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.

Using Cancer to treat Diabetes? Sort of…

Vanessa Kam

Tumour.  The word immediately summons negative connotations, embedded in the general fear surrounding cancer and impounded by the Daily Mail’s endless crusade to classify everything into cancer causes or cures.

While ‘tumour’ is often used as a synonym for ‘cancer’, in science, the two are not quite the same.  ‘Tumour’ is derived from the Latin word for ‘swelling’, and originally referred to any swelling, like a pooling of fluid in inflammation.  Nowadays it is used to refer to ‘neoplasms’ which form a mass, an abnormal growth of cells appearing bigger in size.  These masses can be benign, sticking to one location and easier to treat, or malignant, invading into other tissues and spreading around the body.  Cancer, derived from the Latin word for crab, refers to the malignant tumours, which extend out from their original site like a crab’s legs from its body.

 

2306-preview

(Cancer Cells:  Image source: National Cancer Institute)

Now that it’s clear benign tumours are not cancerous, we move on to a diabetes discovery, lest getting tied down by etymology.

In a study published in October, researchers at the Icahn School of Medicine at Mount Sinai, New York, harnessed critical information from the genomes and expression patterns of insulinoma cells.

Insulinomas are rare, small, benign tumours of pancreatic beta cells.  The pancreas is a pivotal organ in regulating blood sugar, and its beta cells secrete insulin to capture excess glucose from the bloodstream for storage.

In diabetes, beta cells are either destroyed by the patient’s own immune system (type I) or cease to function, with type II diabetes seeing a reduction in working beta cell numbers, often alongside insulin resistance.  Much work has been invested into inducing beta cells from stem cells to transplant into patients with type I diabetes, effectively replacing the destroyed cells, but what about inducing beta cells to regenerate in situ?

This is notoriously difficult, in part due to the normal development of beta cells.  Beta cell proliferation occurs shortly after birth, continues for about a year, then rapidly declines in early childhood.  In adults, the increase in beta cells is virtually zero, bad news for diabetics.  Even at its highest rate, beta cell proliferation is relatively low, with about 2% of cells dividing versus up to 50% in other cell types.  With normal proliferation rates so low in later life, there’s a particularly high barrier to promoting regeneration in adult beta cells.

This is where insulinoma comes in.  In insulinomas, beta cells proliferate.  While this generates tumours which overproduce insulin, causing patients to display symptoms of low blood sugar, identifying the mechanisms by which insulinoma cells overcome division dormancy can be applied therapeutically to diabetics, re-expanding their beta cell populations.

In fact many cancers are undergoing genomic scrutiny under various projects, including the Cancer Genome Atlas and the International Cancer Genome Consortium.  But seeing as insulinoma has a low incidence rate of two in every one million people worldwide and is largely benign—only 10% is cancerous,—insulinoma slipped through the net.

Until now.  Wang and his team at Icahn conducted whole exome sequencing and RNA sequencing on 38 benign human insulinoma samples, analysing the DNA sequence for all the protein-coding genes (exons) in the cells and the transcriptome, the variable, actively expressed portion of exons in those particular cells at that specific point in time, comparing them to normal beta cells.

They found insulinomas to display mutations and differing expression of epigenetic modifying genes—genes coding for proteins which alter the expression of other genes without changing their DNA sequence—and their targets.

One such example is a new potential drug target KDM6A.  KDM6A supports the cell cycle inhibitor CDK1NC, a protein only expressed in pancreatic beta cells and prompts their inability to divide.  CDK1NC is reduced in insulinoma, and allows beta cell proliferation when turned off.

KDM6A was mutated in several insulinoma samples in this study, prompting the team to interfere with it by inhibition using both a drug and a virus.  This resulted in lower levels of CDK1NC, which will allow beta cells to re-enter the cell cycle and proliferate, exciting news for diabetes therapy.  Future work screening for molecules which inhibit KDM6A may identify drugs promoting beta cell regeneration.

In fact, this study reaffirmed the presence of targets of a novel drug another team at Mount Sinai identified.  In 2015, after screening through 100,000 compounds, only one, harmine, was found to drive human beta cell replication in culture.  This was unheard of, with all previous attempts seeing beta cells resist pushes to multiply.

Harmine is derived from the plant harmal, which due to its psychoactive properties, is used in many spiritual rituals, hung around to protect from the ‘evil eye’ in Turkey, for example.  When used to treat mice mimicking human diabetes, harmine tripled beta cell numbers and improved blood sugar control, and is now under early development for diabetes treatment.

However even with harmine, the induced proliferation rates of beta cells are modest.  With new information about beta cell replication gathered from insulinomas, more novel drug targets can be identified and promising compounds highlighted.  This goes to show that studying rare diseases like insulinoma can bring about medical advances for the masses, with beta cell regeneration therapy now an increasing reality for the millions of diabetics worldwide.

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

brainscancoma_web_1024

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.

 

Poison or Peaches?

cyanide-apple-featureChlo McCole

Murder mysteries often feature cyanide as a poison, but did you know you can be exposed to this toxin in everyday life too? Have you ever wondered how cyanide poisons and kills people, how much it takes before its toxic, and whether there is a cure? Here’s what you need to know.

Cyanide is the CN ion (one carbon atom bonded to a nitrogen atom) and as a poison it is commonly administered as one of three compounds: hydrogen cyanide, a volatile, colourless liquid, and potassium and sodium cyanide, both white powders. Both potassium and sodium cyanide react with stomach acid to produce hydrogen cyanide, which can then go on to cause toxic effects.

Though cyanide has been used as a poison for centuries, it was first isolated in Sweden in 1782, by Swedish chemist Carl Scheele. Whilst different sources tell different stories, some claim that his exposure to cyanide was a contributing cause to Scheele’s death at the age of 43. He was also the first person to note the bitter almond smell of hydrogen cyanide – a smell which, it turns out, can only be detected by 40% of people for genetic reasons.

So, what happens when a person is poisoned with cyanide? Upon ingestion, cyanide binds to haemoglobin, the molecule in red blood cells responsible for carrying oxygen to the cells in our body. Haemoglobin then ferries it to the body’s tissues, where it can bind to an enzyme called cytochrome oxidase. This enzyme is a vital tool which cells require to make energy and with cyanide bound to it, they are unable to do so. It’s a bit like using treacle instead of petrol in your car; both fit in the tank but treacle will just clog the system.

The symptoms of cyanide exposure include headaches, nausea, vomiting, and elevated breathing and heart rates. With a high enough dose, these symptoms quickly progress to loss of consciousness, respiratory failure, and death.

How much cyanide is fatal depends on the route of exposure, the dose, and duration of exposure. Inhaled cyanide presents the greatest risk, followed by ingestion. Skin contact is not as much of a concern (unless it has been mixed with DMSO). A fatal dose for humans can be as low as 1.5 mg/kg body weight.

Cyanide is actually a relatively common toxin in the environment, and because of this the body can detoxify a small amount of cyanide. For example, you can eat the seeds of an apple, bite into a peach stone or smoke a cigarette without dying.

Perhaps the most well-known use of cyanide as a poison was in the Nazi concentration camps of World War II. There, the Nazis used Zyklon B, a cyanide-based pesticide to kill millions. Cyanide was also involved later in the war; though it’s commonly thought that Hitler committed suicide by shooting himself in the head, evidence has suggested that he in fact killed himself using a pill containing potassium cyanide, along with his wife of just 2 days, Eva Braun.

Cyanide poisoning is still a not-uncommon occurrence, though the exposure is often accidental. In particular, plastics such as nylon and polyurethanes release cyanide when burnt, so during fires cyanide poisoning can often occur. In the Grenfell Tower Fire of 2017 a number of the deaths were thought to be as a result of the inhalation of cyanide and other toxic gases produced by burning plastics.

As cyanide is such a fast-acting poison, it can be hard to administer any antidote in time. Thiosulfates are commonly administered in combination with nitrites, as they help convert the cyanide to thiocyanate, which can then be eliminated in urine. Vitamin B12a has also been used, which can bind the cyanide to form another harmless form of vitamin B12.

Cyanide poisoning can be detected in a number of ways; the most common is a simple, lab-based test. A tissue sample is added to 5% sodium hydroxide solution, which is in turn added to a solution containing 5% iron (II) sulfate and 1% iron (III) chloride. This is heated to 60˚C for 10 minutes, and then transferred to a solution of hydrochloric acid. The appearance of a blue colouration, caused by the formation of the iron-cyanide complex known as Prussian blue, indicates the presence of cyanide ions in the original sample.

Despite the ease of detection intentional cyanide poisonings still occur. This year the serial killer, Mohan Kumar – nicknamed “Cyanide Mohan” by the news media in India – was convicted of the murders of three young women and is suspected in another 17 deaths. Mohan, a 50-year-old former teacher, allegedly killed strictly for profit – he stripped the gold jewelry off the dead women and sold it. Let us not forget the Zimbabwe poachers who killed more than 300 elephants by poisoning their water hole with cyanide (not to mention the other animals that visited there) in order to sell their ivory tusks on the Asian market.

Makers of thriller movies and writers of murder mysteries tend to like cyanide for its dramatic tendencies – the quick gasping finish, the shocking immediacy of the way it kills. I had thought that an old, easily identified, messily visible poison like cyanide would fade away into our homicidal history. I say thought because if 2017 is anything to go by, that’s not particularly apparent. As the continuation of cyanide murder reminds us, we don’t easily set aside our past and we obviously – if unfortunately – hate to give up on a weapon with a history of working so well.

Diabulimia – an emerging health concern

diabetes-2Gemma North

**trigger warning for those of a sensitive nature***

First off, I want to clarify that this article is not encouraging eating disorders, it is merely trying to bring awareness to the public of a more niche disorder. If you do suspect anyone has or is at risk of an eating disorder I recommend talking to them, a GP or any charities.

With that all done, I hope this article provides an insight into a niche disorder. For most of us we know diabetes as insulin injections, blood glucose tests and often associate it with sugar. Similarly, we know of bulimia as a mental health condition, characterized by binge eating and purging.

Unfortunately, individually they each have a stigma associated with them; together in the form of diabulimia this stigma is only made worse and can have life-threatening effects if not handled and managed properly.

Individually people know of diabetes, they know anorexia and they know bulimia. But Diabulimia is something many don’t know about. Honestly, I didn’t know about it till I saw the headlines, even then I had to research a fair amount to understand just what it is.

But a new ‘trend’ among-st primarily young type 1 diabetic women has now resulted in the death of one, and a need to raise awareness and understanding of Diabulimia.

Admittedly it’s a niche condition, but so little is known about the disease although recent headlines have drawn to the life-threatening effects of it.

Whilst not medically classified, it has been under the radar of physicians and nurses, even academia from as early as 2007. So why hasn’t anything been done? And what can we do about it now? Due to the nature of Diabulimia it is particularly dangerous due to the health needs of diabetics, of type 1 diabetics moreso perhaps.

In recent news, it was noted a young woman passed away following a battle with Diabulimia. Whilst it hasn’t been medically classified yet, it is a growing problem affecting young girls who take insulin to treat type 1 diabetes.

Whilst not as common as more well-known eating disorders it is particularly dangerous in the way it is carried out. This is through the restriction and limitation of insulin injections (foregoing medical advice) to lose weight, with this comes deadly implications. It should be noted that, whilst the condition doesn’t always present as severe weight loss, it can also present as diabetics eating normally but manipulating the insulin dosages. The patients would normally take the bare minimum to function; but this comes at the cost of being consistently dehydrated, fatigued and irritable.

Insulin, as is well known is used to manage blood sugar in response to defective B-islets in the pancreas which are unable to produce it themselves. The restriction of insulin meant there was a significant increase in blood glucose levels resulting in hyper glycaemia, overworking the kidneys. Ultimately this leads to kidney failure and in time will result in death. Pathologies happen at an increased rate as above, such as nephropathy and retinopathy. (death of the kidney and cells of the eyes, respectively.)

As the body becomes starved of calories it becomes reliant on breaking down what it can e.g. muscles to try and gain energy; through a process known as glucosuria. As time goes on more and more organs are broken down leading to eventual organ failure.

The effects are horrific, not only on the individual but also on loved ones and close friends. But because it affects a small subset of individuals it’s not been formally recognized within the medical field. It is estimated 60% of women with type 1 diabetes suffer from it. The treatment is described as patchy at best due to the dietary and psychological aspect leading to the patients who need help most often being turned away due to the complexity.

With growing prevalence and a multitude of factors involved, the need to talk and be aware of this condition is become more and more important.

 

You Have Allergies Because You’re Too Clean

Emma Hazelwood

An allergy is when the body’s immune system is sensitive to a normally harmless
molecule. In most people, this molecule would have no effect, but in those with an
allergy, the body sees it as a threat and reacts abnormally to its presence.

Allergies are becoming more and more common in the Western world. The number
of children with a food allergy has doubled in recent years, and the World Allergy
Organisation recently revealed that the global prevalence of asthma (a common
symptom of allergies) has increased by 50 per cent every decade for the past 40
years. 50 years ago, one in 5000 people were allergic to wheat; this figure is now
closer to one in 130. Allergies are becoming a huge problem, with 50% of children in
the UK having an allergy, and 20,000 people admitted to hospital each year for a
dangerous (and potentially life-threatening) allergic reaction.

Scientists disagree about the explanations for this increase. Theories include genetic
reasons, a change in diet, and something called the ‘hygiene hypothesis’. The idea
behind this is that allergies are so common now because we are kept too clean as
children, when our immune systems are developing. This means that the immune
system is not exposed to as many pathogens, so cannot regulate itself as well.
The basic theory was proposed in 1989 by Strachan, who said that young children
exposed to infectious diseases will be less likely to suffer from allergies. Since then,
it has been developed and is now also known as the “lost friends hypothesis”. It is
believed that, as well as colds, measles and other common childhood infections
(which have only evolved in the last 10, 000 years), it is exposure to ancient
microbes present in the time of human evolution that can prevent allergies; we have
“lost” our “old friends”, whom our immune systems need to develop properly.

Although the hygiene hypothesis has not been scientifically proven, there is lots of
evidence that supports it. Links exist between increased allergy prevalence and
many factors related to cleanliness (e.g. early day care attendance, rural living,
contact with animals, older siblings, large family size, and infection by common
diseases).

Allergy_skin_testing

Image credit: Wikimedia commons

It makes sense that a child in day care will have increased exposure to infections. In
fact, many parents send their child to day care so they will become immune to
diseases such as chicken pox, which can be dangerous if caught later in life. It has
been found that children who went to a large day care with other many children have
a reduced likelihood of developing an allergy.

Several studies report a reduced incidence of hayfever and asthma in the children of
farmers. In particular, factors to thank for this are: contact with animals as a child,
exposure to stables under the age of one, and consumption of farm milk (presumably
raw/ unpasteurized). As farm animals can be considered ‘dirty’, this suggests that
exposure to common farmyard microbes may influence vulnerability to allergies.
One of the most significant links with allergy prevalence is family size. This is
because being in a larger family, with more children, means more microbes and
infections are brought into the home. Hay fever and eczema are less common in larger families, and a study on asthma showed that being from a small family
increases the chances of a child being diagnosed. It has been found that having
many older siblings (at least three) in particular can have a protective effect from
allergies. Sharing a bedroom as a child, which is more likely in large families, also
had a protective effect. This all agrees with the hygiene hypothesis, as this would
provide more opportunity for exposure to microbes or infection.

The huge increase in allergy prevalence has been seen much more dramatically in
the industrialised world than in developing countries. This could be for genetic
reasons, but there is evidence that this too is due to different levels of exposure to
microbes and disease. Firstly, it is known that the average Eastern family is larger
than the average Western family, which, as we know, decreases the likelihood of
developing an allergy. Furthermore, immigrants from developing countries have
been found to increasingly develop autoimmune disorders in relation to the length of
time they have been in the industrialised country. Studies in Ghana demonstrate an
increase in immunological disorders as it grew more affluent and presumably
cleaner.

Allergies are on the rise, and it seems that the increased hygiene in the Western
world may be the cause.

Contact sports and public health.

Hugh McCloskey

Imagine our society lauding people of all ages for activities that were potentially harming their long-term mental and physical health. But how? our society has come on leaps and bounds in health promotion, education surrounding alcohol consumption, numerous initiatives to help people stop smoking. All these things clearly demonstrate our conscious commitment to public health as a nation.

But what if I told you we as a society were actively promoting activities in our young people that could lead to conditions with symptoms similar to those caused by the long-term abuse of tobacco and alcohol in their later lives. And that we were promoting these activities as beneficial.

The activities I am talking about are of course contact sports, anything that involves players sustaining direct impacts to their head, examples include; rugby, boxing, MMA, kickboxing etc. There is a growing body of evidence to suggest that impacts to the head sustained by sports players can lead to chronic traumatic encephalopathy or CTE.

Hockey_goal_cmd_2004

Image credit: Wikimedia commons

CTE has also been identified as a potential environmental factor in many neurodegenerative diseases such as Motor Neuron disease or ALS, Alzheimer’s and Dementia. Although there has been a recent stir in the sporting community around concussion with the programs such as the IRFUS “recognize and remove” campaign (1) being implemented in rugby, this focuses on large traumatic impacts that illicit a loss of consciousness or disorientation.

Perhaps the insidious thing about CTE and resulting neurodegenerative diseases is that they don’t require multiple large concussions resulting in loss of consciousness to occur before they are incurred (but that would certainly help them on their way). In fact, they can be brought on by multiple sub-concussive blows sustained over time causing what is known as mild traumatic brain injury or MTBI.

There is, however, no doubt that extended careers in extreme pugilistic sport bring about neurodegenerative diseases with 97% of NFL players studied post-mortem having evidence of neurodegeneration! (2) . Anecdotally This month a New England Patriots star committed suicide in jail after a conviction for murder (3) When his brain was examined it was found to have one of the most advanced stages of chronic traumatic encephalopathy possible (4). Negative changes to personality and tendency towards paranoia and violence are well-documented symptoms of CTE (5) The fact is we still have no exact values to quantify just how many impacts of what magnitude a person can sustain during a sporting career before they increase their risk of neurodegenerative
disease.

800px-LacrosseGoalie

Image credit: Wikimedia commons

This begs the question; Could a casual career in weekend or school rugby lead to increased risk of depression, paranoia, violent behavior suicidality in the short term and neurodegeneration in later life?

We live in a society where sporting culture is becoming ever more performance orientated. Athletes are becoming larger, faster, and stronger at younger ages meaning the forces they generate and impart during training are greater than ever before. They are also training and competing more regularly which again implies more net impacts.
However, society seems to see no problem with this because what little is entering the collective consciousness about brain injury in sport through that medium of movies like “concussion” tell us that these injuries only happen to professional NFL athletes in other countries. But what if it’s happening to our young men and women competing in boxing, rugby, American football etc right here? The problem is that we don’t know.

I am not advocating a blanket ban on these selected sports, I myself gained a tremendous amount of discipline and self-respect from training and competition in MMA and rugby. However, I believe these sports should at least implement a system of education around the risks faced by players until further investigation can influence their practice and prevent these things happening. Unfortunately, there is no way to avoid impacts to the head in certain sports and in these cases athletes should be educated about the long-term risk of brain injury they may well be exposing themselves to.

Finally, to return briefly to our attitudes on public health as a nation permit me to use some shocking but I believe justified imagery to highlight a paradox. What if there were a competitive children’s smoking league where despite the risk of cancer, heart disease and stroke we allowed children to go head to head in a ring smoking as many cigarettes as possible whilst we cheered from the side-lines?

Sounds ridiculous, right? And yet we allow children as young as 10 to begin careers in boxing and rugby. With evidence that sporting trauma in childhood can bring on neurodegeneration (6) we can only ignore these issues for so long.

1. http://www.irishrugby.ie/downloads/IRFU-Guide- to-Concussion%282%29.pdf
2. Gardner, R.C. and Yaffe, K., 2015. Epidemiology of mild traumatic brain injury and
neurodegenerative disease. Molecular and Cellular Neuroscience, 66, pp.75-80.
3. https://www.washingtonpost.com/news/early-lead/wp/2017/04/19/aaron- hernandez-
found-dead- in-prison- cell/
4. http://www.freep.com/story/sports/nfl/patriots/2017/09/21/aaron-hernandez- cte-suicide-
murder-new- england-patriots/690651001/
5. http://www.alz.org/dementia/chronic-traumatic- encephalopathy-cte- symptoms.asp
6. Keightley, M.L., Sinopoli, K.J., Davis, K.D., Mikulis, D.J., Wennberg, R., Tartaglia, M.C.,
Chen, J.K. and Tator, C.H., 2014. Is there evidence for neurodegenerative change following
traumatic brain injury in children and youth? A scoping review. Frontiers in human
neuroscience.