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Two new studies have provided further insights into the complex links between head injury in elite rugby and potential dementia risks.

In a study of 200 former professional rugby players (aged 30-61 years old), researchers from Imperial College London, University College London (affiliated with the Institute of Sport, Exercise and Health) and the UK Dementia Research Institute found no cases of early-onset dementia.

However, a proportion of players did have increased levels of key brain markers which are potential signs of neurodegeneration and increased risk of developing dementia in later life.

The findings come from baseline assessments taken at the start of an ongoing study. The group will now be followed up over the next four years to monitor for any changes to their brain health.

According to the researchers, their data add to the complex emerging picture of repeated head injury in professional sport and risk of dementia in later life.

They explain that while cases of dementia would not necessarily be expected in these relatively young former players, changes detected using sensitive brain scans and blood tests indicate that further investigation and long-term follow-up is warranted to monitor their brain health.

The findings are published simultaneously in two papers this week in the journal Brain.

Clinical findings

There are growing concerns that elite participants in contact sports, such as boxing, rugby and football, may be at increased risk of developing dementia in later life due to repeated head injuries sustained during their career.

We didn’t see any cases of early dementia in this group of former players, which is reassuring. However, the changes in blood biomarkers and brain imaging abnormalities show some long-term effects of repeated head impacts on the brain. Prof. David Sharp Department of Brain Sciences

Previous studies have suggested a link between exposure to repeated brain trauma and neurodegenerative disorders, including a condition called chronic traumatic encephalopathy (CTE) – a brain condition which can progress to dementia long after exposure to brain injury has stopped.

While neurological symptoms are common in former players, they can have many potential causes.

Whether these symptoms are caused by previous head impacts and represent degenerative brain disease is often unclear.

In the latest studies, researchers recruited 200 retired male and female elite rugby players (median age of 44 years old[1]) with significant previous head impact exposure, along with 33 matched healthy controls who had not played rugby and who had no prior exposure to significant head impacts.

Brain scans

All participants underwent MRI brain scans as well as detailed cognitive tests – including memory, verbal reasoning and spatial awareness – to assess for any evidence of dementia.

Participants also provided self-reported symptoms, including depression, anxiety, pain, behavioural changes, and sleep disturbance. Head impact exposure for players was estimated using measures including their career length, position played, and number of diagnosed concussions over their career.

The results showed that while former players had higher self-reported scores of most symptoms, their performance on cognitive tests did not differ significantly from controls.

In addition, brain scans showed the majority of former players did not have evidence of previous trauma or significant abnormalities and there were no diagnoses of dementia.[2] Many former players had other potential explanations for the neurological symptoms they reported, including treatable mental health issues.

Blood biomarkers

In a second analysis, researchers found higher levels of a protein called p-tau217 in the blood of some former players.

Tau normally helps to provide structural support to nerve cells in the brain, acting as a type of scaffolding. But when brain cells become damaged – such as during a head injury – these proteins can form clumps, or tangles.

Tau tangles and amyloid plaques are the hallmarks of Alzheimer’s disease and are associated with progressive nerve damage and are also seen in CTE. Increased p-tau217 is particularly associated with amyloid and tau pathology in Alzheimer’s disease.

The analysis found that levels of p-tau217 were higher overall (by 17.6%) in former players compared with controls, and levels were significantly increased in 46 (23%) of the retired players.

However, the results show that levels of p-tau217 in former players were not as high as those seen in people with diagnosed Alzheimer’s disease, so the clinical relevance of this finding is not yet known.

Brain volume

MRI scans also revealed former players had reduced brain volume in some areas, compared with the control group. These include frontal brain regions which are involved in regulating behavior and some aspects of cognition.

In former players, volume reductions were seen in the hippocampus, which is particularly important for memory function, with greater reductions in volume in players with longer careers (even accounting for age).

Professor David Sharp, Director of the UK Dementia Research Institute Centre for Care Research & Technology at Imperial College London, who co-led the work, said: “We didn’t see any cases of early dementia in this group of former players, which is reassuring. However, the changes in blood biomarkers and brain imaging abnormalities show some long-term effects of repeated head impacts on the brain.

“We would not usually expect signs of dementia in mid-life, but we need to follow-up our cohort to clarify whether our biomarker results indicate that some retired players have early neurodegeneration that might lead to later dementia.”

Dr Neil Graham, from the Department of Brain Sciences at Imperial College London, said: “Previous research in this area has explored the link between head injury and cognitive decline in older retired players. Our work with former players adds to this complex emerging picture.

“There doesn’t seem to be an increased rate of dementia in the particular cohort we studied, at this midlife stage, but some of the biological hallmarks of neurodegenerative disease are increased, which is concerning. Following up this group over time will be essential to understand the implications of these findings to long-term brain health, and to better understand how head injury interacts with genetics and other environmental factors.”

Dr Thomas Parker, NIHR Clinical Lecturer, from the Department of Brain Sciences at Imperial College London, said: “This study highlights the significant brain health concerns of individuals who have played rugby at the elite level. These findings support the introduction of larger scale brain health screening programmes for former athletes exposed to head impacts. This will help us to better understand the long-term outcomes and provide the appropriate care to these individuals.”

Dr Richard Sylvester, co-lead of the study, from the Institute of Sport Exercise and Health at University College London, said: “These findings suggest that neurological symptoms in former rugby players in mid-life may not all be due to head injuries sustained participating in sport and even cognitive and behavioural changes in this group are not commonly a sign of dementia.

“We would encourage any former players with concerns about their brain health to seek expert clinical assessment as there may be treatable issues that could significantly improve their quality of life and help to reduce the risk of developing dementia in later life.”

The work was funded by the Rugby Football Union (RFU), and Premiership Rugby – neither of whom had input into the analysis of the study – in addition to the UK Dementia Research Institute, Academy of Medical Sciences and the National Institute for Health and Care Research (NIHR).

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‘Brain Health Concerns in Former Rugby Players: Clinical and Cognitive Phenotypes’ by Parker, T., Hain, J., Rooney, E., et al. is published in Brain. DOI: 10.1093/brain/awae416

‘Biomarker evidence of neurodegeneration in midlife former rugby players’ by Graham, N., Zimmerman, K., Hain, J., et al. is published in Brain. DOI: 10.1093/brain/awaf152

[1] The group of 200 former elite players had a median age of 44 years – 90.5% were male, the median career length was 10.5 years, and they had a median of seven self-reported concussions over their career. Of the group, 63% played as forwards during their career and 37% were backs.

[2] The team used a clinical checklist to establish that more than one in ten former players (12%) fulfilled the criteria for traumatic encephalopathy syndrome (TES), which is a research tool that has been developed using data from former NFL players and to assess the likelihood that an individual has the brain pathology associated with chronic traumatic encephalopathy (CTE). The researchers highlight though that there are several limitations with this newly developed measure.

Fish oil capsules have long been sold for heart and joint health, yet new evidence suggests they may also steady tempers and aggression.

A sweeping meta‑analysis from the University of Pennsylvania reports that a daily dose of omega‑3 fatty acids can shrink aggressive behavior by up to 28 percent. Adrian Raine, a neurocriminologist at the university, led the study.

Mood, memory, and fish oil

Brains run on fat, and two key omega‑3 molecules, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), slip into cell membranes, helping neurons fire smoothly.

Low tissue levels of these fats have been tied to mood swings and impulsive violence, while diets rich in cold‑water fish tend to show the opposite pattern.

Because the body converts plant‑based alpha‑linolenic acid to EPA and DHA inefficiently, researchers have wondered whether supplements could fill the gap.

Small trials dating back to the 1990s hinted at behavioral benefits, but sample sizes were too thin to guide policy.

Aggression and fish oil

Raine’s team pored over 28 randomized controlled trials that enrolled 3,918 participates, from children to older adults.

Across genders, diagnoses, dosages, and study lengths, the capsules produced a modest but reliable drop in both reactive and premeditated aggression.

“I think the time has come to implement omega‑3 supplementation to reduce aggression,” said Raine.

The average effect size, about 0.22 on the standardized “g” scale, may sound small, yet public‑health experts note that even tiny behavioral shifts can matter when applied to millions. 

The chemistry of calm

EPA and DHA dampen production of pro‑inflammatory molecules that sensitize the brain’s stress circuits. They also nudge serotonin and dopamine signaling toward a calmer set point, offering a biochemical explanation for the behavioral change.

Notably, the analysis found benefits at doses as low as 250 milligrams of combined EPA and DHA, an amount found in a single soft gel.

Higher intakes did not guarantee bigger gains, hinting that individual genetics and baseline diet modulate the response.

The omega imbalance

Most Americans don’t get enough long-chain omega‑3s from food alone. The average U.S. diet is heavy on omega‑6 fatty acids – often in a 10:1 ratio to omega‑3 – which may fuel inflammation and irritability.

Experts recommend at least two servings of fatty fish a week, such as salmon or sardines.

For those who don’t eat seafood, even a basic supplement may close the gap and improve both physical and mental health.

Supplements that calm behavior

One six‑month trial in 8‑ to 16‑year‑olds reported a 59 percent drop in disruptive conduct that lasted half a year after the study ended.

Similar shifts have shown up in adult parolees and nursing‑home residents, suggesting age is no barrier.

Public‑school cafeterias could offer fish twice a week, while correctional facilities might issue capsules at intake. Raine notes that such steps are “low cost, low risk,” especially compared with medications or restraint.

Beyond behavior, omega‑3s continue to earn cardiovascular praise. In the REDUCE‑IT trial, 4 grams of purified EPA cut fatal heart attacks by 25 percent among statin users.

A calmer mind and a stronger heart in the same pill has obvious appeal for clinicians.

Fewer risks, broad access

Compared to prescription medications for aggression, fish oil has fewer side effects and is easier to access. It doesn’t require a prescription, and many brands are available over the counter at grocery stores or online.

That said, fish oil should not replace professional treatment when serious behavioral issues are involved. It can be a helpful addition, but therapy, structured support, and in some cases medication are still essential tools.

Room to refine dosing

Omega‑3 is “not a magic bullet,” Raine warned, stressing that therapy, education, and social support still matter. Most studies followed volunteers for four months; researchers need longer follow‑ups to see whether tempers stay cool.

Scientists also hope to learn why some volunteers improve more than others.

Genetics that alter fatty‑acid metabolism, baseline inflammation, and even gut microbiota may shape response. Tailored dosing could push the average benefit beyond today’s modest figures.

For now, experts say parents of an irritable child, or adults who catch themselves snapping, might consider swapping a sugary snack for salmon, or adding a budget fish‑oil capsule to breakfast. The risk is tiny, the price is low, and the evidence is getting harder to ignore.

Who needs fish oil most?

Not everyone responds the same to omega‑3 fatty acids. Genetic differences, particularly in the FADS gene, can affect how well the body makes EPA and DHA from plant-based sources.

People of Amerindian or African ancestry may have variations that change their conversion efficiency.

For some, this means supplements could be especially important to meet their brain’s needs and reduce inflammation-driven behaviors.

The study is published in Aggression and Violent Behavior.

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