November 13, 2021
In the predawn hours of Feb. 7, 2014, a pre-med student named Ted Agu, a son of Nigerian immigrants and a walk-on player for the University of California’s football team, the Golden Bears, dropped dead during a team conditioning exercise that involved sprinting up and down a campus hillside multiple times while pulling a thick rope, together with a group of other players.
Amidst the subsequent sentimental gestures honoring a young man who had died “doing what he loved” — while teammates and coaches issued tributes to Agu’s intelligence, compassion and dedication; while Cal paused other campus activities to stage a memorial service; while a plaque with his likeness was installed at Memorial Stadium — what is arguably the world’s most famous public university proceeded, on a different track, to do something quite different. It engineered what could only be termed a cover-up of the cause of Agu’s death. Moreover, the cover-up succeeded.
We’ll get to the elements of the cover-up in a moment. First, it’s important to note that offseason conditioning drill deaths of non-professional football players — who are often minors and thus, by definition, not legally consenting — tell their own collective and gruesome story. This is a vastly underreported aspect of football’s overall vastly underreported public health crisis.
Thanks to a vogue angle of medical research — which most people don’t realize has been around since at least the 1920s — many football participants and fans now have some appreciation of the problem of traumatic brain injury, which can have both immediate and lifelong consequences, as a byproduct of systematic violent contact. However, few know or understand the implications of a phenomenon that causes two or more youth football players to die almost every year — at high schools and obscure junior colleges, as well as at NCAA Division I programs like Cal’s — with no traumatic contact whatsoever, and without helmets or shoulder pads.
These boys or young men are dying of bronchial asthma or genetic heart conditions or exertional heatstroke. And, like Ted Agu, at least some of them, probably far more than we know, are dying of what the medical literature has called “exertional sickling,” or ES. Sickling attacks are overwhelmingly associated with Black athletes, since approximately one in 12 African-Americans carry the sickle cell trait.
You most likely have heard of sickle cell anemia, an inherited red blood cell disorder. But sickle cell trait is different; it is not a disease. Carriers can lead normal lives. But they need to be extra-vigilant, with medical protocols in place to protect them in the event of distress during extreme exertion. The trait makes carriers urgently susceptible to rhabdomyolysis, the poisonous entry of dead muscle tissue into the bloodstream, which can cause sudden death.
I argue that all youth football conditioning deaths add up to more than the sum of their individual etiologies. They are a pandemic, albeit a socially induced one, of deaths from football itself — from the sheer size and scope and power of something our society would be wise to confine to a gladiator class certified to provide late-empire mass divertissement. Football belongs out of our public schools. It belongs off our public fields.
“A teen football player dies suddenly in America, for reason unrelated to collision on the field, and the postmortem investigation produces more questions than answers — particularly whether the stressful sport contributed mortally,” writes Matt Chaney, a Missouri author who has investigated the history of football harm. He cites as one of the key reasons “the reputedly ‘deficient’ state of autopsy in America, especially for children, as part of the death-investigations system that a National Academy of Sciences report characterizes as ‘fragmented’ and ‘hodgepodge.'”
And if you analogize the global, multibillion-dollar football industry’s manufacturing of doubt about its dangers to the “captive research” funded or supported by the Tobacco Institute during an earlier era, then the unappreciated scale and causes of youth football conditioning deaths can be seen as something like the sport’s “second-hand smoke” problem.
Speaking of smoke, there was plenty of that spread by Cal authorities from the moment Ted Agu fell down dead, when everyone inside the football program immediately feared and suspected the worst.
Scott Anderson, the head athletic trainer for the University of Oklahoma football team — one of the sport’s most famous collegiate programs — heard all about it. He is an outspoken critic and monitor of some football coaches’ maniacal conditioning regimes. Often these are performative masculinity “toughness” rituals with zero fitness rationale, offering zero genuine competitive advantage. Anderson has a network of sources across the country. On the day Agu died, Anderson spoke with a former Cal football staffer who in turn was on the phone with an assistant coach at the Berkeley football complex. “The coach told my source, ‘It’s a sickle cell death,'” Anderson reported. A report including this revelation briefly made the front page at CBSsports.com, before mysteriously vanishing. Anderson later told the story directly to me. (CBS did not respond to Salon’s request for comment.)
At a same-day press conference, university officials, including team physician Dr. Casey Batten, deflected questions about whether Agu had any pre-existing medical condition. Working from a script drafted by the sports information office, Batten and others said they could not comment on details that might impinge on the privacy of the deceased student-athlete.
Behind the scenes, Batten was singing a different tune — an outright obstructive one. As Dr. Thomas Beaver, the Alameda County medical examiner, was preparing to perform an autopsy on Agu, he received a highly irregular phone call from Batten. The team doctor said the case looked like open-and-shut “HCM”: hypertrophic cardiomyopathy, or generic heart failure. He did not mention ES, and the university never got around to telling Beaver — or the Alameda County Sheriff’s Office, under which the medical examiner operates — that Agu had been tested for sickle cell trait and found to be a carrier. Beaver never asked.
Indeed, it’s unclear how much the coroner knew in the first place about sickle cell trait or exertional sickling. “I was fully aware of exertional sickling when I did the autopsy, but I had no history of sickle cell disease or trait,” Beaver told Salon. He recalled that in examining Agu’s body, he found “mild to moderate cardiomegaly” (i.e., an enlarged heart) but no evidence of hypertrophic cardiomyopathy (the disease by which the heart muscle grows excessively thick) or hypertensive cardiovascular disease.
“I was given the history that he was perfectly healthy and had participated in this specific drill many times without the slightest issue,” Beaver added. “It was not until I looked at the cardiac biopsy material that I found sickle cell in the microvasculature and could raise the issue.” From that point forward, he said, the investigation was conducted by the sheriff’s office and he was no longer involved. “I was never given the history of documented sickle cell trait, or shown any documentation that I recall,” he said.
The autopsy report was released two months after Agu’s death. To the great relief of university officials, the cause of death was listed as hypertrophic cardiomyopathy.
The truth didn’t begin to emerge until discovery and depositions for the Agu family’s wrongful death lawsuit against the University of California’s Board of Regents. In his own deposition, Beaver recounted the phone conversation in which Batten had put his thumb on the scales of the autopsy investigation. A sheriff’s lieutenant confirmed that the university had faxed over 112 pages documenting its own investigation, while appearing to omit up to 29 other pages.
Asked about his call to the coroner, Batten said under oath, according to the transcript of his deposition: “Um, I don’t recall that I had a conversation where we — I think we did say something along the lines of it appeared to be, but it was — I think it was — it might have been after — I really don’t recall when I spoke with him….”
Batten is now lead primary care physician for the Los Angeles Rams of the National Football League, and is also on staff at the highly prestigious Cedars-Sinai Medical Center in Los Angeles. He did not respond to Salon’s request for comment, and a spokesperson for Cedars-Sinai said the hospital could not respond to questions about events in Batten’s career that predated his employment there.
After the depositions, Beaver — who by then had taken another coroner post in Florida, and is now a faculty member at the Medical University of South Carolina — took the extraordinary step of having Alameda County revise the autopsy report to reflect the new conclusion that ES was a contributing cause of Ted Agu’s death. Not long after that, the University of California’s lawyers reached agreement with the Agu family on a $4.75 million settlement of their wrongful death suit.
But to call ES a contributing factor in this case seems a major understatement. Testimony by Agu’s teammates made clear that he collapsed multiple times and deteriorated in stages, rather than dying suddenly. That sequence is completely consistent with ES-rhabdomyolysis, and not at all consistent with a coronary event.
ES awareness can be funny that way. For football, as we’ll see, it’s a political football. In other walks of life, it’s an excuse. Surveying the overall cluster of litigation over deaths of African-American males, there seems to be only one category of defendants who jump to acknowledging ES. In fact, in that one category, defendants aggressively deploy this explanation. That category is police officers, in fatalities involving criminals or suspects. There, apologists for the brutality that caused the individual in custody to die suddenly are quick to suggest that the culprit might have been ES, rather than the proverbial or actual knee on the neck, as in the infamous case of George Floyd.
Yet even today, if you do a standard Google search for Ted Agu’s cause of death, the result still comes up as “hypertrophic cardiomyopathy.” Adhering to the maxim often attributed to Mark Twain, the lie got halfway around the world before the truth put its shoes on. Which was exactly the way Cal and FootballWorld — my term for the organized football establishment — wanted it.
As a grim illustration of this, my California Public Records Act lawsuit against the University of California is now in its fifth year. As a result of the corresponding public information law requests, some of them enforced or catalyzed by my court petition and court orders, 700 pages of internal university documents have been produced, many of them intensely focused on the university’s PR management of Agu’s death.
The only reason this litigation remains ongoing is that UC apparently is not content with its victory in seeing none of these details, which have only been published at my personal website, picked up by any mainstream news outlet. The university is now asking California’s First District Court of Appeal to reverse a lower court’s ruling ordering reimbursement of my attorney’s fees and costs. (Earlier this year, the parties had settled on a discounted payment of $125,000.)
Demonstrating that Cal football at least knows how to fight the last war, emergency medical services were summoned in a timely fashion during a subsequent conditioning episode in 2018 that involved another Black player on the first day of team conditioning. He had been pulled out of a practice three months earlier, and this time required hospitalization for two nights with what was diagnosed as “non-traumatic rhabdomyolysis.” Again, news of the incident was efficiently hushed up.
For FootballWorld, multimillion-dollar settlements of lawsuits by family survivors are baked in as a cost of doing business. In case you’re wondering how key individual actors in the Agu death and the subsequent cover-up made out, beyond the illustrious Dr. Batten, the answer is that they’re doing fine — and without exception have moved on to bigger paychecks and more prestigious programs.
Damon Harrington, the strength and conditioning coach who designed and supervised the bizarre drill that killed Agu — which is certainly not found in any kinesiology or cardiovascular health textbook — had his contract renewed twice at Cal before moving on to become strength and conditioning coach for the football team at Grambling State in Louisiana, one of the best-known historically Black universities in the nation. Today, he holds the same position at Texas Tech.
Sonny Dykes, who was head football coach at Cal when Ted Agu died — and for whom Harrington was executing a mandate of “culture change” for a football program seen as having grown soft — is now head coach at Southern Methodist University in Dallas. In 2019, he was among the finalists for the Football Writers Association of America’s Eddie Robinson Coach of the Year Award.
Sandy Barbour, the former athletic director at Cal, now holds that position at Penn State, a school whose legendary football program has been tainted by an entirely different kind of scandal.
There’s a broader question here about the persistence of a largely-unaccounted subset of youth football deaths among Black players. Anderson, the Oklahoma athletic trainer, maintains a spreadsheet updating cases of known sickling fatalities in football conditioning. There have been at least 31 since 1963. By his calculation, nearly half of all college football conditioning deaths are from exertional sickling.
There is “a ratio of 4.5 nontraumatic deaths for every traumatic death,” Anderson wrote in the Journal of Athletic Training, meaning that far more players die as a result of training or practice than because they got hit in the head on the field. “On average, 2 NCAA football players die per season.”
On the college football ES list, Ted Agu was No. 29. Because of cover-ups similar to Cal’s but across a longer period, and because of generally poor awareness of sickle cell trait and ES, there may have been many additional deaths that were inaccurately ascribed to “random” heart attacks and the like. Anderson has documented scores of conditioning deaths in college football this century. There could be scores more at lower levels of the sport, all the way down to Pop Warner and pee-wee leagues. Anderson’s colleague, now-retired football team physician Dr. E. Randy Eichner, writes extensively about safety lapses in conditioning drills.
No. 27 on the ES list was Ereck Plancher, who died at the University of South Florida in 2008. That happened on the watch of an athletic trainer named Robbie Jackson, who moved on to California and was head athletic trainer on the scene when Agu died six years later. After being intimately involved with two such similar tragedies, Jackson seems to be the only main figure in the story who suffered noticeable career consequences: He left football and was last reported to be working in medical supply sales.
Anderson wrote that the four most common causes of “on-field (non-trauma) collapse of a football player who takes the field healthy are, by and large, different enough in setting and clinical features that, even judging only from early, sparse, media accounts we can sometimes make an educated guess that proves right.” Those four are ES, cardiac disease, exertional heatstroke (EHS) and asthma.
With more than 150 fatalities at all levels of football since 1955, EHS is the most frequent cause, and it is the one that has captured most of the headlines in recent years. There was 16-year Zachary Martin (who was not Black), at Riverdale High School in Fort Myers, Florida, in 2017. There was 19-year-old Jordan McNair, at the University of Maryland in June 2018.
And just two months after McNair, there was 19-year-old Braeden Bradforth, at Garden City Community College in Kansas. Bradforth had been rush-recruited from New Jersey less than a week earlier. He expired on his first full day in Kansas, at altitude. After the head coach, Jeff Sims, lashed out at him for supposedly not making enough effort in first-day conditioning drills, during which basic hydration was withheld, an assistant coach dismissed Bradforth from the inaugural team meeting — and, seemingly, the team — and he wandered off. Shortly thereafter, teammates found the 300-pound lineman lying unconscious outside the dormitory building where he had just moved in. Team staff directed that his body be crudely hosed down before 911 was belatedly called.
Garden City is one of the “Last Chance U” bottom-feeder football programs in the junior college system; it was where Tyreek Hill, now a star wide receiver for the Kansas City Chiefs, got a leg up before transferring to Oklahoma State and being drafted by the NFL. Sims, a peripatetic coach who was in the middle of taking Garden City to two straight junior college national championship games, blatantly lied in his early spin to the media — which was dutifully amplified on a national scale by Sports Illustrated and others — saying that Bradforth’s death was a random, context-free act of God. Only after the dogged investigations of Braeden’s mother, Joanne Atkins-Ingram, and her lawyer, Jill Greene, did the college begin seriously accounting for its gross negligence. Sims left Garden City for Missouri Southern State, then was let go there around the time Garden City settled the Bradforth family’s lawsuit for $500,000, the maximum amount allowable under the Kansas legal doctrine of “qualified immunity” for state public agencies.
One thing Sims could well have faced, but didn’t, was criminal prosecution for reckless endangerment or manslaughter. There is only one known case of such prosecution in a football conditioning death: the EHS death of 15-year-old Max Gilpin at Louisville’s Pleasure Ridge Park High School in 2008. The Pleasure Ridge Park head coach, Jason Stinson, was acquitted at trial, but Jefferson County Public Schools forked over $1.75 million to the Gilpin family to settle the civil case.
(Two Georgia high school girls’ basketball coaches currently face charges for the 2019 EHS death of one of their players.)
Dr. Eichner has published voluminously on avoidable football conditioning deaths in general and ES in particular. He has consulted in dozens of wrongful death lawsuits involving sports or the military, including the Agu family’s. (A 1987 Army study found that Black recruits with sickle cell trait were 30 times likelier to die during basic combat training than those without the trait.) Commenting on the recent football heatstroke deaths in the newest issue of Current Sports Medicine Reports, Eichner writes: “Global warming and a demanding coach can be a lethal combination [especially] for a huge lineman. This is especially true when the coach lacks common sense. In football, training is often by tradition; athletes become coaches and train young athletes as they were trained. Too often, the focus is on ‘creating’ toughness and discipline more than developing football fitness and skills.”
Black people are around 13 percent of the U.S. population, but Black athletes comprise 46 percent of Division I football players, according to NCAA data. In the NFL, that figure is close to 60 percent.
A basic and understandable explanation for this is what has been called the “Dr. J. Syndrome,” after basketball legend Julius Erving: Lacking a multitude of models for advancement, Black youth cling to the visible and compelling dream of fame, glory and riches in sports and entertainment.
David Karen, a specialist in the sociology of sports at Bryn Mawr College, also sees fundamentally rational economic choices playing out. “There is serious tracking happening with sports, by race and class,” Karen said. “What do parents and kids perceive the sports opportunity structure to look like? People are going to gravitate toward opportunities that appear plentiful and well-used. Additionally, what kids choose to do in college is structured by what they’d had access to before — from very young ages onward.”
Hamilton College sociologist Alex Manning specifically studies the dynamics of racism, inequality, families, youth, sports and culture. He told me: “It comes down to how we treat sports institutionally. A lot of sports require substantial private resources in order to get to elite levels, but football is something supported and invested in by public schools. That’s where the funneling happens.”
In Manning’s analysis, football’s touted benefits to the commonweal, such as forging teamwork and wider community-building, as well as time management and other disciplines said to be individual life skills, stem from the same structural determinism: “Especially in the South — rural, urban and suburban — football has become that rare open space and institution for Black youth-centered activity. It is where young African-American men can build recognition and attain some agency in their lives.”
Passivity regarding the lethal risk of ES is a challenging extra piece of the puzzle around football, racialization and death. The University of California and other higher-education football factories, major and minor, couldn’t so easily get away with burying the complications of providing for both athletic opportunity and safety if the most conspicuous constituency didn’t largely remain silent. Many Black people in or around football who I have spoken with about this have expressed sentiments that could be summarized this way: “Why do we have to take the lead in raising sickle cell trait consciousness? That will just be one more thing used to stigmatize us and retard Black progress.”
Activists for sickle cell anemia research and treatment don’t necessarily want to hear evidence about exertional sickling and football deaths, fearing it could draw oxygen away from their fundraising efforts. This statement appears on the Sickle Cell Disease Association of America website: “Given the lack of scientific evidence that substantiates a significant correlation between sickle cell trait in athletes and training related sudden death, SCDAA does not support screening of athletes for sickle cell trait as a means to reduce heat related illness or death in athletes who are carriers.”
That disclaimer relies on a restricted definition of what constitutes a “significant correlation.” The families of Ereck Plancher and Ted Agu might consider the link not insignificant. So might the loved ones of Aaron O’Neal (University of Missouri, 2005), whose death was not nailed down as ES until long afterward. The larger public health point is that greater awareness would almost certainly establish greater correlation.
Here’s the language from the Centers for Disease Control: “Some people with SCT have been shown to be more likely than those without SCT to experience heat stroke and muscle breakdown when doing intense exercise, such as competitive sports or military training under unfavorable temperatures (very high or low) or conditions.”
The CDC recommends sickle cell trait screening for athletes, and the NCAA mandates that football programs offer optional screening. Ted Agu was among those who opted in, but it’s not known what percentage of Black student-athletes opt out. Anyway, screening itself is meaningless if, as in Agu’s case, a school knows about a player’s sickle cell trait vulnerability but does nothing about it when a life-saving intervention is needed — and then proceeds to skew and cover up the record after the worst happens.
And what ES awareness safety measures could give to young Black men, they could also take away. Football “scholarships” are not the bootstrapping grants-in-aid portrayed in sports mythology; they are semester-to-semester contracts at the almost sole discretion of the coaches. Players who are perceived as not able to cut it are dropped, just as ruthlessly as NFL players under the imperfect protections of their union. There is good reason for Black athletes to be concerned that greater caution around ES could mean a reduction of scholarship opportunities.
So it goes in the stormy cultural marriage between young Black men and organized football. Until death do they part.