The NFL was supposed to be impervious to overall TV viewership decline.
So, it turns out the NFL is mortal. It seems only now do we realize its players are too.
The return of the NFL on September 6 makes me think of the NBA; basketball is the sport on which I was raised, and after my father installed the floodlights in the driveway, almost nothing could pull me away from the regulation free throw line we measured out, the addicting splash of the chain net with every clean jumper.
Despite our "Basketball Jones," Sundays were still for football. Between games, I'd run routes on the lawn against my brother and flex my dance moves with each end-zone catch. My brother and I didn't play football in high school, so the gravity of basketball and the NBA began pulling us away from football, especially when the NBA season started in October.
The two leagues are the most popular in America, but they are experiencing quite different moments in their histories.
Declines in NFL viewership pass the eye test when looking at plummeting ratings for television as a whole. But compared to the NBA, the picture gets clearer.
Football is still America’s sweetheart, with 37% of people calling it their favorite sport (about 11% for basketball). And despite these declines in viewership, the NFL brought in more money than ever before through broadcast. Each NFL team made about $255 million in 2017, up to about $8 billion total across the league–a 4.9% growth. The 2017 NBA season garnered $7.4 billion for teams, up 25%.
Let’s be clear: the NFL is still more popular and valuable than the NBA. Its viewership is still supreme at 20.3 million sets of American eyes on Sunday night, but even that is down 10% from the previous year. ESPN and TNT broadcasts of NBA games captured 2 million viewers, one-tenth the size of Sunday Night Football. But those telecasts are up 15% from the previous year.
A league worth billions of dollars doesn’t exactly need answers, but that doesn’t stop people from looking. The NFL had its issues in 2017: a contentious relationship with the President, player protests, domestic violence, rule changes; all these have been pointed to as potential reasons for the descent.
In actuality, it may just be a lack of visible star power. Look at the list of top-ten selling NFL jerseys. Only Tom Brady made it to the playoffs without being injured or suspended. In the NBA, players with nine of the top-ten selling jerseys are projected to make it to the playoffs.
The brightest stars drive professional sport. When the best teams aren’t doing well, or the best players aren’t competing, ratings will naturally decline (like in the NFL wildcard game that featured the Titans-Chiefs).
NFL players can be out for a laundry list of reasons. But one, somewhat unique in sports to the NFL, might have long-term health implications. Fans are starting to notice and maybe, that’s turning them off to the game they love.
Neurons are the brain’s superhighway: there are over 90 billion neurons connecting a complex network that enables us to interpret and react to our surroundings. Neurons are composed of the cell body, the axon and the axon terminal, communicating with each other by sending electrical signals down axons and off to adjacent cells.
When we hit our heads, the brain can bounce around in the skull; a concussion is a traumatic brain injury (TBI) that’s a result of the rapid motion of the brain inside the skull. On a neurological level, individual neurons can be stretched and damaged, affecting brain chemistry.1 Symptoms range from loss of consciousness to disorientation to sensitivity to sound and light.
Axons are like wires; they help neurons reach cells in different parts of the brain. But they’re fragile and injury-prone, and after a concussion, axons are usually more damaged than other parts of the brain’s cells. This damage to the transportation system makes it difficult for the brain to send signals and thus function.
Microtubules are also part of this transportation system, much smaller than axons but still important in the delivery of materials within the cell. They’re susceptible to even smaller impacts than concussions.
And because they’re so small, microtubules gain structural support from a special protein called tau. In healthy brains, tau supports the microtubules, which help the brain function and operate normally.
With repeated microtubule breakdown, tau protein can float freely inside the cell. Free tau protein can change shape and clump together–at this point, it can spread to surrounding brain areas, growing even without additional head trauma.
Chronic traumatic encephalopathy (CTE), is a degenerative brain condition believed to be caused by repeated hits to the head.
A unique pattern of tau spread is associated with the disease, killing brain cells.
Symptoms of CTE include everything from impaired executive brain function and short-term memory loss, which can lead to depression, substance abuse, emotional instability and suicidal thoughts or behavior.
It seems obvious. Put some of the best athletes in the world on a field together, have them run full speed to collide and twist and tackle, and there will likely be some brain injuries.
But after a hit, players get up. Maybe they stay down for a moment, but more often than not, they’re jogging back to the sidelines, out for the next play and out of sight to the fan. Of course, there are those moments when a stretcher comes out and we hold a collective breath, but those happen far less than the hundreds of small injuries that together, may have a cumulative effect.
So, why is CTE found frequently in football players? Because concussions are commonplace.
Concussions happen pretty often in the NFL. From 2016 to 2017, there was a 13.5% increase in diagnosed concussions during the preseason and regular season: a total of 291 in 2017. The league is taking precautions to help avoid these types of injuries, from rule changes to new gear to heftier fines. But those efforts haven’t yielded better results.
The repeated head injuries are likely linked to the increase in CTE. And it’s not just diagnosed concussions; it seems even less-severe hits to the head can lead to CTE.2
Scientists have known about the brain damage caused to professional boxers since the 1920s, with the disease originally being called dementia pugilistica.3 In recent years, studies have looked at professional football players, and the findings have been so eye-opening it’s impossible to look away.
One study, which analyzed the brains from 202 deceased football players, CTE was neuropathologically diagnosed in 177 (87%). When looking specifically at those who played in the NFL, that number rose to 110 of 111 samples (99%).4 Remember, these samples were donated, which means donators likely suspected CTE even before the diagnosis. That skews the samples, but the findings remain important.
The first confirmed case of CTE in an NFL player was documented in 2005 by Dr. Bennet Omalu.5 The study was made famous through the film “Concussion,” in which Will Smith portrayed Omalu.
Part of Omalu’s conclusion was a desire for continued research on the subject, because his study was conducted on a single research sample. Dr. Ann McKee, director of Boston University’s Chronic Traumatic Encephalopathy Center, has been leading much of that research. She and her team have studied tauopathy after repetitive head injury, detailing the patterns found by the spreading of tau.3 The difficult thing about CTE diagnosis is that it can only happen postmortem with a neuropathologic examination of brain tissue.
Even those who don’t pay attention to sports have likely heard of Aaron Hernandez, the former New England Patriots tight-end and convicted murderer who ended his own life while in prison. McKee and CTE BU researchers found his case to be the most severe they’ve seen in a young person.
More studies continue to uncover unsettling results. In 2016, she and her team concluded that there is increasing evidence that CTE affects amateur and professional athletes, as well as military veterans, citing CTE as a “major public health concern.”6
While the spotlight on the NFL may have helped illuminate CTE, military professionals are also at risk, specifically those who have experienced blast injuries.7 TBI and CTE are both being studied in postmortem military veteran brains, linking blast exposure to persistent impairments in neurophysiological function, learning and memory.8
When analyzing symptoms of military veterans diagnosed with CTE, researchers found some individuals were also diagnosed with PTSD, drawing lines between commonalities in symptoms and possibly shared pathogenetic foundations.9 More research is needed to understand the connection, but the suggested linkage could exacerbate symptoms.
The bottom line? Concussions are more serious than we thought.10 These injuries, occurring on the battlefield of the football field (or even accidentally in everyday life), can change personality, cognitive performance and can increase the risk for suicide. They can change a life forever, or end it.
Not everyone in the military or NFL have CTE or other brain injuries. Since many of the brains are donated to research, they can’t provide a representative sample.
Still, research suggests that duration of exposure to hits can impair cognitive function. A study in former NFL players who started playing football before age 12 inconclusively demonstrated an association between preteen football and cognitive impairment later in life.11 Those results were supported by another study in deceased athletes linking early football play to cognitive and behavioral symptoms of CTE 13 years earlier on average (when compared to players who started later in their teenage years).12
One study, which looked at the link between cognitive impairment and depression of 65 year-olds who played football in the 1950s, didn’t illustrate a risk for symptoms later in life.13
Problem is–we’re not playing 1950s football anymore. Athletes are bigger, stronger and faster than they’ve ever been, and despite the technological advancements in gear, we’re still seeing an increased risk of brain injury.
The NFL is taking steps toward making the game safer: helmet-to-helmet hits are banned and penalized, kickoffs have been changed to limit full-speed collisions, the amount of contact in practices have been lessened, and the league is analyzing artificial playing surfaces to soften the impacts.
There’s even a concussion protocol, where players suspected of having a concussion are immediately removed from the field. If diagnosed, they can only return to play after completing the league’s concussion protocol, including a period of tests, supervised exercise and examinations from both team and independent doctors.
The league has even donated millions to concussion-related research.
But none of this changes the countless hits that can lead to brain injury on an NFL field.
It seems these are occupational hazards for football players, similar to military personnel.
For the military, head immobilization during blast exposure prevented side effects of learning and memory deficits.8 More research is needed, but some suggest TBI recovery practices might focus on mechanisms that promote innate neuroplasticity, like graded exercise, restorative sleep and nutritional support.9
There has also been growing research that suggests certain nutrients have emerged as a potential strategy to prevent or reduce the deleterious effects of concussions. Things like creatine and curcumin were used in a recent study,14 along with omega-3 fatty acids, which are present in Kado-3 by HVMN.
We at HVMN are dedicated to understanding traumatic brain injury. Exogenous ketones, like HVMN Ketone, could help.
Many studies have been done on animals, with research suggesting that the ketogenic diet could be useful for children suffering from TBI injuries.15 Similarly, fasting (which leads to ketosis) studies on rats showcased that, after moderate cortical impact, fasted subjects showed a significant increase in tissue sparing.
In patients with cerebral injury, one study found that administering ketones may provide a significant benefit.16 While dosage, timing, and administration methods all need further research, the results are exciting, as ketones could be employed to manage acute brain injury. Two to three days after an impact, there is a hypometabolism of glucose and the brain is starved of energy. Ketones can bypass glucose metabolism and maintain brain energy levels, thus potentially limited damage.
Despite different methods to achieve ketosis (both exogenously and endogenously), results indicate that the presence of elevated ketone levels in the blood can help recovery for those who suffered a brain injury.
As science continues to explore the subject, we’ll continue learning about how brain injuries happen, how to treat them and hopefully, how to prevent them.
What’s clear now? They’re a problem in the NFL and the military, two occupations where some of the world’s elite performers push their bodies to the absolute limit. Sometimes, the result is a concussion or another type of TBI, and later down the line, the result is increasingly becoming CTE. These types of injuries aren’t exclusive to the NFL and military. You could slip, fall and hit your head. You could accidentally run into something. The possibility for brain injury is ever-present.
But they’re more susceptible than the rest of us, given the nature of their jobs. These athletes and military personnel are more than just elite performers; they’re heroes to many. They’re fathers and mothers and siblings and children, who put their bodies on the line for us (in one way or another).
The scientific community is committed to finding answers, and we hope to be part of the solution.
If you're interested in learning more, check out our podcast featuring Connor Barwin, outside linebacker for the New York Giants.
|1.||Giza CC, Hovda DA. The Neurometabolic Cascade of Concussion. J Athl Train. 2001 Jul-Sep; 36(3): 228–235.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC155411/|
|2.||Tagge CA, Fisher AM, Minaeva OV, et al. Concussion, microvascular injury, and early tauopathy in young athletes after impact head injury and an impact concussion mouse model. Brain, Volume 141, Issue 2, 1 February 2018, Pages 422–458, https://doi.org/10.1093/brain/awx350.|
|3.||McKee AC, Cantu RC, Nowinski CJ, Hedley-Whyte ET, Gavett BE, Budson AE, Santini VE, Lee HS, Kubilus CA, Stern RA. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol. 2009 Jul;68(7):709-35.|
|4.||Mez J, Daneshvar DH, Kiernan PT, et al. Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football. JAMA. 2017;318(4):360-370. doi:10.1001/jama.2017.8334|
|5.||Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL, Wecht CH. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. 2005 Jul;57(1):128-34; discussion 128-34.|
|6.||McKee AC, Alosco ML, Huber BR. Repetitive Head Impacts and Chronic Traumatic Encephalopathy. Neurosurg Clin N Am. 2016 Oct;27(4):529-35.|
|7.||Mez J, Stern RA, McKee AC. Chronic Traumatic Encephalopathy: Where Are We and Where Are We Going? Curr Neurol Neurosci Rep. 2013 Dec; 13(12): 407.|
|8.||Goldstein LE, Fisher AM, Tagge CA, et al. Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model. Sci Transl Med. 2012 May 16;4(134):134ra60. doi: 10.1126/scitranslmed.3003716.|
|9.||McKee AC, Robinson ME. Military-related traumatic brain injury and neurodegeneration. Alzheimers Dement. 2014 Jun; 10(3 0): S242–S253. doi: 10.1016/j.jalz.2014.04.003.|
|10.||Peskind ER, Brody D, Cernak I, McKee AC, Ruff RL. Military- and Sports-Related Mild Traumatic Brain Injury: Clinical Presentation, Management, and Long-Term Consequences. J Clin Psychiatry. 2013 Feb; 74(2): 180–188. doi: 10.4088/JCP.12011co1c.|
|11.||Stamm JM, Bourlas AP, Baugh CM, et al. Age of first exposure to football and later-life cognitive impairment in former NFL players. American Academy of Neurology, Jan 28, 2015. doi: https://doi.org/10.1212/WNL.0000000000001358|
|12.||Alosco ML, Mez J, Tripodis Y, et al.Age of first exposure to tackle football and chronic traumatic encephalopathy. Annals of Neurology. 2018; 83(5); 886-901.|
|13.||Deshpande SK, Hasegawa RB, Rabinowitz AR, et al. Association of Playing High School Football With Cognition and Mental Health Later in Life. JAMA Neurol. 2017;74(8):909-918. doi:10.1001/jamaneurol.2017.1317|
|14.||Oliver JM, Anzalone AJ, Turner SM. Protection Before Impact: the Potential Neuroprotective Role of Nutritional Supplementation in Sports-Related Head Trauma. Sports Med. 2018; 48(Suppl 1): 39–52. doi: 10.1007/s40279-017-0847-3|
|15.||Hu ZG, Wang HD, Qiao L, Yan W, Tan QF, Yin HX. The protective effect of the ketogenic diet on traumatic brain injury-induced cell death in juvenile rats. Brain Injury, 23:5, 459-465, DOI: 10.1080/02699050902788469|
|16.||White H, Venkatesh B. Clinical review: Ketones and brain injury. Critical Care. 2011;15(2):219. doi:10.1186/cc10020.|