where the synapse is given a sheath that helps them transmit signals more quickly. That is why the teenage years are so critical to your future development! Skills and habits laid down at this point are likely to stay in the long run.

Interestingly, the prefrontal cortex is the last part of the brain to fully mature (or finish pruning). However, this is the part that allows us to be an adult – it controls our emotions and helps us to empathise with others. Therefore, if your prefrontal cortex isn’t functioning fully, you tend to be impulsive and insensitive to other people’s feelings. Sound familiar? Don’t worry though – as teenagers mature, the prefrontal cortex is used a lot more when making decisions, showing that they start to consider others when making choices.

What about that stereotype that teenagers are “hormonal”? Well stereotypes usually come from some truth! Teenagers are hypersensitive to pleasure; rewards such as the neurotransmitter dopamine release is at its peak during adolescence. Any action that causes dopamine release is positively reinforced, but the actions that cause the most dopamine release are usually associated with a stereotypical teenager – reckless driving, drug taking, and/or risk taking. Or in my case, 7 hours of dungeons and dragons on a Friday night – please don’t judge. This reward system is also closely harmonious with the brain’s social network, which uses oxytocin, a neurotransmitter that strengthens bonding between mammals. This causes teenagers to strongly associate social interactions with happiness  and so constantly seek out social situations. This explains why we usually see a dynamic shift from kids being close to parents to teenagers having friends being their emotional centres.

So the next time the teenager in your life is threatening to throw a chair at you, just remember that parts of their brain are literally being destroyed. Cut them some slack, bro.

What Causes Alzheimer’s? Emma Pallen

Alzheimer’s disease is a chronic neurodegenerative disorder with a wide range of emotional, behavioural, and cognitive symptoms. It is the most common cause of dementia, causing around 60-70% of dementias and is primarily associated with older age, with around 6% of the global population over 65 being affected and risk increasing with age. This is especially concerning considering our ageing population and, by 2040, it is expected that there will be 81.1 million people suffering with Alzheimer’s worldwide. It is also one of the costliest conditions to society, costing the US $259 billion in 2017.

Symptoms of Alzheimer’s can be grouped into three categories. Perhaps the most recognisable category is cognitive dysfunction, which includes symptoms such as memory loss, difficulties with language, and executive dysfunction. Another category of Alzheimer’s symptoms is known as disruption to activities of daily living (ADLs). Initially this can be difficulty performing complex tasks such as driving and shopping, later developing to needing assistance with basic tasks such as dressing oneself and eating. A third category of AD symptoms are related to emotional and behavioural disturbances. This can range from depression and agitation in earlier stages of the disease to hallucinations and delusions as the disease progresses.

What causes Alzheimer’s Disease?

We know that the symptoms of Alzheimer’s are caused by a gross loss of brain volume, also known as atrophy, in a number of regions that progress as the disease develops. As brain tissue is lost, symptoms associated with the function of the lost area emerge, such as personality changes developing as tissue is lost in the prefrontal cortex.

We also know that this brain atrophy is caused by a loss of neurons and synapses in the brain. However, what we don’t know is exactly why this neuronal loss occurs. One way to attempt to solve this question is to compare the brains of Alzheimer’s patients to normally ageing brains. This has led to the observation that the brains of Alzheimer’s patients have two distinct biochemical markers: amyloid plaques and neurofibrillary tangles, which are both abnormal bundles of proteins. While these features are often present to some degree in normal ageing and are not always observed in Alzheimer’s, they are often more associated with specific brain regions, such as the temporal lobe, in Alzheimer’s than in regular ageing. There are a number of theories as to how these biochemical markers may be linked to neuronal and synaptic loss, however none are fully conclusive.

One such theory is the amyloid cascade hypothesis. This hypothesis suggests that amyloid plaques, which are made up of a protein known as amyloid beta, are the primary cause of the disease and that all other pathological features of Alzheimer’s are as a consequence. This theory suggests that the accumulation of amyloid beta into plaques leads to disrupted calcium homeostasis in the cells, which can lead to excitotoxicity and ultimately cell death. Evidence in support of this theory comes from the fact that Down’s Syndrome, a condition in which almost all sufferers display some degree of Alzheimer’s disease by age 40, is associated with a mutation on chromosome 21 which is also the location for the gene coding for Amyloid Precursor Protein (APP), a precursor protein that leads to the formation of amyloid beta.

However, if the buildup of amyloid plaques are the cause of cell death in Alzheimer’s disease, it stands to reason that the removal of these plaques should at the very least stop the progression of the disease, which has not been found to be the case. Furthermore, whilst APP producing transgenic mice do end up having more amyloid beta and amyloid plaques, this does not lead to other features of the disease such as neurofibrillary tangles and most importantly, no neuronal loss. This suggests that there may be some other cause for the neuronal loss seen in Alzheimer’s.

Another theory about the cause of neuronal loss in Alzheimer’s focuses on hyperphosphorylated tau, a protein that is the main component of neurofibrillary tangles. The tau hypothesis suggests that the hyperphosphorylation of tau leads to the formation of these neurofibrillary tangles which can result in depleted axonal transport, a potential cause of cell death. This idea is supported by the fact that the number of neurofibrillary tangles is linked to the degree of observed cognitive impairment. Additionally the progression of where tangles are found is similar to the known progression of atrophy observed in Alzheimer’s. Dysfunction of tau is also known to be linked to another type of dementia, frontotemporal dementia, so it seems plausible that similar mechanisms may be at work in Alzheimer’s.

Whilst these are the two of the most prominent explanations for neuronal death in Alzheimer’s, there are a multitude of other potential explanations, and it is likely that no single explanation will capture all facets of the disease. Rather, it is more likely that there is a complex interplay of biochemical reactions along multiple pathways that lead to the clinical features we see in Alzheimer’s disease. These are likely affected by many other risk factors, such as genetics, or environmental factors such as smoking or head trauma.

Dyslexia: In the eye of the Beholder?

Dyslexia Word Cloud

Bethany Firmin

Dyslexia is a specific learning difficulty (SpLD) affecting between 5-10% of people. The disorder is characterised by difficulties in phonological awareness (this refers to the ability to focus on and manipulate individual sounds in spoken words), verbal memory and verbal processing speed.

As well as difficulties with spelling and reading, there are a broad range of other symptoms – this can include concentration issues, trouble understanding certain jokes/expressions and difficulties with time management. Dyslexia is a broad spectrum, with some individuals experiencing some of the associated difficulties but not others, and with varying levels of severity. While some may have mild dyslexia, which can (personally, I was only diagnosed in my first year of university) be managed, others may always struggle significantly with reading and spelling. Intelligence is not affected.

For someone to be diagnosed with dyslexia, diagnostic tests are carried out, the content of which varies depending on the age of the individual. While these tests are very useful in giving information about an individual’s specific strengths and weaknesses, they can be very time-consuming.

Currently, there is no cure for dyslexia, but there are many strategies to help people, such as alternative exam arrangements and extra tutoring. With adequate support, many people with dyslexia go on to be very successful in life. The importance of early intervention is emphasised.

Dyslexia is widely believed to be a neurological problem, but a recent study suggests they may have found a possible cause of dyslexia – not in the brain, but the eyes!

Photoreceptors in the eye

In the eye, there are two types of photoreceptor (structures that respond to light) – the rod and cone cells. Rod cells, the more plentiful (around 120 million), respond to low levels of light but do not detect colour, which allows you to see in the dark. There is only one type of rod cell, and they are absent from the fovea (the region of the retina responsible for the highest visual acuity) but concentrated elsewhere. Cone cells (6-7 million) are only activated at higher concentrations of light, but detect colour. There are three types of cone cell – blue, red and green. There is a ‘blind spot’ in the fovea of about 0.1-0.15 millimetres, in which there are no blue cone cells.

Eye Dominance and Dyslexia

Similarly to the way in which most people have a dominant hand (apart from those who are ambidextrous), most people have a dominant eye. Both eyes record slightly different versions of the same image, so the brain decides which one is likely to be the most accurate. Signals from this dominant can override signals from the other. Lots more people are right-eyed than left.

This study investigated the presence or absence of eye dominance in 30 non-dyslexic students and 30 dyslexic students, using a method called the afterimage test. For the non-dyslexic participants, 19 were right-eye dominant and 11 were left-eye dominant – therefore, all had a dominant eye. On the other hand, 27/30 of the dyslexic participants had no dominant eye.

Furthermore, there were correlations between lack of eye dominant and apparent physical differences in eye. In the dominant eye, the shape of the blind spot is circular, while the shape in the non-dominant eye is elliptical. In the dyslexic participants with no eye dominance, however, the shape was circular in both eyes. For one of these participants, five family members who also had dyslexia were studied – there was no asymmetry in the arrangement of cone cells, as well as no eye dominance. This suggests a possible genetic cause of dyslexia, and could lead to new diagnostic strategies for dyslexia

Lack of asymmetry would mean the brain has to process two slightly different ‘mirror images’, which researchers believe would confuse the brain. Perhaps this could explain why dyslexic people commonly make ‘mirror image errors’ – for example, mistaking ‘b’ and ‘d’, or ‘3’ and ‘E’ – and often get confused between left and right.

So, what else does this study mean for dyslexic people? Firstly, lack of afterimage dominance could lead to a potential new, quicker way to diagnose the condition. In addition, researchers were able to use an LED lamp to “cancel” one of the images in the brains of the dyslexic participants, which reduced reading difficulty. Some participants referred to this as the “magic lamp”.

Considerations & Limitations

While this study seems very promising, it is important to remember that only 30 dyslexic participants were studied – this sample size is too small to draw any absolute conclusions. Also, all participants were students, so these would not have been representative of the whole dyslexic population.

A further problem is that the study cannot establish cause-effect relationships. It cannot be said whether the visual differences are the trigger of dyslexia, or simply a consequence.

As well as that, the findings from the study may explain some people’s dyslexia symptoms, but may not necessarily explain the symptoms of other people. As mentioned before, dyslexia has many symptoms and manifestations, which this study does not necessarily explain. For me, I don’t experience ‘mirror image’ distortions when reading, but the words sometimes start to go wobbly after I’ve been reading for a while. There are a range of other distortions experienced by other dyslexic people too, such size distortions of letters/words or gaps between words appearing narrower/wider.

In conclusion, while the study seems promising, significantly more work is needed before any proper conclusions about the cause of dyslexia can be drawn.

Why do we Procrastinate?

do it - procrastination concept

Emily Farrell

Everyone procrastinates. No one wants to write that essay, or clean the bathroom. If it’s not food, sex or sleep, your body is just not interested. Sure, in the long run you might need to write that essay, to get that degree, to get that job, to earn money to buy food to survive. But your body doesn’t understand, or care, about that. Your body is a thing made in simpler times. It is built for when survival entailed going off to pick some plants to eat, some reproducing and maybe a bit of sleep afterwards. But modern, western lifestyles are a horrible mismatch for this way of living. Imagine giving a caveman a long, boring, task to do such as moving numbers from one column to another (maybe with sticks, it could take a while to explain the concept of computers). Why should he do it? He gets no food from it. He gets no joy from it. Doing this task does not make him any more attractive to cavewomen who might then want to have his babies. It takes a reasonable amount of energy that is better spent in other labours. So why should he do it? To him, the answer is he shouldn’t. And this is the thought process your brain goes through when faced with a task. While the conscious parts of your brain know the real reason for the task, your ancient parts of the brain, which we share with our ancestors and other animals, do not.

Think about it. How do you procrastinate? Making a snack? (means you won’t starve to death) Taking a nap? (means you won’t be too tired to see the tiger of death headed your way) Talking to friends? (maintaining social bonds which one day might lead to you making tiny replicas of yourself vis someone else’s genitals) Watching cat videos? (evolution can’t explain the internet, but taking joy from something which takes away no resources you may have gained from the other tasks means your body agrees to it).

Cleaning your own room is therapeutic and has actually been shown to improve your mood while doing it and afterwards when you’re in your nice clean room. But when it comes to the gross shared bathroom every uni student has encountered, you put it off for longer. You procrastinate away from it. This is because you gain no real benefit from it. It’s not dirty enough to give you diseases (yet), and you don’t spend enough time in it for it to benefit your mental health. If you can’t see an immediate advantage, you won’t do it.

Procrastination is all about cost and benefit and finding the balance between the two. If the immediate payout does not equal or outweigh the energy expenditure required to perform the task, then the inclination to do it will disappear.

Think about this the next time you put something off and do something else instead. Would what you are putting off benefit a caveman? Would he benefit by doing what you are doing now? But don’t listen to your inner caveman. Listen to your inner modern human who wants that essay done, because they know that you really need to do it. Don’t let them in only at the last second to write it. Go and do something productive! Go!

Regaining signs of consciousness after 15 years in a vegetative state!


Emma Hazelwood.

A man in France has regained some signs of consciousness after being in a vegetative state for fifteen years.

A vegetative state is defined as the absence of responsiveness and awareness due to brain damage, although some motor reflexes are maintained as normal. The issue of consciousness has baffled humans for centuries – there is no one test to determine whether someone is conscious. Instead, there is a scale known as the Coma Recovery Scale, which looks at various aspects of consciousness (including communication and auditory and visual functions).

The 35-year-old went into a coma after being involved in a car accident in 2001, and had shown no signs of improvement since. That is, until scientists tried a new treatment, involving using electricity to stimulate a nerve in the man’s body, known as the vagus nerve. This nerve runs from the brain to several areas of the body, including areas involved in emotion, alertness and memories. It was thought that after this treatment the patient may be able to regain some consciousness, without the risk of side effects from medication.

Improvements in the subject’s condition could be seen within a month of treatment. At first, this just meant being able to open his eyes more often. His brain showed activity in areas which had previously been quiet, and eventually he was able to follow an object around the room with his eyes, and even respond to requests to turn his head from one side to the other. He reacted with surprise when the examiner’s head suddenly approached his face. Amazingly, he shed tears and could smile with the left side of his face when he was played his favourite music.

According to medical professionals, this is known as a “minimally conscious state” – the man has not fully regained consciousness to the extent he had before the accident, but he is able to show some self and environmental awareness.

Although the test needs to be repeated in other patients, the results have neurologists very excited for future potential treatments involving this technique.

However, this experiment further demonstrates how little we know about consciousness, and brings into question the ethics surrounding treatment of people in vegetative states. Recently, the Court of Protection in England and Wales ruled that if doctors agree it is in the patient’s best interests, families of people in vegetative states no longer need the court’s permission to let their loved one die.

We do not have a perfect way of deciding whether someone is conscious or not. A 2010 study by the New England Journal of Medicine found that 40% of patients who had been assumed to be completely vegetative were actually able to communicate, even if it was just through yes or no questions.

If someone can “wake up” after fifteen years of no environmental awareness, this may complicate the already complex issue of whether it is right to decide to stop artificially feeding people in vegetative states. This could add to the guilt and emotional distress of families trying to decide whether or not to keep their loved one alive through machines, not knowing whether or not they are in pain or will ever wake up; or letting them die, never knowing whether they would have recovered.

The process may also be emotionally distressing for the patient. In this example, doctors have not yet asked the man whether he is in pain. Furthermore, doctors agree that he has such severe brain damage that it is unlikely he will ever be able to walk or talk again – even if he is eventually able to fully regain consciousness. This brings into light concerns around whether it is right to bring back someone who has been unconscious for so long (so many things have changed since he went into a coma in 2001), and to a lower quality of life than before, especially when we do not fully understand the process.

This treatment has been a breakthrough discovery for neurologists, and opens up a new world of possible treatments. However, it is essential that as we discover more about consciousness and how it is regained, we continue to consider the ethical consequences of our actions.


Savant Syndrome

Ellie Marshall

Can you think of any talents you possess? Perhaps you’re a great runner or are skilled at
playing an instrument? Now imagine that you didn’t have to work for those talents at all, and that they are beyond all normal human capabilities. This is what it is like to have Savant syndrome.

Savant syndrome is a rare phenomenon where a person possesses unexplained and
remarkable talents despite mental or physical disabilities. Almost all congenital savants have some form of brain damage, usually to the left hemisphere and around 50% of savants have autism. The remaining 50% either have some form of damage to or disease of the central nervous system. Due to this, some people can acquire savant like abilities later in life after a head injury, dementia, concussion, epilepsy or other brain disturbances.

Exceptionally deep but narrow memory is common to all savants, which allows them to excel at certain activities. For example, one boy could recite the route and time table of every bus in the city of Milwaukee, Wisconsin.

Such talents can be placed into 5 categories: music, usually performance and mostly piano, with perfect pitch but sometimes composing instead or playing multiple instruments (up to 22 in some cases); art, usually painting drawing or sculpting; lightning calculation, including the ability to calculate prime numbers; calendar calculation; and visual-spatial ability, including the capacity to precisely measure distances without the use of instruments, the ability to construct complex models with painstaking accuracy and map making. Skills are usually singular, although multiple skills can be possessed in some cases. The most common savants are ‘human calendars’ and have the ability to rapidly calculate the day of any given date or recall personal memories from that particular date.


Image credit: Derek Amato

One of the most famous savants is the late Kim Peek, who inspired the character ‘Raymond Babbitt’ in the 1988 film ‘Rain man’. Kim was born with a developmental disability but memorised over 6000 books and had an encyclopaedic knowledge of history, sports, geography, music, literature and nine other areas of expertise. He could name all the US area codes and major city zip codes. He also memorised maps found in the front of telephone books and could tell you exactly how to get from one city to another and then how to travel around that city street by street. One of his most remarkable qualities was his ability to read books at lightning speed by simultaneously scanning one page with the left eye and the other with the right eye. MRI scans showed he lacked a corpus callosum (part of the brain that transfers information between hemispheres) with other central nervous system damage. Despite his brilliant mind, Kim had an IQ of 87, markedly lower than average and struggled to follow certain directions.

Contrastingly, Derek Amato was born without any brain dysfunction. However, aged 39 he suffered a head injury in a pool that caused him to suffer from headaches, memory loss and 35% hearing loss in one ear. Several weeks later something dramatic happened. Whilst round at a friend’s house, he spotted a cheap electric keyboard and without thinking he sat at it. He had never played the piano, nor had any previous inclination to, but his fingers found the keys by instinct and to his amazement rippled across them. He started with his right hand, playing arpeggios and climbing in lyrical chains of triads. His left hand followed, laying down bass and picking out harmonies. Amato sped up, slowed down, varied the volume and was soon playing chords as if he had been playing for years. When he finally stopped and looked up, his friend was in tears. Amato found he an overwhelming compulsion to play and would shut himself in for as long as two to three days exploring his new skill.

So, what is the mechanism behind this? There are many theories as to why this occurs, but the most widely accepted theory is as follows: When the left hemisphere and higher-level memory circuits of the brain become damaged, parts of the undamaged brain are recruited to compensate. Lower level memory capacities are also recruited. This is known as cross-modal neuroplasticity. It has been established that some savants operate by accessing low level, less processed information that exists in all human brains but is not usually available to conscious awareness. For example, instead of seeing a whole tree, they would see every individual leaf and branch. However, some argue that this ‘recruitment’ of new areas of the brain to replace damaged areas and develop new skills is a ‘release’ of pre-existing areas, previously masked by more dominant areas of the brain.

Savantism occurs in males more often than females in a ratio of 6:1, the reason being for
this that males are more likely to develop disorders involving damage to the left hemisphere such as autism, dyslexia and delayed speech. The left hemisphere develops slower than the right, meaning it has greater susceptibility to pre-natal influences. Testosterone has a neurotoxic effect and can slow the growth of the left hemisphere, allowing the right hemisphere to become bigger and more dominant in compensation. The right hemisphere of the brain is responsible for art awareness, creativity, imagination, intuition, insight, music awareness and holistic thought.

We cannot fully model brain function until we can account for and incorporate savant
syndrome. Understanding this condition has wide implications regarding buried potential in some, if not all of us. If such potential could lie dormant in Amato, who knows what spectacular abilities lie dormant in us?