Category: 8. Health

In 2015, Andre Hoelz, the Mary and Charles Ferkel Professor of Chemistry and Biochemistry and a Howard Hughes Medical Institute investigator, learned he had a rare brain tumor that was pressing on his acoustic nerve. The chemist, who normally focuses on solving the structure of protein assemblies in the lab, set out to learn everything he could about the workings of the auditory system.

Eventually he teamed up with his surgeon, Rick Friedman , who is also a research scientist and vice chair at UC San Diego specializing in disorders of the ear. The two have taken on the search for methods of protecting the inner ear against hearing loss. Now Hoelz and Friedman have received a grant to extend their experimental agenda.

The inner ear is a remarkable but somewhat fragile vehicle for carrying sound from the outer ear to the brain. It does this by means of tiny bundles of hair-like cells that respond to incoming sound waves by releasing neurotransmitters that send sonic information to the brain along the acoustic nerve. These inner ear hair cells are crucial to our hearing. Sadly, however, they cannot be regenerated. Once lost, they are gone forever, and the hearing they enabled is gone with them.

“There are some cells in our body that are so specialized that they cannot be replaced,” Hoelz explains. “The cells that make us hear, along with other sensory cells, fall into this category. We have 37 trillion cells in our body, and only 16,000 of those are involved in hearing. When these cells die, our hearing is gone. And when it comes to inner ear hair cells, it’s not a question of whether they will die, it’s a question of when.”

Inner ear hair cells (IHCs) perish for a variety of reasons, including viral infections, exposure to excessive noise, and normal aging processes. One cause of particularly devastating hearing loss is associated with cisplatin chemotherapy, a robust and taxing regimen of cancer treatment used to treat adult-onset cancers (testicular, head and neck, ovarian, cervical, endometrial, and lung, for example) and pediatric cancers (such as neuroblastoma, osteosarcoma, medulloblastoma, retinoblastoma, and Wilms tumor).

“Especially for pediatric patients, you want to kill as many cancer cells as possible. Children have another 80 years ahead of them, we hope. So, treatments for childhood cancers are aggressive,” Hoelz explains. “Unfortunately, cisplatin chemotherapy may cause severe damage to the ear hairs we need in order to hear. A full 70% of patients that are treated with cisplatin will end up with some degree of hearing loss.”

“There exist no ideal solutions to this toxicity,” Friedman adds.

Hearing loss is particularly damaging for children who are still in the early phase of developing speech and communication. About 2,000 children are exposed to cisplatin each year in the United States. The only currently available treatment approved by the Food and Drug Administration to avoid hearing loss in patients being treated with cisplatin has a serious drawback: It inactivates cisplatin, thereby weakening the effectiveness of the chemotherapy. “This drug is basically an antidote for cisplatin,” Hoelz says.

Cisplatin therapy saves lives that would otherwise be lost to cancer. If the choice comes down to losing one’s hearing or dying, there is usually little debate.

Hoelz himself confronted a similar dilemma in 2015 when he experienced severe vertigo and temporary hearing loss. Doctors discovered that a very rare brain tumor was exerting pressure on his acoustic nerve, affecting his balance and hearing. Since Hoelz’s symptoms came and went, he and his doctors chose to regularly monitor the tumor via MRI and periodically test his hearing. During this time, Hoelz began to see Dr. Friedman. “I had a very distinct feeling that eventually I would need to have surgery, and that Rick was the person to do it,” Hoelz remembers. “But Rick told me I was not the best candidate for ear preservation, so I hesitated. I thought, ‘I may not be lucky, but if not, at least I can keep my hearing for a while.’”

As Friedman monitored Hoelz’s tumor, the two men began to talk science. “It was strange,” Hoelz says. “I was debating whether or not to have the surgery, but alongside that, I was fascinated by Rick’s data on protein complexes involved in hearing and I began to think about how the work I did in my lab could shed light on these processes.”

When Hoelz’s symptoms became markedly worse, he opted to have the surgery and lost hearing in his left ear. But at the same time, he began a collaboration with Friedman that has already shown promising results.

For his part, Friedman says, “Meeting and collaborating with Andre is the best thing that has happened in my scientific career.”

Over the last five years, Hoelz, Friedman, and other scientists in the field have identified a gene that makes people more susceptible to hearing loss-whether from noise, cisplatin, or age-and started exploring ways to strengthen the inner ear hair cells to protect hearing.

Hoelz and Friedman first identified a gene, Prkag2, that encodes part of the AMPK (5′ adenosine monophosphate-activated protein kinase) complex. AMPK is an enzyme that works throughout the body, from the liver to the brain to skeletal muscle, to regulate metabolism. IHCs are highly metabolically active. The synapses that connect IHCs to the auditory nerve rely on AMPK to deliver neurotransmitters-in this case, glutamate-when they are stimulated by sound. Without these deliveries from the AMPK complex, the IHCs cannot communicate auditory information to the brain.

Hoelz and Friedman have shown that they can in fact protect IHCs, and the hearing that relies on them, if an AMPK-activating drug is properly delivered prior to cisplatin treatment. With a grant from Curebound , a philanthropic organization based in San Diego that funds cancer research, they are now learning the correct dosage and timing required to protect the hearing of cisplatin-treated cancer patients. Efficacy is being assessed in murine models. Once an optimal therapy is designed, it will be tested in guinea pigs, whose auditory system is more similar to our own, and finally in humans.

“The hope is that it will be comparatively easy to recruit people for a study of these treatments,” Hoelz says. “If you are being treated with cisplatin, you may lose your hearing anyway, so any chance to preserve at least some hearing should be attractive.”

The possibilities for this therapy do not end there. “We hope that in the long run this will be a sort of ear vitamin that could work for everyone. The treatment would make IHCs sturdier and less susceptible to all sorts of damage, not only that from cisplatin. Just as you can put a veneer on teeth to protect them from cavities, you could use this therapy to boost the longevity of IHCs, potentially allowing them to survive for people’s entire lifespans,” Hoelz says.

“While mammals cannot regenerate IHCs, some fish and birds can,” Hoelz explains. “Somehow as we evolved we lost this ability. Scientists are studying what developmental program might make it possible for humans to regenerate IHCs,” he adds. “But in the meantime, it would be wonderful if we could develop a therapy to protect them. Working with Rick has been a thrilling dive into the world of hair cell biology, opening new scientific doors and sparking a deeply personal hope that this research might one day help preserve hearing-including my own.”

Adopting a Mediterranean diet helped older adults shed weight and improve metabolic health, but new research shows it may not be enough to enhance cognitive function, highlighting the need for longer or more intensive interventions.

Study: Long-term outcomes of a Mediterranean diet with or without calorie restriction on cognition and cardiometabolic health: The building research in diet and cognition trial. Image Credit: Liubomyr Tryhubyshyn / Shutterstock

In a recent study published in the journal Preventive Medicine Reports, researchers in Chicago, USA, investigated whether adopting a Mediterranean Diet (Med Diet) lifestyle, with or without calorie-restricted weight loss, improves cognition and cardiometabolic health over a 14-month period.

Background

Could a plate of olive oil-dressed vegetables protect the aging brain as effectively as expensive drugs? Alzheimer’s dementia impacts about 6.9 million Americans older than 65 years, and pharmacologic options offer only modest relief.

Observational data link both a Med Diet pattern and intentional weight reduction to sharper cognition, yet rigorous evidence is scarce for African American adults, who shoulder disproportionate dementia and obesity burdens in the United States (US). Existing randomized trials are often short, enroll predominantly White volunteers, or fail to distinguish between dietary and weight-loss effects.

About the study

The Building Research in Diet and Cognition (BRIDGE) Randomized Controlled Trial (RCT) enrolled 185 community-dwelling adults aged 55-85 years with obesity. Eligibility included Body Mass Index (BMI) 30-50 kg/m2, low Med Diet adherence, Montreal Cognitive Assessment scores ≥19, and 91% identified as African American. Participants were randomized 2:2:1 to the Med Diet with Weight Loss (MedWL), the Med Diet alone (MedA), or the control group. Stratified blocks balanced age, cognition, and cohort; outcome assessors were blinded.

Both intervention groups attended twenty-five weekly classes for eight months, received extra-virgin olive oil and almonds, and learned to cook using the Mediterranean diet. MedWL additionally pursued 5-7% weight loss via a 25% calorie deficit and 150 minutes per week of moderate-to-vigorous physical activity coached by certified trainers.

All participants then completed a six-month low-contact maintenance phase. Cognition, attention, and information processing (AIP), executive function, and learning, memory, and recognition (LMR) were assessed with standard neuropsychological tests. Secondary outcomes encompassed diet quality, body weight, body composition assessed by Dual-energy X-ray Absorptiometry (DXA), Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), High-Sensitivity C-Reactive Protein (hs-CRP), Hemoglobin A1c (HbA1c), and six-minute walk distance. Investigators analyzed intention-to-treat change from baseline to 14 months with linear mixed-effects models that adjusted for cohort, age, and baseline cognitive performance.

It is important to note that, for the third cohort, several physical activity and functional outcome measures, including the six-minute walk test, were affected by the COVID-19 pandemic, as data collection for these outcomes had to be conducted virtually or was omitted due to restrictions.

Study results

Among 185 randomized participants, 162 (88%) contributed outcome data at 14 months. The baseline mean age was 66 years, and the mean BMI was 37.1 kg/m²; 86% of the participants were female.

During the eight-month active phase, adherence to the Med Diet rose markedly in both intervention arms, and weight loss occurred primarily in the MedWL group; these trends largely persisted through the maintenance phase.

Over the full 14 months, adherence scores increased by 3.2 points for MedWL and 3.4 points for MedA, compared to 0.2 points for controls (P < 0.05), indicating sustained dietary change.

MedWL participants recorded an average weight reduction of 3.8 kg, compared with a non-significant 1.7 kg in MedA and 0.5 kg in controls; the difference between MedWL and both comparators was statistically significant.

Visceral adipose tissue mass declined by 151 g in MedWL, representing a significant reduction compared to the control group, but not in the other groups. Additionally, BMI fell by 1.4 kg/m² in MedWL only.

Despite these favorable metabolic shifts, cognitive composites changed similarly across groups.

AIP, Executive Function, and LMR scores each improved modestly within all arms, likely reflecting practice effects; however, no between-group differences emerged from baseline to 14 months or from 8 to 14 months.

Significant between-group differences were also seen in secondary outcomes, including Med Diet adherence, weight, BMI, and visceral adipose tissue mass.

For hs-CRP, the only statistically significant between-group difference was a larger drop in the MedWL group compared to MedA. Changes in other cardiometabolic outcomes such as HOMA-IR, HbA1c, fasting lipids, blood pressure, and six-minute walk distance were modest and did not differ significantly between groups.

Sensitivity analyses excluding measures collected virtually during the Coronavirus Disease 2019 pandemic or omitting tests unavailable to the third cohort yielded similar findings, supporting the accuracy of null cognitive results.

Notably, adherence to the Med Diet waned slightly during maintenance, dropping 2.9 points in MedWL and 1.4 points in MedA; yet, it remained higher than baseline, and weight regain in MedWL was limited to approximately 0.9 kg.

Physical activity, as measured by the Godin questionnaire, increased during classes but remained essentially unchanged from baseline at the end of maintenance in MedWL (change of +0.2). The six-minute walk distance declined in some groups, although for the third cohort, this outcome was omitted due to pandemic-related restrictions.

Systolic and diastolic blood pressure remained unchanged. Insulin and triglyceride values showed wide confidence intervals and no group differences. The paper does not report on adverse events attributable to diet or exercise. These activity trends did not measurably mediate cognitive change.

Conclusions

To summarize, an eight-month Med Diet lifestyle intervention, delivered with or without calorie-restricted weight loss and followed by six months of low-contact maintenance, did not enhance cognition in older African American adults with obesity compared with a usual diet. Nevertheless, participants safely improved dietary quality, and the weight-loss arm achieved clinically meaningful reductions in body weight and visceral adiposity.

These gains underscore the practicality of culturally sensitive group programs for cardiometabolic risk management but suggest that stronger or longer exposures may be required to translate metabolic benefits into cognitive protection. Replication in larger, multi-ethnic cohorts and extended follow-up is warranted. Further research is needed to clarify long-term cognitive influence in diverse communities.

You may have heard that eating before bed is a no-no if weight loss is a goal. However, that couldn’t be further from the truth. And, there’s science to prove it.

A small snack can benefit cardiovascular and metabolic health, as well as promote muscle protein synthesis. You don’t have to avoid snacking at night. And that advice stands if you’re aiming to lose weight. It’s the quality of your snack that matters.

So when you’re looking for a late-night bite, read on. We talked to registered dietitians about what late night snack they’d choose to support weight loss.

The Best Late-Night Snack for Weight Loss

Dig into this creamy Cottage Cheese Snack Jar with Fruit when hunger strikes at night.

If you haven’t embraced the cottage cheese craze, here’s your opportunity. The best late-night snack for weight loss that dietitians swear by is the trendy staple that has social media buzzing. This recipe for a cottage cheese snack jar adds diced peaches and chopped pecans for a sweet and crunchy snack.

“Cottage cheese and fruit is an amazing and delicious late-night snack,” says Lauren Harris-Pincus, M.S., RDN, founder of Nutrition Starring You and author of The Everything Easy Pre-Diabetes Cookbook. “The slow-digesting protein, fiber from the fruit and unsaturated fats from a sprinkle of nuts is a fabulous combo to help balance blood sugar, feed your muscles while you sleep and provide an antioxidant boost,” she explains.

Here’s more about why this snack staple is such a superhero before bed.  

It Contains Sleep-Promoting Tryptophan

Just like turkey on Thanksgiving, dairy foods are a great way to up your intake of tryptophan, says registered dietitian and certified personal trainer Nicole Rodriguez, RDN. Tryptophan is a naturally occurring amino acid that plays an important role in the production of serotonin and sleep-regulating melatonin for sleep. Thanks to this and other amino acids found in dairy, foods like cottage cheese may help support sleep quality.

It’s High in Protein 

Dairy is a powerhouse when it comes to high-quality protein, meaning it contains a complete package of essential amino acids. A ½-cup serving of 1% fat cottage cheese provides 14 grams of protein for just 80 calories and 1 gram of total fat. In fact, research shows that pre-sleep protein, specifically casein, can help your body build muscle when you are engaged in a strength training program. This supports earlier research that suggested that higher-protein diets may also help with appetite and weight management. Choosing a low-fat dairy food like cottage cheese is a great way to add a solid source of protein into your nighttime routine.

It’s Packed with Vitamins and Minerals

Cottage cheese contains calcium, magnesium, zinc and B vitamins. Magnesium and zinc, in particular, play an important supporting role in helping convert tryptophan in dairy foods into melatonin (that circadian rhythm-regulating good sleep hormone).

One caveat when it comes to cottage cheese is its sodium content. Traditional cottage cheese is rather high in sodium, with a ½-cup serving clocking in at 459 milligrams, 20% of the recommended daily limit. If you are trying to reduce the sodium in your diet, choose a no-salt-added cottage cheese or compare the sodium content between brands and pick a lower-salt product.

It Has Fiber

While cottage cheese on its own lacks fiber, the addition of fruits and nuts gives it a nice fiber boost. This recipe supplies 3 grams of fiber. Plus, when some of that fiber comes from fruit, you’re in luck. “The addition of fruit can satisfy sweet cravings that you may be trying to minimize while pursuing a weight-loss goal,” says Rodriguez.

It Has Fat 

Healthy fat sources contribute to snack satiety and satisfaction, says Rodriguez. The Cottage Cheese Snack Jar with Fruit has 2 tablespoons of chopped pecans, though you can change up the nuts if you’d like. Other ideas include slivered almonds, walnut pieces or chopped pistachios.

What to Consider When Choosing a Late-Night Snack

Late-night snacks do not have to involve heading to the pantry to grab potato chips or cookies. (Classic TV munchies, of course.) Those snacks taste good, but there are better choices that align with weight loss. “While I encourage my patients to embrace an ‘all foods fit’ philosophy, nighttime presents its own challenges,” says Rodriguez. For example, eating spicy, fatty or fried foods can cause indigestion, while foods with a lot of added sugars can cause blood glucose spikes. Both of these can disrupt your sleep, and lack of sleep can affect your appetite and may make weight loss more difficult.

But there are two nutrients you should focus on when it comes to nighttime nibbles: protein and fiber, says Harris-Pincus. These provide staying power, she says. “Sticking with these options will help to keep blood sugar levels more stable and offer an opportunity to maximize your nutrient intake for the day.”

• Here are the nutrition parameters to focus on when finding a late-night snack:
• Calories: Aim for roughly 200 calories per snack, depending on your personal energy needs, to avoid feeling overly full before bed. 
• Protein: Make sure your snack choice has protein. Aiming for 7 or more grams provides a good source of protein. 
• Fiber: Fiber helps keep you fuller for longer, and can also support your weight-loss goals through offering satiety, meaning you’re less likely to mindlessly munch. Aim for a snack that provides some fiber, ideally 3 or more grams. 
• Fat: Fat is your friend; it also helps to satiate you. Choose a snack that packs a little bit of unsaturated fat to help provide that staying power until your morning meal. 

Our Expert Take

You can enjoy a late-night snack, even if weight loss is on your radar. Consider your individual calorie, protein and nutrient needs as you explore what foods will satisfy you as well. Dietitians recommend pairing low-fat cottage cheese with fruit and nuts for a late-night option that provides protein, fat and fiber, all nutrients that support weight-loss goals.

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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High blood pressure, also called hypertension, is one of the most common long-term health conditions worldwide, and it can lead to serious problems like heart disease, stroke and kidney issues. It’s a big concern not just for personal health, but also for healthcare systems everywhere due to the costs associated with treating and managing it. That’s why finding ways to prevent and manage high blood pressure is so important.

One area of research getting a lot of attention lately is diet. Some studies have indicated that eating patterns like the Mediterranean diet, the DASH diet, plant-based diets and low-salt diets, may help reduce the risk of high blood pressure and improve heart health overall. Interestingly, scientists have also discovered that the collection of tiny organisms living in your gut, known as gut microbiota, might play a key role in how diet affects blood pressure. Your gut microbiota includes bacteria, fungi and viruses that help with digestion, immune health and even inflammation. When the balance of these microbes is off—often called “gut dysbiosis”—it may increase the risk of conditions like high blood pressure. For example, studies have shown that people with hypertension tend to have less diversity in their gut microbiota and fewer helpful bacteria.

While there’s growing interest in how diet and gut health are linked to conditions like high blood pressure, there’s still more to learn, especially about how a test called DI-GM specifically relates to hypertension. DI-GM stands for Dietary Index for Gut Microbiota, and this index looks at factors like the amount of fiber, prebiotics, fermented foods and plant-based foods in your diet—all of which help grow good microorganisms and improve gut diversity. To bridge this research gap, a new study aimed to dig deeper into the connection between blood pressure and gut health using data from the National Health and Nutrition Examination Survey (NHANES), and the results were published in BMJ Nutrition, Prevention, and Health.

How Was The Study Conducted?

To evaluate the association between dietary index for gut microbiota and hypertension, researchers used data from NHANES, a large-scale survey run by the CDC to look at the health and nutrition of people living in the United States. NHANES has been collecting detailed health information every two years since 1999. For this analysis, researchers used data from six survey periods between 2007 and 2020. They focused only on participants aged 20 and older, eliminating those who didn’t have complete dietary or health data, as well as those with extremely high or low BMI or calorie intake. Pregnant participants were also excluded. After applying all these filters, a total of 20,804 participants were included in this study.

Blood pressure levels were measured regularly from 2007 to 2020 by a trained healthcare professional. High blood pressure, also known as hypertension, was defined as having an average systolic blood pressure of 130 or higher, having an average diastolic blood pressure of 80 or higher or being on blood pressure-lowering medication.

The DI-GM used in this study was created using information from NHANES. Participants shared details about what they ate over two separate 24-hour periods, spaced three to 10 days apart, to make sure the data was thorough and accurate. Researchers identified 14 key foods and nutrients that impact gut health, scoring them based on their effects on gut bacteria. If someone ate certain beneficial foods at or above the average for their gender, they earned 1 point; if they consumed too much of less gut-healthy foods, they scored 0 points. The total score ranged from 0 to 13, showing how much a person’s diet supports healthy gut bacteria. A higher score indicates more foods that positively affect gut health.

What Did The Study Find?

After adjusting for other factors, DI-GM (a dietary index score capturing certain nutritional patterns) showed a slight protective effect against hypertension, with those in the high DI-GM group having a 13% lower chance compared to the low DI-GM group. Analysis also suggested that this relationship between DI-GM and hypertension is steady and consistent.

An important detail to note is that this study did not directly measure the gut microbiome. Instead, it looked at how diet patterns, measured using the DI-GM, might reflect gut health. The authors explain that while this method isn’t as precise as directly analyzing the microbiome, it still offers useful insights into how diet may impact gut health and, in turn, blood pressure. 

Another limitation to note is that the study used data from NHANES, which only provides a snapshot in time, and it’s difficult to say for sure if one thing causes another. For now, it would be safer to say that a gut-healthy diet is associated with lower risk of high blood pressure. 

Plus, the dietary information relied on people’s self-reports, which can sometimes be inaccurate. Additionally, the DI-GM is just an indicator and doesn’t fully capture the complexity of gut microbes. While the results are relevant to U.S. adults, they might not apply to people elsewhere who have different diets or gut health profiles. Future research could build on these findings by using long-term studies and more precise methods to confirm these relationships.

How Does This Apply to Real Life?

Gut health and heart health may be more closely connected than you think. Emerging research suggests that by supporting your gut through diet, you could unlock surprising benefits, like better blood pressure. Incorporating fiber-rich foods like whole grains, fruits and vegetables into your diet not only nurtures a healthier gut microbiome but also promotes heart health. Foods like yogurt, kimchi and other fermented options add an extra boost, helping to cultivate beneficial bacteria for your gut. 

Here are a few approachable diet tips for supporting your gut and overall well-being:

• Prioritize fiber-rich foods. Add more whole grains, fruits, and vegetables to your meals to promote a diverse and healthy gut microbiome.
• Include fermented foods. Yogurt, kimchi, sauerkraut, and kefir are great for increasing probiotics in your diet.
• Explore plant-based options. Swap out some animal-based meals for plant-based alternatives rich in fiber and nutrients.

Small, consistent changes like these may make a big difference over time, helping to manage blood pressure and improve your overall health. After all, good health truly starts on your plate.

Our Expert Take

This new study published in BMJ Nutrition, Prevention, and Health highlights the intriguing connection between diet, gut health and blood pressure. Researchers found that individuals who ate more gut-friendly foods were less likely to have high blood pressure. Although the study didn’t directly measure the gut microbiome, it underscores the role nutrition plays in fostering a healthy microbiota and, by extension, supporting cardiovascular health. 

As science continues to uncover the links between what we eat, our gut microbiome and overall health, the message becomes clear: small, intentional dietary changes can lead to meaningful improvements in long-term well-being. Whether it’s adding more fiber-rich foods like fruits and vegetables, incorporating fermented options like yogurt or kimchi, or shifting toward plant-based meals, these steps are accessible and impactful.