Transcriber: Priya Kalyanakrishnan Reviewer: Maria Pericleous
Sport challenges and changes society unlike anything else.
It is a culturally powerful,
multi-billion commercial industry
that transforms lives, businesses and nations.
And whilst life comes with risk,
contact sport heightens those risks thrillingly so.
But the early development of dementia, due to a condition known as CTE,
almost unique to contact sports,
is now the most feared risk
for millions of amateur and professional athletes
across the globe.
Despite the 2013 landmark multi-million NFL settlement
for retired American football players with brain injury
and the 2015 Will Smith movie Concussion,
the fear and reality of dementia in contact sports
is still not widely known,
it is not adequately addressed, and it is not going away.
We rely on experts to identify and explain these risks.
But many have downplayed the reality.
Consequently,
too many players, coaches, parents and fans
remain unaware of what is now known.
Let me share with you what we do understand today
about brain injury and dementia in contact sports.
The relationship between dementia and repetitive brain injury
was known by the ancient Greeks.
And 100 years ago
the condition punch-drunk
was formally recognized as a complication of boxing.
in 1940,
the term chronic traumatic encephalopathy, or CTE,
was introduced to describe a combination of symptoms,
including mood changes, memory loss, disturbance in thinking,
leading eventually to dementia
and arising from repetitive impacts to the head.
But medical scientists
were not really able to progress their understanding of these symptoms
until 2002,
when Mike Webster, a brilliant athlete,
honoured by the NFL Hall of Fame,
died, aged 50.
From his early forties, Webster's behaviour became increasingly strange.
He became lethargic and angry,
he threatened to kill strangers.
When his teeth fell out,
he stuck them back in with superglue.
And he zapped himself with a taser gun
to try to help him sleep.
His cognition and his memory became increasingly worse,
and he died with severe dementia.
Doctor Bennet Omalu examined Webster’s brain.
At first glance, there was no evidence of any brain injury.
But when he looked inside his brain,
he found an abnormal version
of a protein called tau
in regions of Webster’s brain responsible for mood,
memory and intellectual function.
And this abnormal form of tau protein was identical to the tau protein
that had been found in boxers who had died with dementia.
Doctor Omalu then searched and found the same protein
in other contact sports players
who had died with dementia at an early age.
And somehow, in each case, the normal, healthy tau protein,
which is designed to protect the brain cells,
had changed into this new, harmful version,
capable of spreading through the brain relentlessly,
killing more and more brain cells.
Then, given this similarity between this abnormal tau protein
and the abnormal protein found in Alzheimer’s disease
and other dementias,
scientists realized that this disease, CTE, in Webster’s brain,
was progressive, and, like Alzheimer’s,
had most likely started many years
before Webster developed even his first symptoms.
This same year, 2002,
Jeff Astle, a famous English soccer player,
died with severe dementia, aged 59.
Examination of his brain confirmed CTE.
An intense debate, linking
heading of the ball in soccer to CTE commenced.
Over the next decade, it was wrongly assumed
that CTE was a very rare condition,
affecting only professional boxers,
American football players, ice hockey and soccer players.
And that it started late in the player’s career.
Then in 2015,
a very significant event occurred.
Zac Easter suspected he had CTE.
Zac had started playing American football at eight,
but by 11, he started to complain of headaches.
Shortly after, problems with his memory,
then slurred speech, mood swings and depression.
He developed dependency upon drugs
to try to manage his declining brain function.
Zac stopped playing contact sports at 18.
Then at age 24,
Zac wrote a suicide note to his parents,
explaining that he wanted his brain to be examined after his death
to help future players.
Then Zac shot himself in the chest.
Doctor Omalu
examined Zac’s brain, and he found advanced CTE.
This tragic event prompted new questions.
How early does CTE actually develop, and why?
And why does it affect some, but not all players?
In 2020, answers started to emerge.
Doctor Ann McKee, Director of Boston University’s Brain Bank,
confirmed a strong positive link
between the cumulative dose of head impacts in contact sports
and the subsequent development in life
of problems with extreme behavior,
memory loss and other cognitive symptoms.
And players with confirmed CTE after life
were ten times more likely
to have played American football for more than 14 and a half years.
And for every additional year played,
the odds of having CTE after life increased by 30%.
Separately, studies found children
who started playing American football under the age of 12,
grew up to have worse thinking and learning ability than their peers
who started playing after their 12th birthday.
And this is not too surprising,
as a critical and dynamic period of brain development
occurs between the ages of nine and 11.
The next critical discovery was possibly the least expected.
That is, that the risk and severity of CTE
is not caused primarily by the single big hit concussions,
but by multiple smaller sub-concussive impacts
to the head and body.
And, 20% of people diagnosed with CTE after life
had never had a single recorded concussion.
Failure to grasp this critical discovery is too common,
and it presents a huge issue in understanding how we tackle CTE.
So it is crucial to understand the difference
between a concussion and a sub-concussion.
A concussion occurs when the force of impact to the brain
is sufficient to cause an acute brain injury
with symptoms, headache, brain fog, irritability, slowed reaction time.
Quite different from a sub-concussion,
a lower force of impact, which damages brain cell function
but does not cause any symptoms.
So these impacts go largely unnoticed.
And the force to the brain to cause a concussion
is about two to four times greater than a sub-concussion,
but sub-concussions are more than 500 times more frequent.
Whilst a single concussion is never a good idea
and can be life-changing,
so too are multiple, repetitive sub-concussions.
And how resilient is the brain to these lesser impacts?
Well, in 2016, the Wake Forest Report
shed some light on the danger of sub-concussions
by demonstrating evidence of structural brain injury
in a group of eight to 12 year olds
playing American football for just one season.
Whilst no child received a concussive impact,
each child received an average of about 200 sub-concussions.
And the higher the cumulative dose of sub-concussive impacts,
the greater the degree of structural brain injury.
Remember, Zac started playing American football at eight,
developed symptoms of CTE by 11.
Now, compare the number of sub-concussive impacts
with NFL players who receive, in one season
between 1000 and 1500 sub-concussive impacts.
And in Rugby Union and Rugby League this number is significantly higher.
This frequency of sub-concussive hits
explains why CTE is ten times more common
in rugby and American football players,
and symptoms begin in their thirties to forties,
compared to soccer players,
where CTE begins in their fifties or later.
And whilst the intense focus on dementia in soccer
has been related to heading the ball,
it is not widely known that only 13% of all sub-concussions in soccer
are actually due to head-to-ball impacts.
So CTE in football, or soccer,
is so much more than heading the ball.
Now, what about women in sport?
Almost no women’s brains had been studied
until two years ago,
when superb athlete and Aussie Rules football player Jacinda Barclay
took her own life, aged 29,
after short, intense mental illness.
Her parents donated her brain to sports injury research.
Jacinda’s brain demonstrated a degenerative disease
known to be associated with the development of mental illness
and suicide.
And whilst not CTE,
the degenerative changes were attributed 100% to the multiple head impacts.
And the same degenerative disease has been found in other players,
some of whom have played only one season of contact sports.
Jacinda had only one reported serious concussion during her career.
So given the significant increase
in the participation of girls and women in contact sports,
they too now face a very real and serious risk of CTE.
So why is CTE primarily the result of numerous, unnoticed minor head impacts?
The brain is the most sophisticated and complex thing on the planet.
And it has, of course, evolved self-protective mechanisms
to respond effectively to one or two impacts.
But when the brain is subjected to multiple impacts,
especially the dangerous rotational forces from angled hits,
the brain rotates inside the skull,
and eventually the delicate nerves and tiny blood vessels are torn.
A protective structure, the blood brain barrier is disrupted,
and the normal protective neurochemical response to a single impact
is massively exaggerated.
This triggers a huge, inflammatory, harmful response.
Which instead of protecting, it damages the brain cells
and leads eventually
to the accumulation of abnormal tau protein.
We are at the tip of a global CTE iceberg,
and three critical areas of focus are required.
Brain protection, CTE diagnosis in life,
and treatments.
Firstly, brain protection for every player.
We need effective interventions to reduce the number and force
of both concussions and sub-concussions.
Instrumented mouth guards,
identify concussions and detect silent concussions,
whilst removing a player from the pitch
with a concussion is accepted practice now.
Removing a player with a cumulative dose of sub-concussions
is unlikely to be popular, or even practical,
when the player has no symptoms.
And whilst collecting this data is important,
the threshold dose to direct removal of a player with sub-concussions
is not yet known.
Immediate on-pitch, sideline assessments,
eye movements, saliva tests and others
may facilitate identification of a concussion,
but irrelevant to sub-concussions.
Changes in the rules and style of play also underway, but controversial,
dependent upon compliance and monitoring,
unpopular with fans,
and not working for sub-concussions.
Protective headwear sounds like an obvious solution.
Ironically, the hard helmets
increase rotational forces to the brain by permitting greater impacts,
as the skull is protected from fractures.
But the brain is not protected,
and receives the full force of the impact.
Effective brain as opposed to skull, protection is desperately needed.
A new product, Rezon Halos®, entered the market earlier this year.
Rezon Halos® is the only legal CE marked protective headband in the UK and Europe,
and it is designed specifically to decrease by at least 60%
all rotational forces to the brain.
Often it is the simple but fit-for-purpose items
like seatbelts
that make the most sense and hopefully a big difference.
Secondly, diagnosis.
The mantra that CTE
can’t be diagnosed in life with meaningful clinical accuracy
is simply no longer true.
Our team, at Re:Cognition Health and King’s College London
have demonstrated evidence of brain injury
consistent with CTE
in one of the biggest groups of retired contact sports players globally
using our novel sophisticated MRI, DTI sequences.
For these individuals with CTE, the diagnosis is instantly life-changing.
Our discovery, however, is groundbreaking.
It now creates the possibility
to provide potential treatments for CTE,
which takes me to future treatments.
Given the billions already invested to develop new treatments
to remove abnormal tau protein in Alzheimer’s and other dementias,
surely we can use some of these potential treatments for CTE too.
At Re:Cognition Health, we are starting to do exactly this,
under a special early-access drug licence.
We will provide HMTM,
a potential new treatment for Alzheimer’s,
to a number of the ex-professional contact sports players
in whom we have confirmed evidence of brain damage
consistent with CTE.
HMTM was developed by Professor Claude Wischik,
co-founder of TauRx Therapeutics.
Our objective, for the first time ever,
is now to try to halt,
or at least slow progression of CTE symptoms.
We cannot escape that CTE is a complex global political scientific challenge,
which is just about to be understood in sport.
And probably should no longer be considered as a great unknown.
And by focusing on brain protection,
CTE diagnosis in life and treatments,
we will change the future.
And if this TED talk has caused
one parent, one coach or one player
to think differently about how they protect their brain in contact sports,
it will have served its purpose.
Thank you.
(Applause)