I think the venn diagram is probably somewhat intersecting, but not total or near-total. The debate over the appropriateness of the protests (And certainly also the question of whether they have a valid complaint) is a matter of politics; the second issue here, over the continuing "manliness" or entertainment value of the sport, is - though dickish to raise in this manner - a valid sporting question, and one which far more people might debate without the same level of intensity. The correlation between the two may be positive, but I'd imagine it's not very strong.Buried in Trump's anthem rant was the other thing he was saying about football, that liberal weenies were ruining the sport by not allowing the players to hit each other anymore. I wonder how many people who agree with him on the anthem also agree with him on that, and would reject this entire discussion out of hand? Seems like it would be a significant number, and those people would more likely be located in parts of the country where we get a lot of our elite football talent. I dunno, I think football may be in trouble due to a decline in the talent pool and the "ick" factor that fans are already feeling watching these guys literally kill each other, but I also think this entire discussion is evaluating those issues through an entirely different lens than lots and lots of people who love watching football and have no qualms about their kids playing.
This is assuming that CTE is relayed to diagnosed concussions, which may not be true. A lot of the theory seems to suggest is is the repetitive nature of blows to the head in football rather than the concussions. Hockey and other sports are staying mum about testing payers for CTE, but I expect there is something to worry about there. Certainly the problems of several enforcers seem to fit the CTE profile.Second, what is the safe sport alternative? The NFHS also keeps track of concussion data for high school sports. Football has a concussion injury rate of .4 per 1,000 athletic exposures, which ranks behind hockey and women's soccer. Men's soccer comes in at .28, about 75% of the risk. Is a 25% difference in injury rate enough to shift players from one sport to another? If so, then everyone should play baseball as it is MUCH safer than every other sport at a rate of 0.07.
I didn't read the Wired story as saying that about soccer players. What did I miss?We DO know however that soccer players, similar to football players, have a significantly elevated risk of CTE:
I think the relevant quotes are these:I didn't read the Wired story as saying that about soccer players. What did I miss?
More than half the football players on the field at any time get hit in the head at least once on every single play. I think that, applying common sense, parents might opt for sports where their kids are being hit in the head fewer times. Whether that turns out to result in less brain damage remains to be seen.
The point is that it's easy to point football and say, "Oh my god, we need to eliminate this sport because it's so dangerous". It's harder to say "We need to eliminate almost ALL sports because they are dangerous".Yeah, but who really cares if they stop playing soccer?
I don't know man. I got hit by a golf ball in the back of my head while I was walking down the middle of a fairway once. I could have been concussed!The point is that it's easy to point football and say, "Oh my god, we need to eliminate this sport because it's so dangerous". It's harder to say "We need to eliminate almost ALL sports because they are dangerous".
Tennis and golf are probably okay
Just a brief tangent, those NFHS documents are ascinating.I don't think football is going anywhere, for several reasons. First, the participation numbers sound alarming but I don't think they really are. I looked at the NFHS data going back the last 5 years, and football participation has dropped a little over 2% since 2011 (From 1,109,936 players in 2011 to 1,085,182 in 2015). Not insignificant, but that won't cause the death of football. But in the same timeframe, basketball participation also dropped 1.5% (984,777 players in 2011, 970,983 in 2015). Nobody is worried about basketball dying due to lack of participation, and with good reason.
The above data can be found directly from the National Federation of High School statistics: http://www.nfhs.org/ParticipationStatics/ParticipationStatics.aspx/
Second, what is the safe sport alternative? The NFHS also keeps track of concussion data for high school sports. Football has a concussion injury rate of .4 per 1,000 athletic exposures, which ranks behind hockey and women's soccer. Men's soccer comes in at .28, about 75% of the risk. Is a 25% difference in injury rate enough to shift players from one sport to another? If so, then everyone should play baseball as it is MUCH safer than every other sport at a rate of 0.07.
Many will take umbrage at the statistics above, and state that CTE is probably caused by sub-concussive hits whose relative risk may not be captured in the concussion statistics. Unfortunately, we don't know with hard data if soccer has 25% fewer sub-concussive hits or far fewer. We DO know however that soccer players, similar to football players, have a significantly elevated risk of CTE:
As the research continues, I can't see parents removing their children from playing football so they can watch them play a sport they enjoy far less with similar brain injury risk. And as much as I love baseball, I don't see it as the only surviving sport in this country.
I think the relevant quotes are these:
"But neurologists involved in this new study, as well as other experts, say another sport may rival football’s impact on the brain: soccer."
“Soccer has repetitive impacts, from player to player and players heading the ball,” says Boston University’s Ann McKee, an author of this week’s study of NFL players. “It doesn’t matter how you do it, just that you do it and do it repetitively.”
"Scientists say that it may be the less powerful “sub-concussive” hits that both football and soccer players receive all the time that could trigger the disease. "
"McKee’s group in Boston has set up a “brain bank” where families of ex-football players (pro and college athletes) who are worried about their mental state can donate their brains for research. So far they have received 425 brains; CTE has been found in 270 of them. That kind of focused research effort hasn’t yet been developed for soccer."
Basically the article / neurologists imply that they believe soccer may be as dangerous, but they haven't been able to do any full-scale studies yet because nobody has donated their brain despite the fact that many soccer players develop cognitive impairments (See: https://www.einstein.yu.edu/docs/labs/michael-lipton/Soccer_heading_is_associated_with_WM.pdf)
We DO know however that soccer players, similar to football players, have a significantly elevated risk of CTE:
I’m going to respectfully disagree with the statement specific to any degree of certainty. I can conclude with some certainty that CTE is having a negative effect on the popularity of the game. Based on comments within this forum as well as outside discussions with friends and family, CTE is souring people’s view of football and the NFL which directly translates to popularity of the game. The extent of which is entirely unknown to me however is certainty greater than zero. I am digressing into semantics now however in the converse it is highly unlikely that CTE is favorably contributing to the popularity of the game.You’re projecting what those results mean. It may but you cannot say that with any degree of certainty.
http://www.espn.com/nfl/story/_/id/21730219/tom-savage-houston-texans-taken-locker-room-seen-hands-twitching-hitHOUSTON -- Texans quarterback Tom Savage remained on the ground with his hands twitching following a hit in the first half of Sunday's game against the San Francisco 49ers.
[. . .]
He was checked out in the medical tent for less than three minutes then returned to the game for one series and threw two incomplete passes. He went to the locker room with two minutes remaining in the half and was replaced by T.J. Yates.
After taking the hit, Savage spent time talking to the team's medical staff. Before the Texans' next offensive series, a team official held on to Savage's jersey and arm as he tried to go on to the field. Savage could be seen arguing with the team official before he was escorted to the locker room by the team's trainer.
The Texans have ruled Savage out with a concussion.
It's worse than described here. It looks low he had a seizure or something after his head hit the ground.This league really is disgusting:
“He took a hit. But when he walked off and he told the trainers he got poked in the eye, then they did take him into the tent and checked him for a concussion, which he did not have,” Hurney said.
“And it was really getting poked in the eye. He took a knee because they told him to take a knee so we could get the official timeout and Derek could warm up.”
I think the claim (from the broadcast) was that it was actually the padding of his helmet that got smushed around and into his eye.Love to see a recreation of how he got poked in the eye past his visor, face mask, and the tackler having his hands wrapped around his head.
"I know it was precautionary things for a concussion, but it wasn't a hit to the head it was my eye," Newton said, per ESPN. "My helmet had came down low enough over my eyelid and it got pressed by the player's stomach, I believe. I thought somebody stuck their finger in my eye, but I've got my visor, so that couldn't happen."
"My helmet had came down low enough over my eye lid and got pressed by a player's stomach, I believe. I thought maybe somebody stuck a finger in my eye."
Granted. Of course his story is that he knew he had to come out of the game, so kneeling on the field gave Anderson (he's still in NFL???) a few more minutes to warm up.Ahhh... at least it makes more sense it was bad translation from Rivera. But thinking back to all the times I’ve gotten poked in the eye, can’t think of the last time I staggered like that so long after it happened.
Depends on how hard it was poked and from what direction. If the eyeball was rotated by an external object, the rotation could cause some unusual integration of visual and vestibular ("inner-ear balance") information; which could cause one to stagger if one were trying to move around or get up from the ground. The opposite can happen if the vesitbular system is interfered with (e.g. through alcohol consumption).Ahhh... at least it makes more sense it was bad translation from Rivera. But thinking back to all the times I’ve gotten poked in the eye, can’t think of the last time I staggered like that so long after it happened.
I agree. I still remember that game against the Broncos in 2016 (or was it 2015?) when he took hit after hit to the head.Cam Newton is going to have a really, really tough time in his 40s and 50s. He's probably gotten beat up more than any other player.
The actual study was published in the neurologic journal Brain.“It’s the hits to the head, not concussion, that trigger CTE,” says study coauthor Lee Goldstein, a School of Medicine associate professor of psychiatry, who also has an appointment at the College of Engineering.
The study’s finding is important because efforts to protect athletes focus on preventing concussions rather than repeated hits to the head, says Christopher Nowinski, codirector of BU’s Chronic Traumatic Encephalopathy Center.
“In order to reduce CTE risk” in athletes and military veterans, “there must be a reduction in the number of head impacts,” says Ann McKee, director of the CTE Center and another study coauthor. “The continued focus on concussion and symptomatic recovery does not address the fundamental danger these activities pose to human health.”
I think one of the differences is that soccer, and to a lesser extent hockey (I will not comment on lacrosse as I think I have seen one game in my life), have the possibility of changing up their rules to alter the sport in ways that can reduce the amount of head trauma their players (I think that soccer without headers, and hockey without fighting, as an example are still perfectly viable sports).So this basically means football as we know it is over in ~20 years, right?
Can't imagine many parents, at least not in wealthy or educated households, will allow their children to participate in the future.
Not good for US soccer either. Hockey and lacrosse maybe also will see a significant reduction in enrollment.
Ann's group makes a really important point here; insult to the brain via head trauma does not equate to severe concussions, as diagnosed by clinicians (mild TBI is still probable here).
In terms of design, and given practical limitations, the study is neat. However, Rich Barlow seems to be misquoting the authors in a misleading way.“In order to reduce CTE risk” in athletes and military veterans, “there must be a reduction in the number of head impacts,” says Ann McKee, director of the CTE Center and another study coauthor. “The continued focus on concussion and symptomatic recovery does not address the fundamental danger these activities pose to human health.”
Case 2:We included four cases in the acute-subacute post-TBI cohort. Case 1, an 18-year-old male high school athlete (American football, baseball, basketball, weight-lifting) who died by suicide from hanging 4.2 months after sustaining a mild closed-head injury while snowboarding. The decedent’s head injury exposure history was notable for amateur participation in American football (9 years total). He played fullback and middle linebacker, positions associated with frequent high-magnitude head impacts (Crisco et al., 2011). He sustained 10 concussions, none other than the last with loss of consciousness. Four months before death, he sustained a concussion while snowboarding and briefly lost consciousness (∼2 min).
Case 3:Case 2, an 18-year-old male high school athlete (American football, rugby, soccer, in-line hockey) who died suddenly 10 days after the second of two sports-related head injuries. The decendent’s head injury exposure history was notable for four sports-related concussions. He played American football at the amateur level starting at age 11 and continued intermittently through high school (3 years total). In his junior and senior year of high school, he played rugby (amateur then semi-professional level). One month before death, he sustained a severe concussion during a rugby match that resulted in post-traumatic somnolence. Two weeks later he sustained a second rugby-related head injury that resulted in sideline collapse and a 2-day hospitalization for clinical observation and recuperation. Seven days after hospital discharge, he engaged in light weightlifting after which he collapsed suddenly while eating dinner with his family.
Case 4:Case 3, a 17-year-old male high school American football and lacrosse player who died by suicide from hanging. The decedent was diagnosed with two sports-related concussions during life, the last sustained 2 days before death. He was evaluated in an emergency room after his last head injury (no reported loss of consciousness) where he was noted to be confused, could not recall events and circumstances surrounding the injury, and was unable to recite the days of the week in reverse order.
In all the human cases, moderate to severe concussions occurred. Here is the history reported for the controls:Case 4, a 17-year-old male high school American football player who sustained three sports-related concussions (26 days, 6 days, 1 day) before death from second impact syndrome. During the football game in which he sustained a terminal head injury, he received a hard tackle, landed on his helmet, and was rendered immobile and unresponsive. A tonic-clonic seizure ensued. He was intubated and ventilated on the field, then transferred to a hospital emergency ward.
In the human component, the number and severity of diagnosed concussions varies greatly between the cases and controls -- unless the results show no differences between the two groups (i.e. lots of atrophy on the controls part) -- I interpret the human findings as inconclusive (its a sample size of fucking 8) regarding the effect of concussion diagnoses on neural atrophy, save that every case with a severe concussion observed here had neural atrophy.We included four cases in the control athlete cohort. Case 5, a 19-year-old male high school American football player who died of multiple organ failure and cardiac arrest. The intact brain (1430 g) was obtained as a formalin-fixed tissue specimen with an unknown post-mortem interval. Grossly, the brain did not show evidence of atrophy, asymmetry, herniation, or contusions. Case 6, a 19-year-old male college hockey player with a history of six concussions who died of a cardiac arrhythmia. The intact brain (1500 g) was obtained as a formalin-fixed tissue specimen with an unknown post-mortem interval. Grossly, the brain did not show evidence of atrophy, asymmetry, or contusions. Case 7, a 17-year-old male high school American football player who died from oxycodone overdose. The brain was obtained as formalin-fixed coronal slabs of available tissue with an unknown post-mortem interval. A 0.3-cm cavum septum pellucidum was noted. Case 8, a 22-year-old male former high school American football player who died by suicide (unknown mechanism). The decedent’s head injury exposure history was notable for three remote concussions, one with loss of consciousness of indeterminate duration, all sustained more than 7 years before death. He was diagnosed with bipolar disorder and had two suicide attempts prior to the completed suicide. The intact whole brain (1630 g) was obtained as a fresh tissue specimen with a 2-day post-mortem interval. Grossly, the brain did not show evidence of atrophy, asymmetry, or contusions.
Previously, Ann's rodent model research suggested that the intensity of concussions mattered. However, these mice were on anesthetics, which may have preventative effects on head trauma (long story short -- dissociatives like ketamine and PCP may protect the brain in rare circumstances). Obviously, this is a far cry from the conditions that athletes are normally in, so by experimenting on awake mice, they may hopefully reduce the confound; although it's still not even close to the state (i.e. highly active) that athletes usually find themselves in prior to receiving head trauma.We hypothesized that closed-head impact injury is mechanistically linked to, causally determinative of, and temporally associated with early CTE brain pathologies.
To test this hypothesis, we developed an experimental instrument that uses momentum transfer to produce traumatic head acceleration without gross skull deformation in awake (anaesthesia-naïve) mice. Experimental parameters were optimized to match head kinematics in our companion blast neurotrauma mouse model (Supplementary Fig. 1A) was designed for use in unanaesthetized young adult male mice to model subject variables, injury conditions, and brain pathology as in the human cases (Goldstein et al., 2014; Wojnarowicz et al., 2017). The instrument incorporates a gas-driven momentum transfer mechanism to deliver a lateral closed-head impact that induces traumatic head acceleration without gross skull deformation (Fig. 2A and B). The rationale for this design was to enable evaluation of acute neurobehavioural responses and cellular-molecular effects without confounding interference of systemic anaesthetics (Statler et al., 2006; Planel et al., 2007, 2008; Fish et al., 2011; Luh et al., 2011; Whittington et al., 2013; Gao et al., 2016). Unanaesthetized mice were restrained across the thorax in the prone position such that the inner pad of the sled contacted the left temporal-zygomatic region of the head. Linear translation of the sled resulted in left-lateral closed-head impact, right lateral flexion at the cervical spine, and traumatic acceleration of the head in the horizontal plane of motion (Fig. 2A and B). Head motion was assessed by high-speed videography (100 000 fps, 100 kHz).
To me, this last point is critical for a different reason than Ann suggests: the reason we have trouble identifying biomarkers based on brain areas is because the immediate injury varies depending on where the trauma occurs. Behavioral markers are borderline impossible, because the immediate injury means different mechanisms will be affected (as a boxer may attest -- where one gets punched in the head produces different types and gradations of motor impairment). However, the long term pathophysiological process that occurs after is essentially the same (and very difficult to dissociate from other dementias, in this case, AD). However, the sample sizes to draw this conclusion are fucking small as balls. They literally conducted statistical tests where some groups comprise one or two cases.Previous research in our laboratory and others pointed to the intensity of traumatic head motion, rather than the type of insult, as the causally determinative mechanism that triggers CTE brain pathologies (Goldstein et al., 2012; Huber et al., 2013; Kondo et al., 2015). To test this hypothesis, we set experimental parameters in our impact injury mouse model such that head motion was kinematically comparable to our blast model (Supplementary Table 2). We hypothesized that impact injury would initiate shearing forces in the brain, thereby causing microvascular injury, reactive neuroinflammation, and accumulation of pathogenic species of phosphorylated tau protein similar to the cascade triggered by blast exposure (Goldstein et al., 2012; Huber et al., 2013; Kondo et al., 2015). To investigate this hypothesis, we examined brains from mice sacrificed 24 h, 3 days, and 2 weeks after single-repeat left-lateral impact injury (24 h post-injury: impact-injured mice, n = 7; uninjured sham control mice, n = 3; 3 days post-injury: impact, n = 6; sham, n = 2; 2 weeks post-injury: impact, n = 7; sham, n = 3; 5.5 months post-injury, cis-p-tau only: impact, n = 3; sham, n = 1). In contrast to the diffuse brain pathology noted after blast exposure (Goldstein et al., 2012), the brain lesions observed after lateral impact injury localized predominantly to ipsilateral cerebral cortex subjacent to the impact contact zone (Fig. 3).
This is a really interesting notion, the hit itself matters more than the shearing motion (e.g. as visualized by the NYT). However, I think there are some limitations to this interpretation. I've already stated the first limitation, this is a small sample size. The second problem is the assessment of behavioral response. In order to compare studies, both experiments primarily relied on motor tasks, but a diffuse brain injury may produce different deficits that cannot be uncovered through motor experiments. The failure to observe a lack of behavioral response in the blast experiments does not exclude loss of function. Certainly in humans, blast exposure can lead to concussions. The third problem is that we don't know what cause the longitudinal pathophysiological process, which is the one associated with dementia. The fourth problem, unfortunately, is that mice are a poor substitute for humans, especially since the orientation of the body with respect to the head is completely different and the organization of the brain areas also differs.By contrast, and to our surprise, mice exposed to blast under conditions matched for head kinematics did not exhibit acute neurobehavioural deficits post-injury (Goldstein et al., 2012). This unexpected observation argues against the concept that kinematic variables are primary determinants of concussive phenomena (Denny-Brown and Russell, 1941; Shaw, 2002). Rather, our experimental and computational results suggest that the observed acute neurobehavioural responses to closed-head impact injury are triggered by force point loading and intraparenchymal shear stress foci in the cerebral cortex that occur before onset of gross head motion.
In other words, the authors suggest that two things are occurring due to focal head trauma: 1) The immediate impact, which causes immediate behavioral changes, are temporary and due to functional, not structural changes. 2) The resultant head motion and slow-shearing initiate the long term pathophysiological process, which also remains highly heterogeneous.Taken together, our results indicate that the transient neurobehavioural impairments triggered by impact result from disruption of cortical function rather than damage to cortical structures, and as such, agree with neuronal excitation theories of concussion (Denny-Brown and Russell, 1941; Walker et al., 1944; Shaw, 2002).
do not appear to be strongly supported by the study's findings. I find the author's quotes quite odd here "provide strong causal evidence" "independent of concussion"; I think Rich Barlow just missed the point of the paper. For he concludes:“The same brain pathology that we observed in teenagers after head injury was also present in head-injured mice,” says Goldstein. “We were surprised that the brain pathology was unrelated to signs of concussion.”
The findings, he adds, “provide strong causal evidence” linking head impacts to both traumatic brain injury and early CTE, “independent of concussion.”
The logic of the concluding sentence gets the study backwards. The trigger for concussion and CTE can be the same, but the pathophysiological processes may be independent.
Absolutely; that's not the point of this study however (this has been known for at least a few decades). The point of the study is that concussion severity may be unrelated to long term effects. If true, then a number of current practices need to be revisited. For example, testing for the concussion protocol in the NFL relies on behavioral symptoms, which may be insufficient to determine future risk of putting the player back in.Okay sample size for this study is small and mice and humans have differently shaped skulls but isn’t it safe to say that parents should not let their kids play tackle football or box because the long term effects really suck?
That's ridiculous by Timberlake.The NFL must be thrilled
Pop singer Justin Timberlake, speaking Thursday at an NFL press conference to promote his Super Bowl halftime performance, said that his own son will never play football.
Timberlake and actress Jessica Biel are the parents of two-year-old Silas. After jokingly offering to suit up himself Sunday as a wide receiver if the New England Patriots needed him, Timberlake was asked by a reporter if he would "support it if [Silas] wanted to run some routes and get in the NFL."
Timberlake responded: "Uh, he will never play football. No, no."
I think it's entirely hypocritical to play the halftime show and get hundreds of millions of viewers watching him and then, before he does this, take a dump on the product giving him this platform.If that's how he really feels, good for him. It's not like they're going to fire him. The NFL is evil and holding it's feet to the fire is the only way to get them to anything.
So you feel bad that the NFL, one of the most hypocritical organizations on earth, got taken advantage of by a hypocrite?I think it's entirely hypocritical to play the halftime show and get hundreds of millions of viewers watching him and then, before he does this, take a dump on the product giving him this platform.
If he feels that way about football, which would be fine, he shouldn't be utilizing the NFL's largess to give him exposure to the world.