Can You Get CTE From High School Football?

High school football players can develop the brain changes associated with chronic traumatic encephalopathy, though the risk appears substantially lower than for those who continue playing through college and the pros. Brain bank studies consistently find CTE in former players whose careers ended after high school, and neuroimaging research on active high school athletes has detected measurable white matter changes over the course of a single season. The picture is more complicated than a simple yes or no, because CTE risk tracks closely with total years of repetitive head impacts, and a four-year high school career involves far fewer cumulative hits than a decade-plus professional one.

What Brain Bank Studies Tell Us

Most of what we know about CTE comes from examining donated brains after death. The largest such collection, maintained by researchers at Boston University, has identified CTE in former football players at every level, including those who never played beyond high school. But the rate differs sharply by how far someone went in the sport. After researchers adjusted for the fact that families of professional players are more likely to donate brains (a well-known source of selection bias), college and professional players still had roughly two and a half times the risk of a CTE diagnosis compared with players whose careers ended after high school.¹ That gap held up even after accounting for the statistical distortions that plague brain bank research, which tend to make all levels look more similar than they really are.

A recent large cohort study of NFL players found that total lifetime duration of football play was strongly linked to more severe stages of CTE, though not necessarily to whether CTE was present at all.² In other words, more years of play pushed the disease further along, making it more likely to reach the severe stages associated with dementia and personality change. For someone who stopped after high school, the total exposure is a fraction of what a professional accumulates, which is consistent with lower severity when CTE does appear.

Years of Exposure Matter More Than Concussions

One of the more important findings in CTE research is that diagnosed concussions are not the main driver. About 16% of confirmed CTE cases in one review had no reported history of concussion at all, suggesting that the hundreds or thousands of smaller, subconcussive impacts players absorb on routine plays are enough on their own to set the disease process in motion.³ The total number of years a person spends absorbing those hits turns out to be the strongest predictor: each additional year of football corresponds to about 30% higher odds of having CTE at death, and about 14% higher odds of that CTE being severe.⁴

This dose-response relationship is central to understanding the high school question. A player who starts tackle football at age 14 and stops at 18 has four years of exposure. A player who goes on through college and then spends a decade in the NFL might have 20 or more. The math favors the high school-only player, but it does not zero out the risk. Four years is still four years of repetitive head impacts, and the biological process that leads to CTE begins with those impacts regardless of the level of competition.

How Many Hits a High School Season Involves

Researchers have used helmet-mounted accelerometers to quantify what high school players actually experience. The average player sustains over 650 impacts in a single season, with the forces involved reaching the threshold for concussion (around 100 g’s of linear acceleration) in some hits.⁵ Over a four-year career, that works out to roughly 2,600 or more impacts, with most of them well below concussion level but still forceful enough to jostle the brain inside the skull.

Not all positions are created equal. Linemen take the most hits per season, absorbing somewhere between 870 and 1,080 impacts depending on the study, largely because they collide on virtually every play.^{6 7} Running backs and linebackers fall in the middle, while quarterbacks and receivers tend to sustain fewer hits overall. However, when certain skill positions do get hit, the impacts tend to be more violent. Kickers and punt returners, for instance, experienced some of the highest peak accelerations in one longitudinal study, because their collisions happen at full speed with less bracing.⁸ Frontal, head-to-head collisions were both the most common and the most severe across positions.⁹

Impacts also increase over a player’s high school career. A study tracking players over multiple years found that the number of hits climbed between the first and third year of participation, reflecting longer playing time, higher intensity, and more contact drills as players became starters.⁸

Measurable Brain Changes in Active High School Players

You don’t need to wait for a brain bank examination decades later to see effects. Researchers have used diffusion tensor imaging, a type of brain scan that measures the structure of white matter tracts, to study high school football players during and after the season. One study compared football players to peers who did not play contact sports and found that the football athletes showed significantly greater white matter changes over the course of a season, with the extent of those changes correlating directly with cumulative exposure to head hits above 20 g’s of acceleration.¹⁰ The researchers concluded that subconcussive impacts were inducing low-level neural damage that accumulated with more exposure.

Another two-season study documented reductions in specific white matter measurements in football players that partially reversed during the off-season, suggesting a cycle of injury and incomplete recovery.¹¹ This is not the same as finding CTE, which is defined by a specific pattern of tau protein deposits and can only be definitively diagnosed after death. But it shows that the kind of structural disruption believed to set CTE in motion is occurring in teenagers playing high school ball, not just in professionals absorbing hits for decades.

Blood biomarkers offer a complementary view. A study of adolescent football players tracked neurofilament light chain (NfL), a protein released when nerve fibers are damaged. Significant elevations appeared during the season, though they were modest and did not persist long after the season ended.¹² NfL spikes are a sign of axonal injury, essentially the stretching and tearing of nerve cell extensions. Whether those transient elevations translate to permanent damage over years of play is one of the open questions in the field, though animal research has confirmed that axonal pathology is the likely source of elevated NfL after mild traumatic brain injury.¹³

Why the Adolescent Brain Might Be Especially Vulnerable

The teenage brain is still under construction. Myelination, the process of insulating nerve fibers for faster signaling, continues into the mid-twenties. So does the pruning and reorganization of synaptic connections that sharpen cognitive abilities. Some researchers have raised concern that repetitive head impacts during this developmental window could be more damaging than the same impacts to a fully mature brain.

An early and often-cited study of former NFL players found that those who started playing tackle football before age 12 performed significantly worse on tests of executive function, memory, and estimated verbal IQ than those who started at 12 or older, even after controlling for total years played.¹⁴ That result prompted widespread calls to delay the age at which children start contact football. But the broader research picture on age of first exposure has turned out to be mixed. A large narrative review of the evidence concluded that the best available data do not show an association between earlier age of first exposure and worse cognitive functioning or mental health in current high school athletes, current college athletes, or middle-aged men who played high school football.¹⁵ The association may be specific to people who ultimately accumulate very high lifetime exposure at the professional level.

This nuance matters for high school players and their families. Starting football at 14 rather than 8 likely reduces total career exposure, but the evidence that the specific age of starting makes an independent difference is still unsettled. What is more firmly established is the total number of years and total volume of impacts, which is something a high school player can influence by choosing not to play year-round or by not continuing into college ball.

The Underlying Biology

CTE is defined by the buildup of a misfolded protein called tau in specific locations in the brain. After repetitive head impacts, the mechanical forces stretch blood vessels and nerve fibers, particularly in the grooves of the brain’s surface known as sulci. This triggers biochemical cascades that lead tau to accumulate around small blood vessels in those grooves, producing what researchers describe as the hallmark lesion of CTE.¹⁶ In its earlier stages, CTE tends to show up in isolated patches. In advanced stages, the tau spreads widely and is accompanied by brain atrophy, memory loss, and personality changes.¹⁷

Genetics influence how the brain responds to all of this. The APOE ε4 gene variant, best known for its role in Alzheimer’s disease, has been associated with greater tau accumulation in the brains of former contact sport athletes. In brain bank donors older than 65, carrying the ε4 variant more than doubled the odds of higher CTE stage and was strongly linked to greater tau burden in the frontal lobe.¹⁸ PET imaging of living former athletes has echoed this, with ε4 carriers showing higher cortical tau than non-carriers.¹⁹ This means two players with identical exposure histories can have very different outcomes, and there is currently no practical way to screen for genetic susceptibility before someone starts playing.

The Diagnostic Problem

One complication in the CTE conversation is that the symptoms associated with it, including depression, impulsivity, anger problems, and memory difficulties, are not unique to the disease.²⁰ A study testing proposed diagnostic criteria for CTE on a sample of men with depression who had no significant contact sport history found that over half of them met the criteria, and if a delayed-onset requirement was loosely applied, more than 80% qualified.²¹ Depression, anxiety, and headaches can produce the same cognitive and emotional profile that gets attributed to CTE.

For former professional players specifically, researchers have found that conditions like sleep apnea, diabetes, ADHD, and low testosterone were all independently associated with the cognitive impairment and behavioral changes that clinicians look for when considering a CTE diagnosis.²² Depression and sleep apnea alone were strongly tied to whether a former player had received a pre-mortem CTE diagnosis, and both are treatable.²³

This does not mean CTE is not real or that football does not cause it. It means that if a former high school football player is experiencing mood problems or memory trouble in his 30s or 40s, the odds are high that something other than CTE is responsible, and that something may be very treatable. Jumping to a CTE explanation can actually be harmful if it leads a person to believe their condition is degenerative and untreatable when it might be depression, a sleep disorder, or another medical issue.

What Rule Changes Have Done

One of the most straightforward ways to lower CTE risk at the high school level is to reduce the number of hits players absorb in practice, where a huge portion of season-long exposure accumulates. After rule changes limited full-contact practices in high school football, researchers measured an average 42% decline in head-impact exposure across all positions, with linemen seeing a 46% drop. The forces involved in individual hits stayed about the same, but players were simply hitting each other less often.²⁴ Given that total cumulative exposure is the strongest predictor of CTE, cutting nearly half of it through a practice policy change represents a meaningful reduction in risk.

Many states have now adopted limits on contact practice time, and some youth leagues have moved to flag football through certain ages. Whether these interventions are sufficient to make high school football “safe” from a CTE perspective is an open question that will take decades of follow-up to answer. The evidence is clear that fewer hits mean less cumulative damage, but it cannot yet tell us how few hits would be needed to eliminate risk entirely, if such a threshold exists.

Declining Participation

Families appear to be making their own risk calculations. High school football participation has been declining more steeply than participation in other sports, and increased attention to head injury risk is considered a significant factor.²⁵ The trend is most pronounced in states and communities where CTE has received substantial media coverage. Whether flag football can serve as an adequate substitute from a participation and development standpoint is a live debate, with the NFL itself investing heavily in promoting flag as a pathway into the sport.

For families weighing the decision right now, the honest assessment is that four years of high school football does carry some risk of CTE-related brain changes, though it is meaningfully lower than the risk faced by college and professional players. The risk is not evenly distributed: linemen absorb more hits than receivers, starters absorb more than backups, and players who practice with high contact frequency absorb more than those under limited-contact rules. Genetic factors that nobody can currently test for in a practical clinical setting also influence individual vulnerability. The science is not yet mature enough to give any individual player a personal risk score, but the direction of the evidence is consistent, fewer cumulative hits to the head means less pathology, and stopping after high school dramatically limits lifetime exposure.