Yes, some studies have found higher ALS mortality among professional football players, but the evidence does not prove that playing football causes ALS. The clearest findings concern small groups of elite athletes, not every player or person who has played the sport.
This distinction matters because ALS is uncommon, and a higher relative rate can still mean a low absolute chance for an individual. The research also has limits: some studies measure deaths rather than new diagnoses, and they cannot fully separate football from other factors.
Here is what researchers have found, how head impacts might fit in, and what the evidence can and cannot tell players and families. You will also learn which symptoms warrant a medical assessment and how to interpret claims about football and ALS.
Are football players more likely to get ALS?
Some research suggests a higher rate among professional players, but it does not establish that football itself causes ALS. Findings have appeared in studies of professional American football players and soccer players. They do not mean that most players will develop the disease, or that recreational participation carries the same risk.
One often-cited study of former National Football League players found that ALS mortality was higher than expected compared with the general population. It measured deaths in a particular group, however, not the lifetime chance of ALS for every football player. Research on Italian professional soccer players has also reported an excess of ALS cases, but that work involved a limited population and does not settle the cause.
So the most accurate short answer is: there is a concerning association in some elite-athlete research, while the overall evidence remains limited and causation is unproven. The findings justify further research, not a claim that football inevitably leads to ALS.
What the football and ALS studies actually measure
Studies can measure different outcomes, and those outcomes are easy to confuse. A study that counts deaths is not the same as one that follows players to see how many develop ALS. Both can provide useful clues, but neither automatically reveals why a difference exists.
| Evidence type | What it can show | Main limitation | Best way to read it |
|---|---|---|---|
| Professional football mortality study | Whether ALS deaths occurred more often than expected in a player group | Death records, group selection, and small case counts affect estimates | A signal for investigation, not proof of cause |
| Soccer-player cohort research | Whether a defined group of players had more diagnosed cases | Results from one country or league may not apply broadly | Evidence from a specific setting, not all football |
| Studies of head impacts | Whether repeated impacts or injury history relate to neurological outcomes | Exposure is difficult to measure over a full career | A possible mechanism to examine, not a confirmed explanation for ALS |
| Population research | How ALS rates vary across larger groups | Often lacks detailed records of playing position and impact exposure | Useful context, but may not explain a football-specific link |
Relative risk and absolute risk are different. Relative risk compares one group’s rate with another’s. If a rare condition occurs more often in one group, the relative increase may sound large even though the absolute chance for any one person remains low.
ALS is uncommon in the general population. A study reporting more cases in a player group does not, by itself, provide a reliable personal prediction. The result can be affected by the number of people studied, how long they were followed, and whether diagnoses were recorded consistently.
Mortality studies have another important limitation: they count people who died from ALS during the study period. They do not necessarily tell researchers how many players developed ALS, when symptoms began, or how the disease rate compares across all former players. This is why headlines about a “higher risk” need to be checked against the study’s actual measure.
Why researchers are investigating football exposure
Football can involve repeated blows to the head and body, including impacts that do not cause a diagnosed concussion. Researchers are studying whether repeated head impacts, concussion history, or other features of a playing career could be related to later neurological disease.
One possible concern is that repeated impacts may affect the brain and nervous system over time. But a plausible pathway is not proof that the pathway causes ALS. Researchers have not established a clear chain from a particular number or type of football impact to ALS in an individual player.
Football exposure also includes more than collisions. Players may differ in training, years of participation, position, other injuries, and health history. Those factors can be hard to reconstruct decades later. If a study does not measure them well, it may not be able to tell which exposure, if any, explains the pattern.
There is also a difference between a concussion and ALS. A concussion is a traumatic brain injury, while ALS is a progressive disease affecting nerve cells that control voluntary muscles. A history of concussion alone does not mean someone has ALS, and current research does not show that every concussion leads to it.
What the research cannot prove yet
Observational studies follow people as they are, rather than assigning them to play a sport. This is necessary for studying long-term health, but it makes cause and effect harder to establish. Researchers can find that two things occur together without knowing whether one caused the other.
Several challenges shape the football evidence:
- Small numbers: ALS is rare, so even a large group of athletes may include relatively few cases. A small number can make estimates unstable.
- Selected groups: Professional athletes are not representative of every player. They may differ in training, health care, fitness, background, and career length.
- Incomplete exposure records: Older records may not capture routine impacts, practice contact, or injuries that were never diagnosed at the time.
- Different comparison groups: A study’s results can change depending on whether players are compared with the general population or a more similar group.
- Long time spans: ALS can appear years after a playing career. Long follow-up is essential, and records may become incomplete over time.
- Other possible influences: Age, inherited variants, and other exposures can affect ALS risk, making it difficult to isolate the role of football.
Researchers also need to consider surveillance. Former professional players may receive more attention from medical staff or researchers than people outside sports, which can affect how diagnoses are identified and recorded. That possibility does not invalidate a finding, but it is one factor scientists must assess.
Association is not the same as individual prediction. Even if a group-level association is real, it cannot tell a particular former player whether they will develop ALS. It also cannot show that a specific injury caused the disease.
Does the evidence apply to all kinds of football?
Not necessarily. In the United States, “football” usually means American football. In many other countries, it means soccer, also called association football. These sports have different rules and patterns of contact, and studies of one should not automatically be treated as evidence about the other.
Much of the public discussion concerns professional or elite athletes. Those players may have years of intensive training and frequent contact. There is less evidence for estimating ALS rates among people who played casually, played youth football, or participated for a short time.
That gap is important. A finding in a professional cohort cannot be used to calculate the risk for a child in a local league or an adult in a recreational club. The exposure, length of participation, and available health data differ substantially.
Researchers need larger, longer studies that track diagnosed ALS cases and carefully record playing history. Better information about position, years of play, practice exposure, concussions, and other health factors would help clarify whether any association varies by exposure. Until then, broad claims about all football players go beyond what the evidence can support.
ALS is not the same as CTE
ALS and chronic traumatic encephalopathy (CTE) are separate conditions. CTE is associated with repetitive head impacts and can only be confirmed after death through examination of brain tissue. ALS affects motor neurons, the nerve cells that control voluntary movement and breathing, and it is diagnosed through clinical assessment and testing.
Both conditions may be discussed in connection with contact sports, but that does not make them interchangeable. A person cannot infer that they have ALS from a history of head impacts, memory problems, or a CTE-related concern. Nor does a CTE diagnosis explain an ALS finding without further evidence.
This distinction helps prevent a common misunderstanding: football-related neurological research covers several different conditions, and evidence for one condition cannot simply be transferred to another. Each disease needs its own studies and diagnostic standards.
What ALS symptoms can look like
ALS affects nerve cells that control muscles used for movement, speech, swallowing, and breathing. Symptoms often begin gradually and can vary between people. A symptom alone does not diagnose ALS; many more common conditions can cause weakness, cramps, or muscle twitching.
Possible early signs include persistent muscle weakness, loss of strength in one hand or foot, increasing difficulty with tasks such as buttoning clothes or walking, slurred speech, or trouble swallowing. Some people notice muscle twitching or cramps, but these symptoms by themselves are not specific to ALS.
ALS usually causes progressive problems: changes tend to continue or spread rather than resolve. If you notice persistent or worsening weakness, arrange an assessment with a health professional. A clinician can consider other explanations and decide whether neurological testing is needed.
Seek urgent medical help for sudden severe weakness, sudden trouble speaking, or sudden breathing difficulty. Those symptoms can have causes that require immediate care and should not be assumed to be ALS.
How ALS is evaluated
There is no single screening test that confirms ALS in everyone. Diagnosis usually involves a neurological examination, a review of symptoms and their progression, and tests that help assess nerve and muscle function or rule out other conditions.
An electromyography test, often called an EMG, measures electrical activity in muscles. Nerve-conduction testing may also be used to examine how signals travel through nerves. Depending on the symptoms, clinicians may order imaging, blood tests, or other assessments to check for conditions that can resemble ALS.
Having played football is relevant medical history, but it is not a diagnosis. A clinician needs to assess symptoms and test results rather than assume that a past sport exposure explains them. If symptoms are progressing, ask for medical advice instead of trying to interpret a study or online checklist on your own.
Practical steps for current and former players
Research uncertainty does not mean players should ignore symptoms or panic about their past. A sensible response focuses on current health, accurate medical history, and reducing avoidable injury during play.
- Get persistent symptoms assessed. Record when weakness or other changes began, whether they are worsening, and which activities are affected. Share that timeline with a health professional.
- Describe your playing history clearly. Include the sport, approximate years played, position, level, and known head injuries. This information can help with an assessment, although it cannot diagnose ALS.
- Follow concussion guidance. A player with a suspected concussion should stop playing and follow appropriate medical advice before returning. Do not use the absence of a diagnosis to dismiss concerning symptoms.
- Use current safety practices. Coaches and organizations should follow applicable rules for contact, protective equipment, and injury evaluation. Equipment can reduce some injury risks, but it cannot eliminate impacts or guarantee protection from ALS.
- Be careful with alarming claims. Look for the original study and check whether it measured diagnoses, deaths, or another outcome. A headline alone rarely supplies enough detail to estimate personal risk.
A useful point many summaries miss: football history is not a substitute for a proper ALS evaluation, and a group-level study is not a personal risk calculator. If a former player has new, progressive weakness, the practical next step is a medical assessment—not a conclusion based on sport history alone.
What stronger future research needs
More informative studies would follow large groups of players over time and compare them with groups that have similar age and health profiles. They would record confirmed diagnoses, not rely only on death records, and include enough participants to study relatively uncommon outcomes.
Researchers would also need better measures of exposure. A useful record might include career length, playing position, practice and game contact, diagnosed concussions, and the timing of injuries. These details could help distinguish a general sport association from a relationship tied to a particular pattern of exposure.
Even strong observational research may not identify one simple cause. ALS can involve multiple influences, and a risk factor may affect some people more than others. The goal is to determine whether football exposure is associated with a higher rate, how consistent that association is, and whether specific factors account for it.
Until such evidence is available, avoid both extremes: it is not accurate to say football has been proven to cause ALS, and it is not accurate to dismiss every reported association. The careful position is that some elite-player studies have raised a concern that needs better research.
Some studies report higher ALS mortality or more ALS cases in groups of professional football players, but they do not prove that playing football causes the disease. The results also do not establish an individual player’s personal risk, especially for recreational or youth participation.
If you have persistent or worsening muscle weakness, arrange a medical assessment and share your full playing and injury history. For claims about whether are football players more likely to get als, check what the study measured before treating a group-level finding as a personal prediction.