Can sport increase our risk for dementia?
We all know that physical activity and in particular exercise is good for us and our brain. Large scale population-level (epidemiological) studies have shown time and again how higher levels of physical activity and exercise can reduce our future risk for dementia by up to a whopping 40%! Clearly worth therefore to dust off those trainers and get moving.
However, what is less known is that injuries from certain sports can actually increase our risk of dementia by up to four-fold. In particular, one condition – Chronic Traumatic Encephalopathy (CTE) – has been shown to increase the risk of neurodegeneration and dementia. What is Chronic Traumatic Encephalopathy and what relevance has it for our risk for dementia?
Let’s find out.
Chronic Traumatic Encephalopathy
Chronic Traumatic Encephalopathy (CTE) is quite a mouthful, so let’s start by unpacking the terminology. ‘Chronic’ means that the condition is of a long-term nature. ‘Traumatic’ refers to the fact that this condition is caused by an injury or multiple injuries. Finally, the big one, encephalopathy, which seems a complex term but is in fact fairly simple to understand, once we know the underlying etymology. Encephalon originates from the Ancient Greek word ‘enkephalos’, meaning ‘brain’ (the literal translation is actually ‘in the head’ from ‘en’ = in and ‘kephalos’ = head – finally all my school Latin and Greek comes to good use!). The final part ‘-pathy’ in encephalopathy, is a short form of the term ‘pathology’ referring to the study of diseases (again Ancient Greek; ‘pathos’ = suffering; ‘logos’ = word, science – although I am not sure pathologists want to be referred to as ‘scientists of suffering’). So, now we can put the terminology back together and hopefully understand better that chronic traumatic encephalopathy means a long-term condition caused by injuries resulting in a disease in the brain.
What are then these injuries?
When people think about injuries to the brain they think often of gruesome injuries which open the skull and damage the brain, such as penetration wounds by bullets. These injuries are indeed very severe to the brain, however, there is another class of injuries to the brain which can be as severe but actually does not involve damage to the skull. Most such injuries occur because there is sudden deceleration (reduction of speed) or torsion (twisting) forces on the head. A classic example is car accidents when the crash causes a sudden deceleration of the head. This deceleration might cause us a sore neck but more importantly, it can actually damage the brain quite severely without the skull being damaged at all.
How is the brain injured by such decelerations/torsion forces?
For that, we have to understand that our brain is ‘floating’ inside of our skull. The reason is that our brain is a very sensitive organ with the nerve cells being highly sensitive to touch. If therefore, the brain and its nerve cells would touch the skull directly, they might misfire causing all kinds of strange symptoms to us. Instead, evolution has devised an ingenious system by having a fluid (the co-called corticospinal fluid – CSF) surrounding our brain, allowing the brain to ‘float’ in the corticospinal fluid. The corticospinal fluid protects, therefore, the brain from touching the skull and its nerve cells to misfire. (The corticospinal fluid has also other functions but we will not cover them here)
The brain is, therefore, nicely nestled inside of the corticospinal fluid, protecting it from being accidentally damaged by the skull. This ‘floating function’ of the corticospinal fluid also allows us to move around. Imagine there would be no such fluid around our brain and we would be walking. Our brain would bounce up and down with each step, which might prevent us from walking at all since all this movement would make the brain misfire. The role of the corticospinal fluid in the protection of the brain should be therefore not underestimated. However, the protection of the corticospinal fluid for the brain has its limits. If our head gets decelerated or twisted too fast, the corticospinal fluid cannot protect the brain anymore and the brain literally bounces against the inside of our skull causing the nerve cells to misfire or worse to get injured. A good example is when we fall and hit the back of our head. The sudden deceleration of our skull when hitting the floor causes the brain to hit the inside of the skull at the back of our head. Often when we fall onto the back of our head, we suddenly ‘see stars’ or other shapes. Of course, our eyes are not really seeing these stars or shapes but it is the visual brain regions (which are at the back of the brain) that hit the skull and their nerve cells misfire, making us ‘see’ these stars or shapes.
Hang on is this not concussion we are talking about?
CTE vs concussion
Exactly, the mechanism we are talking about is the same for concussion, traumatic brain injury and chronic traumatic encephalopathy. So, what’s the difference, you might rightly ask. The difference lies mostly in the severity of the damage to the brain. Let’s start with the worst outcome – traumatic brain injury. If our head decelerates or gets twisted very violently, like in a high-speed car crash, the forces exerted on the brain causes it to violently hit the inside of our skull and severely injuring the brain areas which have hit the skull. A traumatic brain injury is so severe to the brain that people instantly lose consciousness and often even die from the injury. If they survive, they usually have life-long symptoms caused by the brain areas injured during the traumatic event. A concussion is a somewhat milder version of traumatic brain injury, a person having a concussion might still lose consciousness after the impact, but often that is not the case and instead they ‘just’ feel dizzy and disorientated. However, a concussion can, similarly to traumatic brain injury, cause long-lasting symptoms due to the impact on the brain areas affected. Finally, chronic traumatic encephalopathy is the mildest version of the three, as people often have more ‘subconcussive’ events, which means they do not show the classic symptoms of concussion but have milder or no obvious symptoms. However, similar to traumatic brain injury and concussion, chronic traumatic encephalopathy actually damages the brain and could be regarded as even the most dangerous one, since this injury is often not detected in contrast to concussion or traumatic brain injury who have obvious symptoms right after the damage is done to the brain.
How is chronic traumatic encephalopathy caused then?
There is still an ongoing debate as to what actually constitutes chronic traumatic encephalopathy events. Indeed, only this year an international commission tried to come up with improved consensus criteria for chronic traumatic encephalopathy to allow better research in this little-understood but quite serious condition.
So, what do we know so far?
CTE and sport
Chronic traumatic encephalopathy was actually first recognised in the 1920s by Harrison Martland, a US pathologist, who noticed that the brains of former boxers showed signs of brain damage after their death. He also had some clinical symptoms which described how these boxers had changed their behaviour, cognition and movement before their death but long after they finished their careers. In particular, their slurred speech and uncoordinated movements, made him decide to name this condition ‘punch drunk’. Despite Martland’s groundbreaking discovery, the name for the condition – punch drunk – fortunately, did not stick. Fortunately, because the name would imply that it would only affect drunken fighters, which could not be further from the truth, since all those boxers were extremely fit and healthy and were trained to fight. Throughout the 1930s and 1940s reports of this syndrome kept coming up and it was recognised that the cognitive symptoms of these boxers resembled dementia. The syndrome was, therefore, referred to as ‘dementia pugilistica’ (from Latin ‘pugil’ meaning boxer). Again, fortunately, the label did not stick since we now know that chronic traumatic encephalopathy does not only affect boxers but many other sports and laypeople. Finally, the field settled on chronic traumatic encephalopathy as a name in 1949, which might not be the most ‘rolling of the tongue’ term, but at least described the syndrome in a more neutral way. The above description also makes clear that chronic traumatic encephalopathy is a pathological syndrome first and foremost. This means that it can only be diagnosed with absolute accuracy by examining the brain of people post-mortem – so far. Symptoms of chronic traumatic encephalopathy during life are, therefore, only associated with or strongly suggestive of chronic traumatic encephalopathy but not definite proof.
What are then the brain changes in chronic traumatic encephalopathy?
The key brain changes in chronic traumatic encephalopathy are that often ‘subconcussive’ events (events which might make your brain ‘bounce’ but not cause per se a concussion) can cause still damage to the brain cells, including the nerve cells. But not only is there a damage to the brain cells, but also it seems to trigger protein accumulations, similar to the one seen in dementia. Just a reminder, that all dementias, with the exception of vascular dementia, are caused by the accumulation of proteins. The insight in the 1930s that the brain changes in chronic traumatic encephalopathy (or dementia pugilistica as it was called then) shares a lot of the pathological brain changes with dementia. In particular, chronic traumatic encephelopathy seems to affect the accumulation of amyloid and tau in the brain, two key proteins involved in the development of Alzheimer’s disease. The exact mechanism of why chronic traumatic encephalopathy causes the accumulation of amyloid and tau are still being investigated but one thing is clear, similar to dementia, the accumulation of amyloid and tau due to chronic traumatic encephalopathy leads to a progressive nerve cell loss in the brain and specific symptoms.
What are the symptoms associated with chronic traumatic encephalopathy?
As mentioned above, the tricky part of chronic traumatic encephalopathy is that it does not cause any immediate symptoms after a brain injury but those ‘subconcussive’ brain injuries can build up and cause long-term symptoms. There is a variety of long-term symptoms in people with chronic traumatic encephalopathy because it depends on which area is affected by the long-term injuries. However, one major brain region affected by chronic traumatic encephalopathy is are the frontal brain regions – just behind our eyes. In a way, this should not be a surprise as repeated, severe decelerations of our head will make our brain ‘bounce’ forward hitting the inside of our skull at the front. The frontal brain regions are important for many functions, including our behaviour, decision making, but also our attention and memory and even our movements. Damage to the frontal brain regions can lead therefore to a variety of symptoms. But commonly damage to the frontal brain regions lead to often to changes in behaviour and decision-making, in particular people can become more impulsive, less inhibited, such by saying or doing things they would have not said aloud before. Similarly, people with frontal lobe damage can become more irritable or even aggressive in their behaviour, often describes as ‘flying off the handle’ for no obvious reasons. On top of these behavioural and decision-making changes, people often have a shortened attention span than before their condition started and also have problems with their memory (the frontal lobes help to organise and retrieve memories). But as I said, if the chronic traumatic encephalopathy affected other brain regions more commonly, then other symptoms might also occur. However, these cognitive problems can seem very like dementia, although people with chronic traumatic encephalopathy are often younger when presenting with such symptoms and therefore more akin to younger onset dementia. The final critical symptom in chronic traumatic encephalopathy is that it can affect our movements. Remember the original ‘punch drunk’ description by Martland? Like someone who is ‘drunk’, people with chronic traumatic encephalopathy can have slurred speech and movement coordination problems. These movement symptoms can appear similar to Parkinson’s disease and people with chronic traumatic encephalopathy have been shown to have damage in key regions involved in Parkinson’s disease, which might result in these symptoms. The exact reason why those regions are affected is still being explored.
What has that all to do with sport, you might ask?
The reason chronic traumatic encephalopathy is so important for professional and amateur athletes is that it has been shown that certain sports result in a higher risk of chronic traumatic encephalopathy and dementia. Indeed, a condition such as chronic traumatic encephalopathy can increase our future risk for dementia by up to four-fold. Not surprising, boxing is a sport with a well-established history of chronic traumatic encephalopathy, just think of the original studies by Martland on boxers or consider former professional boxers such as the late Muhammad Ali (maybe have a look at some YouTube videos of Muhammad Ali in his later years to get an impression of someone with the symptoms of quite severe chronic traumatic encephalopathy). Having being exposed to repeated blows to the head, boxers are clearly at high risk of chronic traumatic encephalopathy. However, other sports have emerged more recently to also increase the risk for chronic traumatic encephalopathy, such as American Football, Ice Hockey and Rugby. Clearly all of these sports are high-impact sports, which might explain why chronic traumatic encephalopathy is so common in former players but this only came to light in the 2000s when it was increasingly realised that former professional players had a higher incidence of chronic traumatic encephalopathy and dementia. It was recognised that ‘subconcussive’ events in those players over the decades they played those sports increased their risk for chronic traumatic encephalopathy significantly. Often it was not even the playtime but the training time which was one of the largest contributor to these subconcussive events. (As an aside, cage fighting has not been shown so far with chronic traumatic encephalopathy but the sport is still quite young and we might see in the future that former fighters will have a similar risk as boxers to develop chronic traumatic encephalopathy).
More recently, the discovery that heading a ball in football/soccer might similarly constitute a ‘subconcussive’ event for players caused a stir. There are currently several studies investigating this association to determine what the actual risk is of heading the ball for developing chronic traumatic encephalopathy or even dementia. But one thing is clear, these revelations of an increased risk for chronic traumatic encephalopathy or even dementia for formers professional and amateur athletes have wide-ranging implications. Not only makes it clear that people who play and love these sports are at an increased risk for developing a disease later in life, despite them being highly fit and well-trained people. If you are interested, I recommend listening to a BBC Worldservice podcast (link here) with Alix Popham – a former professional rugby player- who has now young onset dementia. Alix and his wife talk very openly about their experience with chronic traumatic encephalopathy and eventually the diagnosis of younger onset dementia.
The other implication is that this increased risk of future disease might actually change the sports themselves in the future. For example, we might see football/soccer with less or no heading of the ball. Indeed, the Scottish Football Association has already banned heading football for under-12s, as a precaution. Maybe we can live without heading balls in football/soccer, even though it would change the game fundamentally, but just imagine American Football, Ice Hockey or Rugby without the physicality – it would be simply not the same sport. Not to speak of boxing or cage fighting. There is therefore currently a re-think occurring as to what way forward these sports should have so that players are better protected from those injuries, which can have an impact long after they have finished their playing careers. All open questions which we do not have the answer for – yet.
Suffice to say, that most of us (including myself) love watching or participating in sport. And that is obviously a good thing. As I have pointed out over and again, physical activity is excellent not only for our cardiovascular health and brain, reducing our risk for dementia by up to 30%. But maybe we need to choose our sport carefully, as not to inadvertently damage our brains and in fact, increase our risk for chronic traumatic encephalopathy and even dementia.