CTE risk factors in older athletes and suicide prevention

When an older retired athlete says, “I think I have CTE,” the room usually gets quiet. A spouse may hear danger. An adult child may hear years of tackles, checks, punches, headers, or falls finally catching up. The athlete may hear something worse: that anger, memory lapses, depression, poor sleep, and impulsive decisions are proof of an untreatable brain disease.

That belief should never be brushed off. Repetitive head impacts are a real exposure risk, and chronic traumatic encephalopathy is a real disease. But “I probably have CTE” is not a diagnosis, and it should not become a reason to stop looking for depression, sleep apnea, chronic pain, medication effects, blood pressure problems, low testosterone, or other treatable conditions that can look frighteningly similar.

If there is any immediate concern about suicide, threats, a firearm in the home, sudden reckless behavior, or a person saying the family would be better off without them, treat that as urgent. In the United States, call or text 988. Former NFL players and families can also contact the NFL Life Line at 800-506-0078. Families looking for CTE-specific support can use the BU CTE Center family resources and the Concussion & CTE Foundation caregiving resources. This article is educational and is not a substitute for professional medical care, emergency evaluation, or individualized mental health treatment.

The Risk Factors Families Usually Mean When They Say CTE

Families often use “CTE” as shorthand for several different worries at once: past head impacts, current behavior changes, fear of dementia, and fear of suicide. Separating those pieces is not just cleaner medically. It gives the family something to do besides watch and wait.

The strongest warning sign in recent research is not only confirmed disease in donated brains. It is what happens to living athletes who believe the story is already over. In a 2024 JAMA Neurology study of 1,980 former NFL players, 34% believed they had CTE; those players were five times more likely to report suicidality than players who did not believe they had CTE, 25.4% compared with 5%.[1]

That association did not disappear when researchers adjusted for depression. Perceived CTE still doubled the odds of suicidality, with an odds ratio of 2.06.[1] For a family, that means the sentence “I have CTE” is not only a medical concern. It is a suicide-prevention concern.

Exposure Risk Is Real, But It Is Not the Same as a Living Diagnosis

The older athlete who played years of football, hockey, rugby, boxing, or soccer is not inventing the exposure history. In Boston University CTE Center research, CTE was found in 91.7% of 376 former NFL player brains studied after death, and each additional year of tackle football was associated with a 30% increase in CTE risk; every 2.6 years of play doubled risk.[2]

That 91.7% number deserves attention, but it also needs its guardrail. Those brains came from a self-selected donation group, not a population-representative sample of all former NFL players.[2] Families should not translate it into “nearly every former player has CTE.” They can translate it into something more careful and still serious: repeated head impacts and years of tackle football are not minor history.

There is another limit that matters in the exam room: CTE can only be definitively diagnosed after death.[2] A clinician can evaluate symptoms, history, function, mood, cognition, sleep, medications, and safety. A clinician cannot confirm CTE in a living person the way they can diagnose high blood pressure, sleep apnea, major depression, or medication toxicity.

This distinction protects both sides of the family argument. It keeps relatives from saying, “You’re fine; stop worrying.” It also keeps the athlete from saying, “There’s nothing anyone can do.”

Why Perceived CTE Can Raise Suicide Danger

The dangerous part of perceived CTE is not that an athlete notices symptoms. Noticing a change can be protective if it leads to care. The danger comes when the athlete decides the symptoms prove permanent brain deterioration and that treatment is pointless.

The Harvard Football Players Health Study reported that NFL players had a 2.6-fold higher suicide rate from 2011 through 2019 compared with MLB and NBA players, and that the rise coincided with growing media attention to CTE rather than with a biomarker change.[3] That finding is correlational, not proof that media coverage caused suicides. But it is enough to make families and clinicians careful about the message an athlete absorbs: “This explains me, and there is no way back.”

Dr. Rachel Grashow of Harvard put the treatment gap plainly: “It is frustrating that most of these symptoms and conditions are treatable, especially depression, which stands as the biggest risk factor for suicide. But so many former players think there's no point to seeking treatment.”[3]

That is the clinical opening. The family does not need to win a debate about whether CTE exists. It needs to interrupt hopelessness, reduce access to lethal means during a crisis, and get the athlete evaluated for the problems that can be treated now.

CTE-Like Symptoms Can Come From Treatable Conditions

One of the most important findings for families is easy to miss because it is less dramatic than a headline about donated brains. Boston University researchers reported in 2021 that 84.8% of former players without CTE pathology would still have met clinical criteria for traumatic encephalopathy syndrome, meaning their symptoms had other causes.[2]

That does not make the symptoms less real. It makes them more actionable. A man who cannot sleep, snaps at his spouse, forgets appointments, drinks more because his knees hurt, and says he is “turning into one of those CTE stories” may need urgent suicide screening. He may also need a sleep study, medication review, depression treatment, pain plan, blood pressure management, hormone evaluation, substance-use assessment, and cognitive testing.

The conditions worth checking are not obscure. In older retired athletes, sleep apnea can worsen memory, irritability, depression, and daytime fatigue. Low testosterone can overlap with low mood, low motivation, sexual changes, and loss of strength. Treatment-resistant depression may look like personality change when it has gone untreated for years. Chronic pain can erode sleep, patience, movement, and judgment. Hypertension-related cognitive effects can appear as forgetfulness or slowed thinking. Medication side effects can produce confusion, dizziness, emotional blunting, agitation, or falls.

None of these possibilities cancels the head-impact history. A good evaluation holds both truths at once: the exposure matters, and the symptom cause still has to be investigated.

A Practical Evaluation Path

• Start with safety: ask directly about suicidal thoughts, firearms, stockpiled medication, reckless driving, heavy drinking, threats, and recent goodbyes.
• Bring the exposure history: years played, positions, combat or collision sports, known concussions, and years of repetitive head impacts.
• List the current changes: sleep, pain, mood, anger, memory, impulse control, balance, motivation, substance use, and daily function.
• Review medications and substances: prescriptions, over-the-counter sleep aids, pain medicines, alcohol, cannabis, and supplements.
• Ask for targeted screening: depression, anxiety, sleep apnea, cognitive impairment, blood pressure, hormone issues when appropriate, pain, and fall risk.
• Do not let one normal test end the search if the household still feels unsafe or the athlete is still deteriorating.

Dr. Robert Stern of the BU CTE Center made the clinician’s job clear: “It's critical for any clinician who hears from a patient that they believe they have CTE to work hard to convince them that it's not necessarily CTE causing their symptoms, and that there is always a reason for hope.”[2]

How a Family Can Talk About CTE Without Feeding Despair

The first sentence matters. “You don’t have CTE” may sound like dismissal. “Yes, that’s probably CTE” may sound like a sentence. A safer response is closer to: “Your history makes this worth taking seriously, and we are not going to assume every symptom is untreatable. We are getting help for the dangerous parts now.”

If the athlete is ashamed, angry, or suspicious, make the appointment about function and safety rather than blame. The goal is not to prove the spouse right. The goal is to find out why sleep is broken, why pain is worse, why temper is shorter, why memory is slipping, why driving feels riskier, or why the person has stopped caring whether they live.

• Use specific observations: “You slept in the chair four nights this week,” not “You are becoming impossible.”
• Name safety directly: “When you said you do not want to be here, I got scared, and we need help today.”
• Reduce lethal access during high-risk periods: secure firearms, large medication supplies, and other immediate means.
• Bring another person to appointments when possible, because memory and pride both interfere with reporting symptoms.
• Ask clinicians to document a plan for nights, weekends, pain flares, drinking episodes, and sudden agitation.

Families also need permission to protect themselves. A spouse can love a retired athlete and still leave the room when threats start. An adult child can respect a father’s career and still take car keys seriously after impulsive driving. Safety planning is not punishment. It is the bridge that keeps treatment possible.

What the Research Does Not Yet Tell Us

The best-studied group in much of this work is former NFL players, which limits how confidently the findings can be applied to other sports or to female athletes. Hockey, rugby, boxing, soccer, and other sports involve different patterns of head impact, different cultures around reporting symptoms, and different medical follow-up. The absence of the same volume of data is not proof of safety.

Age also complicates the picture. A retired athlete in his 60s, 70s, or 80s may have head-impact exposure plus ordinary late-life risks: vascular disease, hearing loss, poor sleep, grief, isolation, pain, alcohol use, or medication burden. The family may see one changed person; the clinician has to look for several overlapping causes.

Younger athlete data still reinforces the seriousness of repetitive head impacts and suicide concern. BU researchers reported CTE pathology in 41% of athletes under 30 who died by suicide.[4] That finding does not tell a family what is happening inside one living older athlete’s brain. It does show why head-impact exposure should not be minimized.

Suicide Prevention and Fall Prevention Belong in the Same Home Plan

In an older retired athlete, the same cluster of problems that raises suicide concern can also raise fall risk. Poor sleep slows reaction time. Depression reduces movement and attention. Chronic pain changes gait. Medication side effects can cause dizziness or confusion. Cognitive decline can make stairs, bathrooms, tools, and driving less safe. Impulsivity can turn a bad moment into an injury.

So the safer plan is not only “watch his mood” or “take away the throw rugs.” It is a combined plan: urgent help for suicidal thinking, a careful search for treatable CTE-like symptoms, medication and sleep review, pain management, safer access to firearms and medications, steadier routines, and fall-risk changes at home.

The hopeful message is not that CTE is imaginary. It is that a living person is not a post-mortem diagnosis. When an older athlete believes he has CTE, the family can take that fear seriously without surrendering to it. The next step is safety, treatment, and a full evaluation of every condition that might still be helped.

References

1. Suicidality and Perceived Chronic Traumatic Encephalopathy Among Former Professional Football Players. JAMA Neurology, 2024.
2. 10 Things BU CTE Center Research Has Taught Us about CTE. Boston University, 2024.
3. Recent Trends in Deaths by Suicide Among NFL Players. Football Players Health Study at Harvard University, 2026.
4. Study Finds CTE in 40% of Athletes Who Died Before 30. Boston University CTE Center, August 28, 2023.