• A new study conducted by researchers in the United Kingdom examined the potential health risks that men versus women may face with type 2 diabetes.
• The researchers were interested in the differences between men and women in comorbid conditions.
• They learned that women with type 2 diabetes developed mental health conditions more often than men.
• Additionally, they found that men experienced higher rates of cardiovascular disease and other issues.

Receiving a diagnosis of type 2 diabetes may involve more than requiring close management of blood sugar levels. People with the disease often face an increased risk of comorbidities, such as heart disease, kidney disease, or anxiety.

However, these conditions may not develop in the same way for everyone. In a new study, researchers examined whether men and women experienced different health patterns following a type 2 diabetes diagnosis and how those patterns varied by age.

The study authors believe the findings could help healthcare providers provide more individualized care.

The study is published in PLOS Medicine.

How does type 2 diabetes affect other aspects of health?

The Centers for Disease Control and Prevention (CDC) estimate that around 40.1 million people in the United States have diabetes, and type 2 diabetes accounts for the vast majority of adult cases.

People can manage type 2 diabetes by making lifestyle changes and taking medications, such as metformin. If it is left unmanaged, diabetes can contribute to serious health issues, such as heart or kidney disease.

For the new study, the researchers used health information from the United Kingdom Clinical Practice Research Datalink (CPRD).

Their analysis included 28,720 people who received a diagnosis of type 2 diabetes between 2010 and 2020. Men made up 62% of the cohort and had a median age of 54 at diabetes onset, while women had a median age of 56.

The researchers excluded anyone who had already received a diagnosis for one of the study’s specified outcomes before developing type 2 diabetes:

• hypertension
• anxiety and depression
• somatoform disorders
• cardiovascular disease
• end-stage renal (kidney) disease.

The team followed participants for a median of 6.8 years. They grouped participants according to whether they developed diabetes at ages 16 to 39, 40 to 59, or 60 and older.

The researchers also tracked the order and timing of comorbid conditions the participants developed after their type 2 diabetes diagnosis.

Mental health conditions more common among women

For the analysis, the team grouped anxiety, depression, and somatoform disorders into one mental health category. They combined cardiovascular conditions and end-stage renal disease into another category and kept hypertension as a separate category.

During follow-up, 39% of participants had at least one of the events included in the analysis.

The most common comorbid condition the participants developed was hypertension, regardless of age and sex group. It affected 20.2% of women and 21.1% of men.

The other categories painted a different picture, however.

About 8.1% of women developed a mental health condition after diabetes, compared with 5.3% of men. Women ages 16 to 39 had the highest probability of developing anxiety, depression, or a somatoform disorder.

Men were more likely to develop cardiovascular or end-stage renal disease, with 8.4% receiving either diagnosis compared with 5.3% of women.

Study author Fabiola Eto, PhD, a postdoctoral research associate at Queen Mary University of London, spoke with Medical News Today about the study findings, and explained that the records showed when clinicians first documented a condition, not necessarily when it began.

Eto pointed out that women averaged 92 primary care consultations compared with 32 among men, so the findings could be possibly explained by women having more opportunities for these conditions to be identified.

“Some conditions may simply be recorded sooner in women rather than occurring at genuinely different rates,” she explained.

The researchers also linked mental health trajectories with the earliest mortality.

Eto emphasized that the study did not establish why these participants died earlier. However, she said the association makes the combination of diabetes and mental health conditions “a red flag worth investigating further, rather than a proven mechanism.”

‘We don’t yet know what is driving these differences’

Cheng-Han Chen, MD, a board-certified interventional cardiologist at MemorialCare Saddleback Medical Center in California, told MNT that the findings could eventually support more individualized diabetes care if future studies confirm them.

Chen, who was not involved in the study, told us:

“We don’t yet know what is driving these differences. Some of the findings may reflect differences in how commonly certain conditions are diagnosed in men and women, rather than a direct effect of diabetes.”

He cautioned against changing guidelines based on one observational study. However, he emphasized that comprehensive preventive care remains “essential.”

“People with diabetes should routinely have their blood pressure, kidney function, cardiovascular risk, and mental health assessed as appropriate,” he recommended.

Jay Luthar, MD, founder and medical director of Lutanen Health and an instructor at Harvard Medical School, told MNT the findings reflect patterns that healthcare providers already observe.

“Type 2 diabetes doesn’t follow the same trajectory in women as in men,” Luthar, who likewise was not involved in the study, said.

He pointed to hormonal differences, men’s lower engagement with preventive care, and women’s greater healthcare use as possible explanations. He also advocated incorporating mental health screening into diabetes care without limiting it by sex.

“The most practical near-term change is routine psychological screening as a standard part of diabetes follow-up visits, for all patients, not just women,” Luthar advised.

• On August 24, 2026, the U.S. FDA cleared a new single-biomarker blood test to help doctors detect signs of Alzheimer’s disease.
• The test helps doctors determine both rule-in (positive result) and rule-out (negative result) assessment of amyloid pathology, a hallmark of Alzheimer’s disease. 
• The blood test is specifically for older adults 55 and older with signs or symptoms of cognitive decline.

On August 24, 2026, the U.S. Food & Drug Administration (FDA) cleared the use of a new single-biomarker blood test to help doctors look for signs of Alzheimer’s disease in older adults 55 and older with signs or symptoms of cognitive decline. 

Called the Elecsys® Phospho-Tau (217P) Plasma (pTau217) blood test, the test was developed in collaboration by pharmaceutical companies Roche and Eli Lilly and Company. 

Medical News Today spoke with four Alzheimer’s disease experts to find out more about the Elecsys pTau217 blood test — how it works, how it’s different from the tests already used today for diagnosing Alzheimer’s disease, how people will be able to take the test, and how they predict this new test will change the Alzheimer’s disease diagnostic landscape. 

What is the Elecsys pTau217 test, and how does it work? 

According to Peter Gliebus, MD, chief of neurology and director of cognitive and behavioral neurology at Marcus Neuroscience Institute, a part of Baptist Health South Florida, the Elecsys pTau217 blood test works by detecting phosphorylated tau 217 in blood, one of the earliest and most specific blood indicators of Alzheimer’s. 

“It rises early in the disease and remains mostly normal in other neurodegenerative conditions,” Gliebus explained. “Although it is a tau marker, blood pTau217 closely correlates with brain amyloid.”

Laura Nisenbaum, PhD, interim chief science officer of the Alzheimer’s Drug Discovery Foundation (ADDF), said the Elecsys test measures pTau217 concentration in plasma and uses validated cutoffs to categorize results as positive, intermediate, or negative. 

“One of its distinguishing features is that it applies the same cutoffs across both primary and specialty care settings, which matters enormously for consistent, scalable implementation,” Nisenbaum told MNT.

How is this blood test different from those already available? 

The Elecsys pTau217 blood test is not the first Alzheimer’s test to be approved by the FDA. 

“The FDA cleared the Lumipulse G pTau217/β-amyloid 1-42 Plasma Ratio [test] in May 2025,” Dung Trinh, MD, an internist for MemorialCare Medical Group and chief medical officer of Healthy Brain Clinic in Irvine, CA, told MNT. “That test measures two biomarkers and calculates a ratio. Roche also received FDA clearance in 2025 for its Elecsys pTau181 test, which is primarily intended to help rule out Alzheimer’s-related amyloid pathology in primary care.”

Trinh explained that what distinguishes the new Elecsys pTau217 test is that it is a single-biomarker assay that Roche says supports both rule-in (positive result) and rule-out (negative result) assessment of amyloid pathology, using the same validated cutoffs in primary and specialty care. 

“That simplicity could be operationally important because one assay can potentially be used throughout the patient journey rather than requiring different testing strategies in different settings,” he continued. 

MNT also spoke with Megan Glenn, PsyD, clinical neuropsychologist at the Center for Memory and Healthy Aging at the Hackensack Meridian Neuroscience Institute at Jersey Shore University Medical Center in New Jersey, who said that while we have seen several other blood markers explored over the last few years, many of them capture general brain inflammation or are easily affected by other neurological conditions. 

“What makes this specific tau marker stand out is its strong connection to the exact amyloid plaques that are characteristic of Alzheimer’s disease,” Glenn explained.

“When compared directly to other options, this marker has consistently proven to be the most accurate at identifying these biological changes. It gives us a much clearer picture of what is happening biologically than previous blood tests could offer. This level of reliability is exactly what we need to confidently use blood testing in a clinical setting.”
— Megan Glenn, PsyD

Who will have access to this blood test and where can it be taken? 

The Elecsys pTau217 is a standard blood draw, the same kind patients already get for routine cholesterol or blood sugar testing, Nisenbaum explained.

“Because it is designed to run on Roche’s existing labs, it should be accessible through many of the same laboratories that handle routine blood work,” she said. “In practice, a patient experiencing cognitive symptoms would discuss testing options with their physician, who would order it as part of a broader evaluation.”

“The result, categorized as positive, intermediate, or negative for amyloid pathology, would then be interpreted alongside other clinical information to guide next steps. It is not a test patients can order themselves, and a positive result should always prompt further conversation with a clinician about what it means and what comes next.”
— Laura Nisenbaum, PhD

Trinh added that the FDA-cleared intended population is important to note for this test. 

“This is for individuals aged 55 and older who are presenting with signs, symptoms, or complaints of cognitive decline,” he said. “It is not currently cleared as a general screening test for healthy, asymptomatic adults.”

How will this test change the Alzheimer’s diagnostic landscape?

Glenn said that the FDA clearance of this new blood test is a massive step forward in making cognitive evaluations more accessible for everyone. 

“By using standard laboratory equipment, it brings advanced testing capabilities to a much wider group of patients who might never have had access to specialized brain scans,” she explained. “The most important thing to remember is that this test supports a careful clinical evaluation and does not replace a comprehensive assessment by a qualified professional.”

“This marks a significant inflection point, not just small news: it is the first FDA-cleared blood test that can both confirm and exclude Alzheimer’s amyloid pathology from a single blood sample, available on lab instruments already in thousands of hospitals,” Gliebus said.

“This is important because approximately 75% of dementia cases remain undiagnosed, mainly due to confirmatory tests like PET scans and spinal taps being expensive, invasive, and limited to specialized centers,” he added. 

“Just over a year ago, there were no FDA-cleared blood tests for Alzheimer’s — now there are four,” Nisenbaum commented. “That is a remarkable shift in a very short period.”

“The broader implication is that blood-based diagnostics are no longer a future promise. They are becoming part of routine clinical practice, and that changes how we think about everything downstream, from trial design to drug development to how patients and families get answers. The diagnostic landscape five years from now will look very different from the one we had just a year ago.”
— Laura Nisenbaum, PhD

What the Elecsys pTau217 test cannot tell us yet

Before incorporating the Elecsys pTau217 blood test into routine care, Trinh said there are several things he would want to very clearly understand. For example, he would want to see the complete FDA labeling and real-world performance data, not only overall accuracy, but the positive and negative predictive values in the types of patients he actually sees. 

“Predictive value can change substantially depending on the prevalence of disease in the population being tested,” he explained. “Second, I would want to know more about the intermediate result group. A test can perform very well overall, but from a clinician’s perspective, the critical operational question is: How many patients fall into the gray zone, and exactly what should we do with them?”

Trinh said he would also want clinicians and readers to understand exactly what the test cannot tell us. 

“Roche specifically states that it is not a stand-alone diagnostic test, and its safety and effectiveness have not been established for predicting who will later develop dementia or for monitoring treatment response,” he explained.

“A biomarker can tell us something very important about Alzheimer’s-related pathology, but caring for the patient still requires determining whether that pathology explains the symptoms, what stage of disease the person is in, what other conditions may be contributing, and what treatment or care plan is appropriate.”
— Dung Trinh, MD

• A new study comparing ketogenic, Mediterranean, and low-fat, plant-forward dietary plans found that they all help with weight loss, with improvements in body fat and insulin sensitivity.
• However, the keto diet produced the largest reduction in liver fat and was also associated with greater improvements in prediabetes.
• Although the study was small and short-term, the findings suggest that diet composition may matter beyond weight loss, and the keto diet showed the greatest changes in hormone and insulin levels linked to liver fat metabolism.

Dietary changes are often an initial approach to support healthy weight loss, as modifying food choices and overall calorie intake can help create a sustainable energy deficit.

In particular, eating plans that emphasize nutrient-dense foods and appropriate portion sizes can support gradual and sustainable weight reduction.

Approaches such as the ketogenic (keto) diet may promote weight loss by substantially reducing carbohydrate intake and increasing fat intake, which can lead to reduced appetite and lower overall calorie consumption for some individuals.

These changes may also influence metabolic health in ways that extend beyond weight loss, such as lowering blood glucose (sugar) and insulin levels, and improving insulin sensitivity.

Now, a new study suggests that the keto diet may also provide greater improvements in liver fat and blood sugar regulation than other popular dietary plans for weight loss.

The study, published in Cell Metabolism, found that people with obesity, prediabetes, and fatty liver disease who followed a keto diet experienced greater improvements in several measures of metabolic health than participants following either a Mediterranean diet or a low-fat, plant-forward diet.

The findings suggest that the composition of a diet may influence metabolic health beyond the effects of weight loss alone.

However, the study was small, involving just 42 participants, and the findings do not necessarily mean that a ketogenic diet is the best choice for everyone.

All 3 diets promoted weight loss

Estimates suggest that obesity affects roughly 40% of adults in the United States, and is associated with an increased risk of conditions, such as type 2 diabetes and fatty liver disease.

Dietary interventions are commonly recommended to help people lose weight. However, it has remained unclear whether one approach provides additional metabolic benefits beyond those associated with losing weight.

In this small study, researchers from Washington University School of Medicine enrolled 42 people with obesity, prediabetes, and fatty liver disease.

Participants were randomly assigned to follow one of three dietary plans:

1. a ketogenic diet, providing 4% of calories from carbohydrates and 73% from fat
2. a Mediterranean diet, providing 50% of calories from carbohydrates and 35% from fat
3. a low-fat, plant-forward diet, providing 70% of calories from carbohydrates and 15% from fat

The research team provided all participants with food and met with them weekly, alongside a dietitian, to support adherence.

Researchers adjusted calorie intake so that participants in all three groups lost approximately 10% of their body weight, which took approximately 4 to 5 months.

“In people with obesity, prediabetes, and excess liver fat, moderate weight loss — 10%, or about 25 pounds on average — improved metabolic function whether it was achieved with a ketogenic, Mediterranean, or very-low-fat plant-forward diet,” lead author Max Petersen, MD, PhD, told Medical News Today.

“Many benefits, including improved muscle insulin sensitivity, were similar across diets. However, the ketogenic diet produced several additional metabolic benefits beyond those seen with weight loss alone, including greater reduction in liver fat content and improvement in liver insulin sensitivity.”

– Max Petersen, MD, PhD

Ketogenic diet produced the largest reduction in liver fat

All three diets were associated with reductions in body fat and improved insulin sensitivity, resulting in better blood sugar regulation. However, the ketogenic diet produced the largest reduction in liver fat.

Those following the ketogenic diet experienced an average 67% reduction in liver fat, compared with 45% reductions in both the Mediterranean and low-fat, plant-forward groups.

The ketogenic group also experienced the greatest increase in glucagon, a hormone that helps regulate blood sugar and promotes fat breakdown in the liver. They also had the largest reduction in circulating insulin levels.

“Blood insulin levels increase after a meal primarily in response to carbohydrate,” Petersen explained. “The ketogenic diet meals contained very little carbohydrate, so we were not surprised to see that insulin levels throughout the day were lower.”

“There are probably two main reasons glucagon levels were higher in the ketogenic diet group: higher dietary protein content (amino acids stimulate glucagon release) and lower insulin levels (insulin suppresses glucagon release),” he added.

The researchers suggest that these changes could explain why the ketogenic diet produced greater improvements in liver fat.

“The ketogenic diet had a much greater effect on several metabolic factors that regulate liver fat than did the other two diets,” Petersen highlighted.

“The ketogenic diet caused a greater increase in blood glucagon concentration, which is a hormone that stimulates liver fat breakdown, and a greater decrease in blood glucose and insulin concentrations which stimulate liver fat production. So together these factors caused a greater reduction in the rate of production of liver fat from blood glucose.”   

– Max Petersen, MD, PhD

Keto was also beneficial for prediabetes

The differences were also apparent when researchers looked at participants’ prediabetes status following the intervention.

Around half of those in the ketogenic group no longer met the criteria for prediabetes after the weight-loss period, compared with 29% in the Mediterranean group and 7% in the low-fat, plant-forward group.

The researchers also reported that participants on the ketogenic diet did not experience an increase in blood fat or cholesterol levels despite consuming considerably more dietary fat than those in the other groups.

“Because the ketogenic meals contained very little carbohydrate, the increase in blood glucose after meals was much lower in the ketogenic diet group than the other diet groups,” Petersen noted.

“So it was not surprising that hemoglobin A1c, a test of average blood glucose, and fasting blood glucose improved most in the ketogenic diet group,” he told us.

What do the findings mean?

The study findings suggest that dietary plans that reduce carbohydrate intake could have metabolic effects beyond those explained by weight loss alone, particularly in people with high liver fat and prediabetes.

Notably, these findings come at a time when medications that target GLP-1 pathways, such as Wegovy, Zepbound, and Foundayo, have substantially changed the treatment of obesity.

However, while these medications can produce significant weight loss, the study findings suggest that the composition of a person’s diet may also provide additional metabolic benefits.

“The results from our study demonstrate that moderate weight loss induced by a ketogenic diet has greater therapeutic benefits, particularly on liver health, than matched weight loss induced by consuming a Mediterranean or very-low-fat plant-forward diet,” said Petersen.

“However, it is important to note that we provided all meals to our study participants to enhance compliance. Achieving compliance with any dietary guidance is difficult in a real world setting and remains the Achilles heal of diet therapy,” he concluded.

Still, the results need to be interpreted cautiously. The small trial included only 42 people and lasted around 4 to 5 months, so it cannot establish whether the observed benefits would persist over the long term.

Additionally, people may find a ketogenic diet difficult to maintain, as its high fat content, which can include large amount of saturated fat from animal products, may not be appropriate for everyone.

While promising, larger and longer-term clinical trials are necessary to determine whether these metabolic advantages can persist over time and whether they translate into fewer cases of health conditions, such as type 2 diabetes.

For now, the study adds to evidence that weight loss alone may not be the sole determinant of how diet affects metabolic health, suggesting that the balance of carbohydrates, fats, and other nutrients may also play an important role.

• Some recent evidence suggests that GLP-1 receptor agonists, used in the treatment of type 2 diabetes, may also help manage polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS).
• A small study has found that GLP-1s can lead to weight loss in people with obesity and PMOS and that, as a consequence, aspects of reproductive system health also improved.
• The evidence, however, remains mixed.
• A gynecologic oncologist and a family doctor specializing in weight management explain how and why GLP-1s might help with PMOS, and who might reap the most benefits.

GLP-1 receptor agonists, known as GLP-1s, for short, are a class of drugs used in the treatment of type 2 diabetes and, in some cases, obesity.

Examples of commonly used GLP-1 drugs include Ozempic and Wegovy, which contain the active ingredient semaglutide, and Mounjaro and Zepbound, which contain tirzepatide.

All of these can be used in the treatment type 2 diabetes, but only Wegovy and Zepbound have received Food and Drug Administration (FDA) approval in the management of obesity, while Ozempic and Mounjaro are more often used specifically in the management of diabetes.

These diabetes medications can help with weight management because obesity and diabetes are often interlinked, as many people with obesity also develop type 2 diabetes.

What is perhaps more surprising is that some recent studies have suggested that GLP-1s could also help with some medical conditions affecting the female reproductive system, particularly polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS).

PMOS is characterized by irregular periods, hormonal imbalances that can present in many different ways, including through unusual hair growth, the development of fluid-filled cysts on the ovaries, and it can co-occur with other metabolic conditions, including obesity.

What is the evidence that GLP-1s can help with PMOS?

One small study published in the Journal of Clinical Medicine in July 2026 found that taking GLP-1s might help not just with weight management, but also with restoring ovulatory cycles in people with PMOS.

This study followed 96 individuals with PMOS, who had a body mass index (BMI) greater than 25 kilograms per square meter (kg/m²), falling in the BMI range of overweight or obesity.

The participants received an individualized semaglutide treatment over a period of 6 months, with the treatment dose increased as necessary.

At the end of this intervention, 95% of participants with PMOS and overweight or mild obesity were able to regulate their menstrual cycles. However, only 25% of participants with moderate or severe obesity achieved the same positive effects.

A systematic review and meta-analysis published in the European Journal of Endocrinology in February 2026 stressed that the evidence suggesting that GLP-1s can aid in the treatment of PMOS remains mixed and uncertain.

The meta-analysis looked at 17 articles that were relevant to the discussion, assessing data from 11 randomized controlled trials between them.

“This rigorous systematic review and meta-analysis show that overweight or obese individuals with PCOS, similar to those with obesity or overweight without this diagnosis, are likely to lose weight following a relatively short course of treatment,” the review authors wrote.

“However, the impact of GLP-1-RAs on other metabolic outcomes in women with PCOS [PMOS] remains uncertain,” they cautioned.

To shed more light on whether GLP-1s are actually a helpful course of treatment in PMOS, and who might benefit the most from this potential addition, Medical News Today spoke with Clare Thompson, MBBS, a general practitioner at the Cadogan Clinic in London, United Kingdom, who leads their Weight Management Service.

MNT also spoke with Steven Vasilev, MD, a gynecologic oncologist specializing in endometriosis and founder of the Lotus Endometriosis Institute in Santa Monica, CA.

• In 2021, there were about 57 million people globally living with dementia.
• Early symptoms of dementia can include signs of mild cognitive impairment (MCI) and sleep issues. 
• Previous research shows certain nutrients may help slow dementia progression, such as vitamin D.
• A new study suggests that consuming a higher amount of vitamin D may improve cognitive function in older adults who have both MCI and problems sleeping. 

According to the World Health Organization (WHO), in 2021 there were about 57 million people globally living with dementia, an umbrella term for diseases that impact a person’s ability to think and remember, such as Alzheimer’s disease.

Early symptoms of dementia can include signs of mild cognitive impairment (MCI) like memory loss, inability to problem solve, or difficulties speaking or remembering words, as well as sleep issues. 

Previous research shows that diet can play an important role in the slowing of progression of dementia. Some foods, such as those that are high in nutrients like omega-3 fatty acids, B vitamins, antioxidants, and vitamin D, may be especially relevant to this equation. 

Now, a new study published in the journal Sleep Medicine says that consuming a higher amount of vitamin D is linked to improved cognitive function in older adults who have both MCI and problems sleeping. 

What’s the link between MCI, sleep issues, and vitamin D?

For this study, researchers recruited 54 adults with an average age of about 67 who had diagnosed or suspected MCI and sleeping problems. 

Study participants’ cognition was assessed through the Montreal Cognitive Assessment (MoCA), and their sleep quality was assessed via the Pittsburgh Sleep Quality Index (PSQI) or the Epworth Sleepiness Scale (ESS).

Study participants also self-reported their daily vitamin D consumption and dosage. 

“Vitamin D is especially interesting because it’s part of everyday life, yet we’re still learning about the role it may play in cognitive health,” Victoria Pak, PhD, MS, MTR, associate professor at Emory University in Atlanta and senior author of the study, told Medical News Today.

“We focused on people with sleep disturbances and mild cognitive impairment because sleep and cognition are closely connected, and we wanted to understand whether vitamin D supplement intake was associated with differences in cognitive function in this group,” added Pak.

Taking vitamin D increased cognitive score by 13%

At the study’s conclusion, researchers discovered that study participants who reported taking 5,000 international units (IU) or more of vitamin D each day scored more than 13% higher on the MoCA, when compared to those who didn’t take a vitamin D supplement. 

“Scores differed by approximately four points on the MoCA,” Pak said. “This was an observational study, so we need to be cautious about how we interpret the finding. What makes the result important to investigate further is that we observed this relationship in people with mild cognitive impairment and sleep disturbances.”

“The amount of vitamin D someone needs can vary, so anyone concerned about their levels should talk with their healthcare provider about whether testing is appropriate,” she added. 

For the next steps in this research, Pak said they plan to test these findings in a clinical trial to determine whether vitamin D supplementation can influence cognition.

“If the trial shows that vitamin D contributes to the differences in cognitive function we observed, that could open up new possibilities for supporting cognitive health,” she said. 

Highlighting a noninvasive intervention for an at-risk group

MNT had the opportunity to speak with Manisha Santosh Parulekar, MD, FACP, AGSF, CMD, chief of the Division of Geriatrics and co-director of the Center for Memory Loss and Brain Health at Hackensack University Medical Center.

Parulekar, who was not involved in this study, commented that her first reaction to this its findings was one of optimism. 

“The findings highlight an accessible, noninvasive intervention for an at-risk group,” she explained. “It reinforces the hypothesis that dietary modifications impact cognitive decline.” 

MNT also spoke with Dung Trinh, MD, an internist for MemorialCare Medical Group and chief medical officer of Healthy Brain Clinic in Irvine, CA, who likewise was not involved in this study. 

Trinh said that he found this to be an intriguing and clinically relevant finding, particularly because sleep disturbance is so common in patients with mild cognitive impairment and may contribute to worsening cognitive health over time. 

“The study found that participants taking 5,000 IU or more of vitamin D daily had better cognitive scores, but I would emphasize that this was a small, cross-sectional study involving only 54 participants, so it shows an association rather than proving that high-dose vitamin D improves cognition,” he continued.

“Still, the magnitude of the observed difference is enough to justify larger and more rigorous studies,” he emphasized.

What are the cognitive function benefits of vitamin D? 

When asked how vitamin D might help improve cognitive function in people with sleep disturbances and MCI, Trinh said one possible explanation is vitamin D’s role in regulating inflammation and immune function. 

“Poor sleep has been associated with increased inflammatory activity, and neuroinflammation may contribute to cognitive decline and neurodegenerative processes. Vitamin D may help modulate inflammatory signaling, and there is also some evidence that vitamin D status is related to sleep quality. That creates a plausible biological pathway in which adequate vitamin D could potentially support both sleep and brain health, although this study did not directly demonstrate that mechanism and the broader research on vitamin D and cognition remains mixed.”

– Dung Trinh, MD

Monique Richard, MS, RDN, LDN, FAND, IFNCP, a registered dietitian nutritionist and owner of Nutrition-In-Sight — who was not involved in this study — added that in addition to inflammation, vitamin D appears to influence other pathways relevant to brain health, including oxidative stress, neuronal signaling, and neurotrophic factors. 

“Sleep disturbance itself can also amplify inflammation and metabolic stress, so vitamin D may be one piece of a much larger sleep–brain–immune connection,” Richard continued.

“My perspective is that the greatest potential benefit may be in identifying someone who is insufficient or deficient rather than assuming that ‘more is always better.’ Evidence from larger trials remains mixed, which is an important part of the story, emphasizing the fact that personalizing recommendations is best,” she told us.

“Vitamin D may not be a magic memory pill, but correcting a deficiency could be one modifiable piece of the brain-health puzzle,” Richard added. 

Should you take a vitamin D supplement? 

For those worrying about their vitamin D intake, Richard recommended first looking at the whole picture rather than immediately reaching for a high-dose supplement of D2 or D3.

“Vitamin D is naturally present in relatively few foods, but fatty fish such as salmon and trout, egg yolks, and fortified milk or plant-based beverages can contribute in meaningful, beneficial amounts. Reading labels, understanding sources and whether that item — irradiated mushrooms, for example — are contributing reliable amounts, are a few additional tips to consider with Vitamin D.” 

– Monique Richard, MS, RDN, LDN, FAND, IFNCP

For people with limited sun exposure, low dietary intake, or other risk factors, Richard said supplementation may be appropriate — but ideally based on an individual’s health history, dietary pattern, medications, ethnicity, conversion rate, and, when clinically indicated, a 25-hydroxyvitamin D blood test.

“Importantly, the 5,000-IU dose in this study should not be interpreted as a universal recommendation,” she continued. “The NIH lists 4,000 IU/day as the tolerable upper intake level for most adults from food and supplements combined, although higher doses may sometimes be used under medical supervision to treat deficiency.” 

“Consulting with a registered dietitian nutritionist (RDN) can help meet people where they are at and tailor an appropriate recommendation and game plan for their needs,” Richard added.

“The goal with vitamin D is to identify whether it is a missing piece of that individual’s health picture and then how that piece can be addressed most appropriately to reap the benefits and support the body and mind’s needs,” the dietitian concluded.

• Research is ongoing regarding COVID-19 and its impact on the human body. 
• One study confirmed reactivation of dormant viruses in over 1,100 participants who were hospitalized with COVID-19.  
• The results suggest that reactivations don’t just occur in people with suppressed immune systems, and that viral reactivation could affect long COVID and severe acute COVID-19.  

When it comes to COVID-19, it’s easy to only focus on the virus that causes it, SARS-CoV-2. But other factors may be at play when it comes to how COVID-19 affects people.

A study published in Nature was able to evaluate the reactivation of dormant viruses in people with COVID-19.

Researchers found that the reactivation of certain viruses occurred, and their activation was linked to both acute COVID-19 severity and possibly to long COVID as well.

Overall, it is possible that the reactivation of dormant viruses could make things worse when it comes to experiencing COVID-19, although more research is needed at this time. 

How does COVID-19 affect dormant viruses?

The authors explain that people often have dormant viruses present in their bodies, and that these viruses can reactivate in certain situations like critical illness. Reactivation of viruses in COVID-19 is an area where there is somewhat limited data. 

Researchers used data from the Immunophenotyping Assessment in a COVID-19 Cohort (IMPACC) study. All participants were adults who had confirmed SARS-CoV-2 and experienced hospitalization with COVID-19.

The research team analyzed data from samples like blood and nasal swabs, looking at some data up to a year after hospital admission. When participants enrolled, they had not received any COVID-19 vaccines. Participants were also divided into categories based on COVID-19 severity. 

The researchers found several viruses present in the samples that participants provided. Participants had experienced the reactivation of viruses, especially viruses that were part of the Herpesviridae and Anelloviridae families.

The study authors explain that they chose to focus on viruses from the Herpesviridae and Anelloviridae families because the cohort had a higher prevalence of these viruses.

Overall, they found that about 48% of participants experienced viral reactivation with severe COVID-19. Of these, about two-thirds “had only one virus detected in the acute period.” 

The activation of different viruses happened at different times. For example, the human alphaherpesvirus (HSV1) and cytomegalovirus — both viruses implicated in herpes — reactivated around 20 days after participants were admitted to hospitals. 

Next, researchers looked at whether detecting reactivated viruses within 40 days of hospital admission was associated with COVID-19 severity. This analysis revealed a number of findings.

For example, they found that some viruses were linked to COVID-19 severity. When looking specifically at participants classified as critical when it came to COVID-19 severity, those who had detectable nasal levels of Epstein-Barr virus (EBV), HSV1, or cytomegalovirus in any part of the respiratory system were at a higher risk for death within a year.

Additionally, certain viruses were also linked to specific comorbidities and complications. For example, detecting Anelloviridae in peripheral blood mononuclear cells, a type of immune cell, was linked to experiencing shock and admission to the ICU.

Viral reactivation ‘far more common than previously thought’

Speaking to Medical News Today, study authors Esther Melamed, MD, PhD, and Cole Maguire, PhD, highlighted the following regarding the study: 

“We studied over 1,150 hospitalized COVID-19 patients across 20 U.S. hospitals for a year, using sequencing techniques to directly detect when these viruses ‘wake up’ or reactivate. Nearly half of patients had at least one chronic virus reactivate during their illness. This was far more common than previously thought, and it was not limited to people with weakened immune systems. Importantly, many of these patients were otherwise healthy before getting COVID-19.”

Analyses further revealed that reactivation of certain viruses was also linked to certain immune responses in the body.

Researchers identified relationships between Herpesviridae and Anelloviridae reactivation and inflammation. For example, certain viruses were linked to increases in certain inflammatory cytokines.

The reactivation of certain viruses was also linked to changes in plasma metabolites, which are the products produced from the breakdown process of metabolism.

Finally, they also found that reactivated viruses were linked to certain changes in gene expression. 

How does viral reactivation affect long COVID?

Next, the researchers looked at how viral reactivation related to long COVID, which is characterized by the continuing experience experience of COVID symptoms for many weeks to months after the initial COVID-19 infection.

One of the major findings was that participants who reported physical disability or fatigue were the most likely to have Anelloviridae in samples from the long-term recovery timeframe. 

Melamed and Maguire explained the following: 

“We also discovered something new about a lesser-known group of viruses called Anelloviridae. Months after patients left the hospital, those who still had active Anelloviridae were more likely to be experiencing ongoing fatigue and physical disability consistent with Long COVID. This is the first time this virus family has been linked to Long COVID.”

What are the study limitations?

Of note, this study doesn’t establish a causal relationship. For example, it can’t prove that reactivation of dormant viruses causes increases in COVID-19 severity.

Researchers were also possibly limited in their findings by the fact that they studied IMPACC participants, who were not vaccinated and who experienced infection with early SARS-CoV-2 strains. Thus, it remains unclear how people exposed to other strains would be affected.

The authors also note that the choice to use transcripts to look at viral load may have produced certain limitations. Further, the specificity of the collected samples may have influenced the findings, since the researchers only looked at three specific sites, and they only had data on endotracheal aspirate samples in participants who were on ventilators. 

Finally, because of the timing of the study, there was no stable definition for long COVID when certain categories were created, so researchers may have been limited in their abilities to look into long COVID and viral reactivation.

Researchers also struggled with participant drop-out.

What do these findings mean?

Microbiology and immunology expert with Johns Hopkins Medicine, Arturo Casadevall, PhD, who was not involved in the study, noted that “the clinical implications at this time are uncertain but it is conceivable that reactivation of other viruses contributes to the disease that we know as COVID-19 and could be promoting the persistent inflammation that is associated with long COVID-19.”

It is possible that addressing these virus reactivations could help with addressing COVID-19 outcomes.

Jimmy Johannes, MD, a pulmonologist and critical care medicine specialist at MemorialCare Long Beach Medical Center in Long Beach, CA, likewise not involved in the study, noted the following to MNT: 

“One possibility is that reactivation of viruses such as EBV, cytomegalovirus, and other chronic viruses could contribute to some of the complications associated with COVID-19, particularly by adding to the inflammatory and immune response. If future studies establish that viral reactivation directly contributes to worse outcomes, it could potentially help doctors identify patients at higher risk for complications or identify new approaches to treatment.”

The findings could also help address ongoing quesrions about long COVID. Melamed and Maguire explained that, “for long COVID, if the Anelloviridae association is confirmed in future studies, it could point toward a new avenue for understanding why some patients develop prolonged symptoms post COVID.“

“It might also open the door to developing targeted therapies for these viruses, which currently have no approved treatments,“ the study authors hoped.

• About 160 million people around the world live with alopecia areata. 
• There is currently no cure for alopecia areata.
• Alopecia areata is currently treated by medications like JAK inhibitors. 
• A new study found a JAK inhibitor medication currently being used to treat rheumatoid arthritis may help people with alopecia areata regrow up to 80% of hair on their scalp within 24 weeks of use.  

About 160 million people around the world live with alopecia areata, a chronic autoimmune skin disease causing hair loss on the head, face, and other parts of the body.

There is currently no cure for alopecia areata. The condition is treated with different types of medications, including corticosteroids, immunotherapy, and Janus kinase (JAK) inhibitors.

“Alopecia areata is an autoimmune condition causing hair loss that carries a profound psychosocial burden for patients,” Arash Mostaghimi, MD, MPH, vice chair of clinical trials and innovation in the Department of Dermatology at Brigham and Women’s Hospital in Boston, associate professor at Harvard Medical School, told Medical News Today.

“Despite the introduction of FDA-approved medications over the past few years, many individuals still do not respond sufficiently to existing therapies. Developing new medications is critical to expanding effective options for these patients,” he noted.

Mostaghimi is the first author of a new study published in the journal JAMA Dermatology, which found that a JAK inhibitor medication currently being used to treat rheumatoid arthritis may help people with alopecia areata regrow enough hair to cover at least 80% of their scalp within 24 weeks of use.  

Why examine a rheumatoid arthritis drug to treat hair loss? 

For this randomized phase 3 clinical trial, researchers recruited almost 1,400 participants — including both adults and adolescents — with severe alopecia areata. 

Study participants received either a 15 milligram (mg) or 30 mg dose of the JAK inhibitor upadacitinib, which is currently used to treat several chronic inflammatory and autoimmune diseases such as rheumatoid arthritis, ulcerative colitis, Crohn’s disease, and atopic dermatitis.  

“Upadacitinib is a once-daily oral medication that targets the JAK/STAT pathway, a key cellular signaling route that drives inflammation,” Mostaghimi explained.

“Given its mechanism of action, along with real-world observations of hair regrowth in patients treated for eczema who also had co-occurring alopecia areata, investigating upadacitinib as a dedicated treatment for alopecia areata was a natural next step,” he told us.

Upadacitinib helps regrow hair to cover at least 80% of scalp

At the study’s conclusion, Mostaghimi and his team found that about half of study participants taking the 15 mg dose of upadacitinib grew back enough hair to cover at least 80% of their scalp within 24 weeks. And 54% of participants taking the 30 mg dose had the same result. 

“These findings demonstrate both rapid onset and substantial depth of response with upadacitinib,” Mostaghimi said. “While this was not a direct head-to-head comparative trial, the data suggest that upadacitinib may be among the most effective systemic treatments evaluated for alopecia areata to date.”

Additionally, researchers reported that study participants had improved eyebrows and eyelashes while on upadacitinib, and said they felt better emotionally and socially. 

“The ultimate goal of treating alopecia areata is not just hair count, but restoring patients’ confidence and quality of life,” Mostaghimi explained. “Achieving regrowth in critical non-scalp areas like eyebrows and eyelashes, along with measurable improvements in emotional and social well-being, confirms that upadacitinib delivers clinically meaningful outcomes.”

“Based on these clinical data, upadacitinib has already been approved for severe alopecia areata in Europe,” he added. “The findings are currently under review by the FDA, and we are hopeful the therapy will be approved for patients in the United States in the near future.”

How does a rheumatoid arthritis drug help regrow hair? 

MNT had the opportunity to speak with Joseph W. Fakhoury, MD, dermatologist, clinical trialist, and director of the Alopecia Clinic at Henry Ford Hospital in Detroit, MI, and spokesdoctor for the National Alopecia Areata Foundation, who commented the results are encouraging.

“Upadacitinib works by blocking certain JAK pathways, which are involved in the abnormal immune response underlying alopecia areata,” Fakhoury, who was not involved in this study, explained. “By decreasing the immune system’s attack on the hair follicle, upadacitinib may help the follicle return to its normal hair-growth cycle.” 

“Alopecia areata affects patients differently, and not all patients respond to currently available treatments,” he continued. “Having more treatment options will allow us to better personalize care and hopefully help more patients achieve meaningful and durable control of this condition.”

Optimistic results with more long-term data needed

MNT also spoke with Alexis Young, MD, a board-certified dermatologist at Hackensack University Medical Center (HUMC) in New Jersey, who likewise was not involved in this study. 

Young said her first reaction to the study’s results was one of tremendous optimism. 

“Seeing that up to 55% of patients on the 30-mg dose of upadacitinib achieved at least 80% scalp hair coverage in just 24 weeks is a massive step forward. It is especially exciting to see such rapid, robust results — with significant improvements observed as early as eight weeks — for both adult and adolescent patients, a demographic that currently has very limited systemic treatment options.”

– Alexis Young, MD

While the 24-week data demonstrates a highly positive benefit-risk profile with safety consistent with its other approved indications, Young said she looks forward to reviewing the longer-term data. 

“This study program includes a 28-week blinded extension period, and seeing the 52-week and beyond results will be critical,” she continued. “That long-term data will help us understand the durability of the hair regrowth, identify any optimal dosing adjustments needed over time, and ensure there are no delayed adverse safety events before routinely prescribing it in clinical practice.”

• The Food and Drug Administration (FDA) has approved Moderna’s mFLUSIVA, the first mRNA-based flu vaccine, for adults ages 50 and older.
• mRNA flu vaccines can be produced more quickly than traditional egg-based vaccines, which may help with matching to rapidly changing influenza virus strains.
• Experts advise that mFLUSIVA provides another option protecting against flu, but it should not replace every flu vaccine.

The FDA has recently approved Moderna’s mRNA flu vaccine. The vaccine, known as mFLUSIVA (mRNA-1010), is designed to protect adults ages 50 years and older against seasonal flu. It is the first mRNA-based flu vaccine, using similar technology as the mRNA COVID-19 vaccine.

The FDA approved the vaccine based on the results of a phase 3 clinical trial involving more than 40,000 adults ages 50 and older across 11 countries. Around half of the participants received mFLUSIVA, and the other half received a standard-dose licensed flu vaccine.

The researchers concluded that mFLUSIVA was superior to the standard-dose licensed flu vaccine in preventing flu-like illness confirmed by real-time polymerase chain reaction (RT-PCR) lab tests.

The vaccine was also granted accelerated approval for use in adults ages 65 years and older. This was following a clinical trial involving over 2,900 adults in the United States. The study evaluated how well the immune system responded to mFLUSIVA compared with a high dose inactivated flu shot.

Moderna expects that mFLUSIVA will be available in the United States for the 2026 to 2027 respiratory virus season.

How important is the development of mFLUSIVA?

There were an estimated 45,000 flu-related deaths in the United States in the 2024 to 2025 flu season, according to the most recent data from the Centers for Disease Control and Prevention (CDC). They noted that vaccination was estimated to have prevented around 12,000 deaths.

As the research found that mFLUSIVA has the potential to be more effective at reducing the risk of flu than other vaccines, it could help further prevent flu-related deaths.

Medical News Today spoke with Dung Trinh, MD, internist, of MemorialCare Medical Group and Chief Medical Officer of Healthy Brain Clinic in Irvine, CA, about the importance of this latest vaccine.

Trinh, who was not involved in the trials, viewed the FDA approval of mFLUSIVA as “an important addition to our influenza prevention toolkit, particularly because adults over 50 begin to experience a progressively higher risk of serious complications from influenza.”

He added: “This is also a significant scientific milestone because it is the first mRNA-based seasonal influenza vaccine approved in the United States, showing that mRNA technology can be applied beyond COVID-19.”

David Cutler, MD, board certified family medicine physician at Providence Saint John’s Health Center in Santa Monica, CA, also spoke with MNT about the new vaccine.

“My overall view is cautiously favorable. The FDA approval of Moderna’s mFLUSIVA (mRNA-1010) is scientifically interesting and potentially important, but I would not interpret it as proof that the mRNA vaccine is necessarily the best flu vaccine for every person over 50,” said Cutler, who was not involved in the trials.

He also explained that the FDA’s approval has important distinctions, with “traditional/full approval” for people aged 50 to 64, and “accelerated approval, with a requirement for additional post-approval evidence confirming clinical effectiveness” for adults ages 65 and over.

“That distinction matters,” continued Cutler, “because people ≥65 are the group in which we most want to know whether the vaccine actually prevents hospitalization, pneumonia, and death, rather than simply producing higher antibody levels.”

Why is it important that the mRNA flu vaccine can match influenza strains more quickly?

Flu viruses are constantly changing. This means that, by the time manufacturing is finished and the vaccines are ready to be administered, the virus may have altered, and the shot might not be as effective as it would have been at the beginning of the manufacturing process.

It can take at least 6 months to manufacture a traditional egg-based flu vaccine, according to the FDA.

However, the mRNA vaccine can be produced more quickly, which means it may be more likely to keep up with the rapid changes of the virus.

Cutler described “a potentially important technological advantage” of the mRNA vaccine, explaining that they “can theoretically be redesigned and manufactured more rapidly when influenza strains change. That could become increasingly valuable for influenza, where vaccine-virus mismatch is a perennial problem.”

Will the mRNA flu vaccine be more effective than the traditional flu vaccine?

Based on study findings, the mRNA flu vaccine has the potential to be more effective than traditional flu vaccines.

“For adults ages 50 to 64, the approval was based on a randomized phase 3 trial involving more than 40,000 participants, in which mFLUSIVA demonstrated approximately 27% greater relative vaccine efficacy against confirmed influenza compared with a standard-dose flu vaccine, while the clinical program identified no new safety concerns,” explained Trinh.

“I think the larger significance of mFLUSIVA may ultimately be beyond influenza itself,” added Cutler.

“If mRNA technology proves capable of producing more effective, rapidly updated influenza vaccines, it could substantially change how we respond to seasonal influenza and potentially to future influenza pandemics,” he said.

Are there any side effects of the mRNA flu vaccine?

Like any vaccine, the mRNA flu vaccine may lead to side effects.

According to Moderna, general side effects that were reported in the clinical trials included:

• headache
• fatigue
• joint pain
• muscle pain
• nausea
• vomiting
• fever
• chills

There were also reactions at the injection site. In rare cases, a severe allergic reaction or anaphylaxis could occur.

As with any vaccine, a healthcare professional can advise on its safety and whether they recommend it based on individual circumstances.

For individuals ages 50 years and over, they can speak with their doctor about the type of flu vaccine they recommend and when they should receive it.

Will mFLUSIVA replace traditional flu vaccines?

The mRNA flu vaccine is not designed to immediately replace traditional flu vaccines.

“I think the appropriate way to view this is not as a replacement for every existing flu vaccine, but as another evidence-based option that could ultimately give physicians and patients more choices in protecting people at higher risk from influenza,” Trinh explained.

Cutler said, “mFLUSIVA is an exciting new option, and its trial results are encouraging. But because its FDA approval in ≥65 is accelerated and confirmatory clinical-outcome data are still required, I would want to see another season or two of real-world evidence before declaring it superior to the established enhanced vaccines.”

He added: “For the 2026 to 2027 season, the most important decision is still to get an appropriate flu vaccine rather than waiting for the ‘perfect’ vaccine. The new mRNA option gives physicians and patients another potentially very useful tool.”

• Researchers believe 50% of all heart failure cases are heart failure with preserved ejection fraction (HFpEF).
• Current treatment for HFpEF includes medications and healthy lifestyle choices, such as following a heart-healthy diet.
• A new study found that a natural compound created in the gut microbiome after eating plant foods containing a certain type of polyphenol may help improve heart function in people with HFpEF, via animal and human tissue models.

Researchers estimate that about 64 million people around the world receive a diagnosis of heart failure — a cardiovascular condition where the heart is not able to efficiently pump blood.

About 50% of all heart failure cases are a type called heart failure with preserved ejection fraction (HFpEF). This occurs when the heart muscle becomes stiff, making it difficult for the heart to refill with blood and relax in between pumps.

It can lead to fluid retention and cause fatigue and shortness of breath when blood is not able to flow throughout the body.

Current treatment options for HFpEF include a combination of medications and healthy lifestyle modifications, such as losing weight, staying physically active, and following a healthy low-salt diet. 

Now, a new study published in the journal Science Advances has found, via animal and human tissue models, that a natural compound created in the gut microbiome when an individual eats plant foods containing a type of polyphenols called ellagitannins, may help improve heart function in people with HFpEF.

Ellagitannins are derived from foods such as pomegranates, berries, and walnuts.

Focusing on urolithin A and PKG1alpha

For this study, researchers used both an animal model and engineered human heart tissue created from human stem cells to test how the natural compound urolithin A might impact HFpEF.

“HFpEF is very common, and the number of people affected continues to rise,” Joseph Burgoyne, PhD, reader in cardiovascular biology within the School of Cardiovascular and Metabolic Medicine & Sciences at King’s College London, and senior author of this study, told Medical News Today.

“Although treatment options have improved, they remain limited and do not directly address some of the underlying problems, such as increased stiffness of the heart and its impaired ability to relax. There is therefore an important need to develop new therapies that target these mechanisms more directly,” Burgoyne continued.

“We screened natural compounds to identify molecules that could target a protein called PKG1alpha, which plays an important role in helping the heart muscle relax. Through this screening process, we identified urolithin A, a compound produced by the body following the consumption of foods such as pomegranates, walnuts, and some berries.”
— Joseph Burgoyne, PhD

Urolithin A improves HFpEF heart function up to 80%

At the study’s conclusion, scientists found that animal models of HFpEF treated with urolithin A experienced improved heart function as much as 80%, when compared to non-treated animal models. 

Via the human heart tissue model created from human stem cells, researchers reported urolithin A helped to significantly improve tissue relaxation in the cells.  

“In our animal model of HFpEF, urolithin A was highly effective at reducing several markers of heart dysfunction, including improving the heart’s ability to relax and reducing stiffness,” Burgoyne said. “These findings provide evidence that targeting PKG1alpha could be an effective new strategy for treating HFpEF.”

“They also suggest that urolithin A, or drugs designed to work in a similar but potentially more potent way, could provide a basis for developing new treatments,” he continued. “Further research will be needed to determine whether these benefits translate to patients.”

Findings need to be replicated in humans

MNT spoke with Kevin Shah, MD, a board-certified cardiologist and Program Director of Heart Failure Outreach at MemorialCare Heart & Vascular Institute at Long Beach Medical Center in Long Beach, CA, who commented that this is an exciting and interesting study as it identifies a new potential treatment target for HFpEF. 

“The findings are encouraging since they were supported in both animal models and engineered human heart tissue,” Shah, who was not involved in this study, said. “We do need clinical studies to translate this to patients.”

“HFpEF accounts for approximately half of heart failure cases,” he continued. “We are gaining momentum on current treatment options, but the treatment likely needs to be refined based on subtypes, e.g. driven by high blood pressure versus driven by kidney disease. Some patients still struggle and have poor quality of life, so identification of new pathways could lead to more effective treatments.”

“The next step is to determine whether these preclinical findings can be replicated in patients,” Shah added. “Longer-term studies and clinical trials to improve symptoms, exercise capacity, and quality of life in patients with HFpEF would be encouraging.” 

Can eating foods that create urolithin A help treat heart failure?  

In a press release, Burgoyne said: “While there isn’t enough evidence to suggest that people should eat pomegranates to treat heart failure, these findings raise the possibility that dietary approaches that enhance urolithin A production may help alleviate this condition.”

Monique Richard, MS, RDN, LDN, FAND, IFNCP, a registered dietitian nutritionist and owner of Nutrition-In-Sight, told MNT that this study’s findings are an intriguing and affirming example of how the gut, diet, and cardiovascular system may be connected in ways we are only beginning to understand.

“Urolithin A is particularly interesting because it is not simply a nutrient we eat by itself, but a metabolite produced by our gut microbiota from compounds such as ellagitannins, found in certain plant foods that can serve as precursors,” Richard, who was not involved in this study, explained.

“This isn’t really a story about eating more urolithin A; it’s a story about what happens when high quality plant food interacts with our microbiome,” she added.

“What’s exciting to me is that this research blurs the line between nutrition for the gut and nutrition for the heart,” Richard continued. “The gut isn’t simply where digestion happens, but a metabolic organ capable of transforming compounds from our food into signaling molecules that interact with the rest of the body.”

How can I get more urolithin A through my diet? 

For those who wish to add more urolithin A in their diet, Richard said that we want to think about urolithin A not as a single compound treatment, but as a component in foods we want more of, that provide its precursors.

Richard said ellagitannins — a type of polyphenol — and related compounds are found in:

• pomegranates 
• raspberries, strawberries, blackberries, and other berries
• walnuts and pecans.

Richard said a practical goal is to incorporate these foods regularly in a dietary pattern rich in whole foods rather than treating pomegranate as a “medicine” or “superfood.”

She suggested trying to add:

• berries to oatmeal or yogurt
• pomegranate arils to a grain bowl or fruit salad
• walnuts to a salad
• or having 4 ounces of pomegranate juice by itself, in herbal iced tea, or as refreshing ice cubes.

“Keep in mind that direct supplementation is very different from eating a pomegranate, and individual production from food varies considerably according to the gut microbiome,” Richard explained. “Food is packaged along with fiber, polyphenols, and additional micronutrients that support vascular health, cardiac function, and may assist in prevention of heart disease.”

“Sometimes the intervention is remarkably unglamorous: Eat a diverse range of plants consistently, feed the microbiome, move your body, get quality sleep, take prescribed medications as directed, and let emerging science help us understand why those fundamentals may be so effective,” she advised. 

• Different stages of melanoma have a higher risk of the skin cancer coming back after being surgically removed.
• An experimental therapy developed by Merck and Moderna aims to help lower the recurrence rate in people with completely resected stage IIB-IV melanoma.
• Participants in the clinical study of their new mRNA-based treatment experienced a 49% reduction in melanoma recurrence or death.

In 2022, about 330,000 people around the world were diagnosed with the skin cancer melanoma, with about 60,000 people dying from the condition. 

Different stages of melanoma have a higher risk for recurrence — coming back after being surgically removed. For instance, past studies show that stage III melanoma carries a high recurrence risk of 40% to as much as 90% at five years following surgery. 

On August 19, pharmaceutical companies Merck and Moderna announced the phase 3 clinical study results for an experimental therapy designed to help lower the recurrence rate in people with stage IIB-IV melanoma who have had their tumor completely removed. 

Medical News Today spoke with seven melanoma experts to find out more about this potential new treatment and how it may help lower recurrence risk in people with higher stages of melanoma. 

Why does melanoma have a high recurrence risk?

According to Joan Levy, PhD, chief science officer of the Melanoma Research Alliance, “completely resected” means surgeons have successfully removed all melanoma they can detect. However, the challenge, Levy said, is what doctors can’t see. 

“Stage IIB through Stage IV describes patients whose melanoma has characteristics that put them at higher risk of recurrence,” she detailed.

“At Stage IIB and IIC, the melanoma may still be localized to the skin, but features such as the depth of the tumor or ulceration make it higher risk. Stage III generally means melanoma has spread regionally, such as to nearby lymph nodes. Stage IV means it has spread to distant parts of the body — although in the patients in this trial, that disease had been completely removed surgically.” 
— Joan Levy, PhD

“So these patients may have no detectable cancer after surgery, but they can still have microscopic melanoma cells remaining somewhere in the body,” Levy continued. “Those cells can eventually begin growing again. That’s why preventing recurrence is such an important goal. We don’t want to wait for melanoma to come back before treating it if we can safely intervene earlier.”

How does mRNA-based intismeran autogene therapy work?

The experimental therapy, intismeran autogene, is an investigational messenger RNA (mRNA)-based individualized neoantigen therapy (INT), used in combination with immunotherapy drug Keytruda (pembrolizumab), currently used to treat a number of cancers, including skin cancer. 

Every cancer has mutations in its DNA, Michael B. Atkins, MD, FAIO, FASCO, deputy director of the Georgetown Lombardi Comprehensive Cancer Center at Georgetown University, and board member of the Melanoma Research Foundation, explained to MNT, and melanoma is known to have a high number of these mutations due to damage from ultraviolet irradiation.  

“Many of these mutations lead to abnormal proteins which can be recognized as foreign by the immune system. In order to escape immune recognition and destruction, cancers express proteins which disable the immune response. Pembrolizumab can block this disabling function (by) enabling the immune system to once again recognize and kill the tumors. After the tumor is resected, there are often insufficient immune cells around that can recognize the tumor as foreign.” 
— Michael B. Atkins, MD, FAIO, FASCO

“Moderna has addressed this problem by taking a piece of resected melanoma, identifying the most likely DNA mutations to be recognized by the immune system, and creating a personalized mRNA vaccine that encompasses these mutations,” Atkins explained.

“In simple terms, this therapy is like creating a custom-built ‘wanted poster’ for your immune system to hunt down your specific cancer,” added Andrew Pecora, MD, co-division chief of the Skin and Sarcoma Service at the John Theurer Cancer Center at Hackensack University Medical Center in New Jersey. “After your tumor is surgically removed, scientists analyze its DNA to find unique mutations, or ‘flags,’ that are only present on your cancer cells.” 

How mRNA vaccines work

“Using mRNA technology — the same kind used in some COVID vaccines — they create a personalized vaccine containing the instructions for your body to produce these harmless cancer flags. Once injected, your cells make these flags, and your immune system recognizes them as dangerous, training a highly specialized army of cells to seek and destroy anything that carries them.” 
— Andrew Pecora, MD

“This newly trained immune army then acts as a long-term surveillance force, patrolling your body to eliminate any microscopic cancer cells that may have been left behind after surgery, thereby preventing the melanoma from ever coming back,” Pecora added. 

What do these study findings mean for people with melanoma? 

According to Moderna and Merck, after a 5-year follow-up, study participants given the new therapy experienced a 49% reduction in the risk of recurrence or death, and a 59% lower risk of distant metastasis or death, compared with those receiving Keytruda alone. 

Kim Margolin, MD, medical oncologist and medical director of The Borstein Family Foundation Melanoma Program at Providence Saint John’s Cancer Institute in Santa Monica, CA, told MNT that doctors already have effective adjuvant treatments that can reduce the risk of recurrence in patients with high risk melanoma, including immune checkpoint inhibitors such as pembrolizumab and nivolumab. 

However, Margolin said, these therapies don’t eliminate the risk of recurrence for everyone, and some patients will still develop metastatic melanoma. 

“We also have increasingly effective treatments for melanoma that has recurred or metastasized, but preventing recurrence remains an important therapeutic goal. The ideal strategy would identify and eliminate microscopic residual disease before it has an opportunity to grow and spread.” 
— Kim Margolin, MD

“Therefore, the question is not whether we have effective treatments today, but whether we can improve upon them and identify which patients are most likely to benefit from additional or alternative approaches,” Margolin said. 

Hilary Gomolin, MD, a medical oncologist and hematologist at the Eugene M. & Christine E. Lynn Cancer Institute, part of Baptist Health South Florida, agreed: “Currently, we have excellent options for treatment of high risk melanomas that have been resected with a number of different immunotherapy drugs that have shown improvement in disease-free survival. There is always the need to move science forward and improve outcomes for our patients.”  

What we still need to know about intismeran

All experts agree that there are still questions and research to be done to continue evaluating this new potential therapy.

For instance, Christina M. Annunziata, MD, PhD, senior vice president, extramural discovery for the American Cancer Society, said that she would like to see the detailed results of the clinical trial, especially the length of the follow-up period, and to see the patients followed long-term to understand how durable the effect will be. 

“From a safety perspective, the report indicates that the side effects were similar to Keytruda alone,” Annunziata told MNT. “For the patients who did not benefit from the vaccine, it would be interesting to sequence the cells in the relapsed cancer to see whether the mutational profile had changed.” 

Shirin Bajaj, MD, a board certified dermatologist and Mohs micrographic surgeon starting at Mount Sinai in September, said she would also like to see the practical realities of this treatment option. 

“Making a personalized vaccine currently takes on the order of six weeks from when a patient’s tumor and blood samples reach the central lab (the company’s stated turnaround target), though independent estimates run longer, roughly two to four months — so manufacturing turnaround, cost, insurance coverage, and equitable access will all matter a great deal for real-world use.” 
— Shirin Bajaj, MD

The bottom line, she added, is this is one of the most promising advances in both melanoma care and personalized oncologic care in years.

“And a positive phase 3 result is a major step, but it’s not yet standard treatment,” Bajaj continued. “The study is still ongoing, and the detailed, longer-term data will tell us just how big a difference it truly makes.”

• Researchers examined whether higher dietary antioxidant intake, including vitamins A and C and zinc, was associated with the prevalence of cervical cancer.
• They analyzed data from more than 1,000 women who participated in a large U.S. health and nutrition survey.
• Women with the highest antioxidant intake had about 56% lower odds of having a history of cervical cancer compared with those with the lowest intake.
• Researchers say more studies are needed to better understand the relationship between antioxidant intake and cervical cancer risk.

Cervical cancer, which is primarily caused by persistent infection with high-risk human papillomavirus (HPV), is a significant global health concern.

Cervical cancer is less common in the U.S., but is one of the most common cancers that affects women worldwide, especially in lower-income countries.

A new study examined the relationship between dietary antioxidant intake and cervical cancer and found that higher antioxidant intake was associated with a lower prevalence of the disease.

The study was published in the International Journal of Gynecology & Obstetrics.

How researchers measured dietary antioxidant intake

There were more than 600,000 cases of cervical cancer and about 342,000 deaths from the disease worldwide in 2020.

Although HPV vaccination and cervical cancer screening can help prevent the disease, access to these preventive measures is uneven, particularly in lower-income countries.

Researchers are also interested in identifying additional modifiable factors that may contribute to the development of cervical cancer, including nutrition.

For the new study, scientists analyzed data from the National Health and Nutrition Examination Survey (NHANES), a program that assesses the health and nutritional status of people in the U.S.

The researchers included 1,044 participants in their analysis. Of these, 174 had a self-reported history of cervical cancer, and 870 participants without cervical cancer served as matched controls.

The team analyzed the participants’ diets using two nonconsecutive 24-hour dietary recall interviews. They then calculated each participant’s Composite Dietary Antioxidant Index (CDAI).

The CDAI provides an overall measure of dietary antioxidant intake based on six components: 

• vitamins A, C, E
• zinc
• selenium
• carotenoids

Higher CDAI scores indicate higher overall dietary antioxidant intake. Antioxidants may help protect against oxidative stress and inflammation, which the researchers thought may contribute to HPV infection and cervical cancer development.

The researchers used CDAI scores to examine whether overall antioxidant intake was associated with the prevalence of cervical cancer.

They also accounted for factors such as age, race and ethnicity, income, smoking and alcohol use, and BMI.

Higher antioxidant intake linked to lower cervical cancer prevalence

After accounting for these factors, the researchers found that each 1-unit increase in CDAI score was associated with 11.4% lower odds of having a history of cervical cancer.

Participants with the highest dietary antioxidant intake had about 56% lower odds of having a history of cervical cancer than those with the lowest intake.

The study authors said that antioxidants may affect oxidative stress, inflammation, and immune responses, which could help explain the association. However, the findings do not show that a higher antioxidant intake prevents cervical cancer.

The study had several limitations, including its cross-sectional design. Since the researchers assessed participants’ diets and cervical cancer history at a single point in time, they could not determine whether diet influenced cancer development or whether participants changed their diets after diagnosis.

Participants also self-reported their cervical cancer diagnoses, and researchers did not have information about cervical cancer stage at diagnosis.

The authors say that future studies should follow participants’ diets over time to better understand whether antioxidant intake affects cervical cancer development.

Can antioxidants help with cervical cancer prevention?

Jagdish Khubchandani, PhD, MPH, a public health professor at New Mexico State University, shared his thoughts on the study with Medical News Today.

Khubchandani noted that while studies using NHANES data can provide valuable insights, dietary research has limitations, including relying on participants accurately recalling what they eat.

However, he said there are several biological mechanisms that could help explain the findings. 

“Antioxidants in many dietary items (e.g., fruits and veggies) neutralize these toxins that can damage DNA in cells,” Khubchandani explained. “Furthermore, antioxidants, vitamins, and minerals in healthy diets also protect our tumor-suppressing proteins.”

“The science is well established that healthy diets reduce the risk of cancers,” he said, adding that greater attention should be paid to improving “access, cost, and lifestyles.”

5 servings of fruit and veg a day as a starting point

Khubchandani recommends aiming for five servings of fruits and vegetables daily when possible, while emphasizing that diet cannot prevent HPV infection when other risk factors are present. 

“Good diets can ensure a strong immune response to any infection,” Khubchandani emphasized.

Laurie Brunette-Masi, MD, a board certified gynecologic oncologist at City of Hope Orange County in Irvine, California, told MNT that the findings should be interpreted cautiously.

“It is important, however, not to interpret this as proof that antioxidants prevent cervical cancer,” said Brunette-Masi. “This was an observational study that shows an association, not cause and effect.”

Brunette-Masi noted that antioxidants are part of a healthy lifestyle and may help support immune function, but emphasized that HPV vaccination and recommended cervical cancer screening are “the foundation” of cervical cancer prevention.

“A healthy diet may be another piece of the prevention picture, but it should complement, not replace, these proven measures,” said Brunette-Masi.

• There are several factors that can play an important role in establishing a person’s cardiometabolic health, such as body composition. 
• Previous research has also linked certain foods to better cardiometabolic health, including coffee. 
• A new study found that drinking coffee regularly may help improve a person’s body composition and metabolic markers, such as visceral fat and insulin markers. 
• Researchers discovered male sex-specific hormone patterns as well for habitual coffee drinkers.

There are several factors that can play an important role in establishing a person’s cardiometabolic health, such as blood sugar levels, blood pressure, and body composition, including visceral or abdominal fat, subcutaneous fat, and muscle mass.

Having poor cardiometabolic health can increase your risk of developing health conditions like type 2 diabetes, chronic kidney disease, fatty liver disease, and cardiovascular disease.

Previous research shows it’s possible to improve your cardiometabolic health by making healthy lifestyle choices, such as being physically active, not smoking, and eating a healthy diet. 

Past studies have also linked certain foods to better cardiometabolic health, such as leafy greens, fatty fish, berries, and coffee. 

Now, a new study published in the European Journal of Nutrition provides more evidence linking coffee consumption to cardiometabolic health.

Researchers found that drinking coffee may help improve a person’s body composition and metabolic markers, such as visceral fat. 

Why focus on coffee? 

For this study, researchers analyzed health data for more than 2,200 participants from the 46-year follow-up of the Northern Finland Birth Cohort 1966. Study participants were asked questions about their coffee consumption habits and completed numerous health assessments, including body mass index (BMI), waist-to-hip ratio, body fat percentage, and skeletal muscle mass. 

“Poor body composition and metabolic health are closely tied to the risk of conditions like type 2 diabetes and cardiovascular disease, which remain among the biggest public health burdens worldwide,” Luca Verroest, doctoral researcher at the University of Oulu in Finland, and lead author of this study, told Medical News Today.

“Much of this risk is shaped by everyday, modifiable factors like diet, so understanding how common dietary components, such as coffee, relate to these markers helps build a more complete picture of prevention, alongside established factors like physical activity and body weight,” he explained. 

“Coffee is one of the most widely consumed beverages globally, and Finland has the highest per-capita consumption in the world, so it’s a highly relevant exposure to study in a Finnish cohort,” Verroest continued.

“Coffee is also far more than just caffeine: it contains over a thousand bioactive compounds, of which many may have biological effects of their own. Yet despite how commonly it’s consumed, we still don’t fully understand how it relates to metabolic and hormonal health.”
— Luca Verroest, lead author

Drinking more coffee leads to lower visceral fat, better muscle mass

At the study’s conclusion, researchers discovered that study participants who drank the highest amounts of coffee had lower total and visceral fat and better skeletal muscle mass, when compared to participants who did not drink coffee, regardless of them both having similar BMIs. 

“(This) suggests that BMI alone may not capture some of the more meaningful differences in body composition associated with coffee consumption,” Verroest said.

“People with the same BMI can have quite different amounts of fat versus muscle, and our findings point to habitual coffee drinkers having a comparatively leaner profile (lower total and visceral fat, more skeletal muscle) that BMI alone wouldn’t reveal,” he explained.

Additionally, consuming higher amounts of coffee was linked to lower circulating levels of branched-chain amino acids (BCAAs) — a known biomarker for cardiometabolic health that are also linked to an increased risk for obesity, type 2 diabetes, and heart disease. 

“Coffee itself isn’t a meaningful source of BCAAs, so this isn’t about coffee adding or displacing amino acids in the diet,” Verroest explained.

“Finding that higher coffee consumption correlated with lower circulating BCAA levels in both men and women adds an interesting angle to how coffee might relate to this metabolic pathway, though as a correlational finding, it can’t tell us whether coffee directly improves this clearance process or simply tracks alongside better metabolic health for other reasons.”
— Luca Verroest, lead author

Male coffee drinkers experience additional benefits

When looking at male vs female participants, Verroest and his team found that in men, higher coffee intake was associated with a more beneficial glucose–insulin profile, as well as increased amounts of total and bioavailable testosterone and sex hormone–binding globulin (SHBG). 

“This was one of the most distinct findings in our study,” Verroest said. “Both total testosterone and SHBG have been linked in other research to a lower risk of conditions like metabolic syndrome and type 2 diabetes, so this hormonal pattern fits coherently with the more favorable glucose-insulin profile we observed in the same men.”

“Coffee appears to leave a measurable fingerprint on the body’s metabolism and hormones, and that fingerprint looks different in men than in women.”
— Luca Verroest, lead author

“It’s a new piece in the puzzle of how a beverage most of us drink without a second thought may relate to long-term health. That said, this is an observational study, so it shows associations rather than proof that coffee causes these changes,” Verroest added.

Coffee may not improve weight and health for everyone

MNT spoke with Mir Ali, MD, a bariatric surgeon, bariatric medicine specialist, and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, who commented that this study’s findings verify what we’ve seen from other studies that caffeine does have some benefit to weight loss and overall health in general, though the specific mechanism is not clearly understood.

“There’s some benefits that we’ve seen from other research in coffee that it does have a mild appetite suppressant effect,” Ali, who was not involved in this study, explained.

“[Coffee] may stimulate the metabolism to some extent. And in this study, it showed that it stimulates some hormonal function as well. So it’s probably a combination of all of these things that improve visceral fat and other benefits.” 
— Mir Ali, MD

As obesity continues to increase worldwide, Ali said it’s important for researchers to continue to find new ways in which people may be able to improve their body composition and metabolic markers as there’s no one thing that works for everybody to improve their weight and their health. 

“So the more information we have, different things that may be beneficial, the better, because one thing that may be beneficial to one person may not help another,” he added. 

Coffee may be one small piece of a much larger metabolic picture

MNT also spoke with Monique Richard, MS, RDN, LDN, FAND, IFNCP, a registered dietitian nutritionist and owner of Nutrition-In-Sight, who likewise was not involved in this study.

Richard said it’s important to note that while this is an interesting study, coffee may not be the only contributing hero of the story.

“Because this was a cross-sectional observational study, we cannot say that coffee caused people to have less visceral fat or more muscle, but that it could be associated with the observation,” she explained.

“Coffee is a chemically complex food containing caffeine, chlorogenic acids, trigonelline, and other bioactive compounds, and the biological response may depend on the whole coffee matrix, not simply caffeine alone. There probably isn’t one coffee compound responsible.”
— Monique Richard, MS, RDN

Richard noted that coffee may be one small piece of a much larger metabolic picture. 

“I would much rather see coffee complement adequate protein, fiber-rich whole foods, resistance training, physical activity, sleep, and stress management than see someone add several cups of coffee while neglecting those foundational behaviors,” she said. 

And Richard also reminded readers that what is in the coffee you’re drinking matters. 

“A plain brewed coffee is metabolically very different from a 500-calorie coffee beverage loaded with added sugar, syrups, and saturated fat,” she explained. “We want to consider coffee consumption related to what kind, how much, when, and what is being added to it.” 

• A new large study suggests that daily sugary drink consumption is linked to a higher risk of developing stomach cancer, compared with those who drank them less than once a month.
• In particular, a higher consumption of fructose, a sugar commonly found in these beverages, was associated with a greater incidence of stomach cancer.
• However, as an observational study, the findings cannot establish that sugary drinks directly cause stomach cancer. Other factors, such as bacterial infections, diet, weight, and other lifestyle choices, may also influence risk.

Sugar-sweetened beverages, such as regular soft drinks, sweetened teas and coffees, sports and energy drinks, and fruit drinks, are a common part of many people’s diet. Many of these beverages contain substantial amounts of fructose, which often derives from high-fructose corn syrup.

Older data from the Centers for Disease Control and Prevention (CDC) suggest that nearly 65% of U.S. adults report consuming one or more sugar-sweetened beverages every day.

Regular consumption of these beverages is associated with a range of adverse health outcomes, including weight gain, obesity, type 2 diabetes, and cardiovascular disease. There is also growing interest in a possible relationship between high consumption of sugary beverages and cancer.

Now, a large observational study suggests that people who regularly consume sugar-sweetened beverages may have a 2.45-fold higher risk of developing stomach cancer.

The findings, published in Gastro Hep Advances, add to growing research indicating that the consumption of sugary drinks may contribute to cancer risk. However, as an observational study, it cannot establish that sugary drinks directly cause stomach cancer.

What did the study find?

Researchers from Mass General Brigham analyzed dietary and health information from more than 112,000 U.S. adults drawn from two long-running U.S. studies: the Nurses’ Health Study and the Health Professionals Follow-up Study.

Participants were grouped according to how frequently they reported consuming sugar-sweetened beverages. These included carbonated beverages, punch, lemonade, and sports drinks. Over the course of follow-up, 278 participants developed stomach cancer, also known as gastric cancer.

Compared with people who consumed fewer than one sugar-sweetened beverage per month, those drinking these beverages daily had more than twice the risk of developing gastric cancer after the researchers accounted for a range of potential risk factors.

The association appeared particularly strong among females who consumed more than one sugar-sweetened beverage per day. The study also found that higher total intake of fructose was associated with a greater incidence of gastric cancer.

“Based on data collected from more than 100,000 people over decades, we found that consuming at least one sugar-sweetened beverage per day was associated with more than twice the risk of developing gastric cancer compared with those never consumed these beverages,” senior study author Andrew Chan, MD, MPH, a gastroenterologist and epidemiologist with the Mass General Brigham Cancer Institute, told Medical News Today.

“In contrast, artificially sweetened beverages were not associated with increased risk of gastric cancer,” he said.

Sugar vs. artificial sweeteners

“[T]he evidence on artificial sweeteners and cancer risk overall is still evolving and somewhat mixed. The insulin and metabolic pathways that might underlie the risk of stomach cancer are specific to sugar sweetened beverages and not artificially sweetened beverages.”
— Andrew Chan, MD, MPH

Why might sugary drinks be associated with stomach cancer?

While the study found an association, it was not designed to determine why sugar-sweetened beverages might be associated with stomach cancer, so any explanation remains speculative.

One possibility is that frequent consumption of sugary drinks may contribute to weight gain and metabolic changes. Previous research highlights an association between excess body weight and an increased risk of several cancers. However, the relationship between obesity and individual cancer types can be complex.

“We don’t know the exact mechanism but several biological pathways have been proposed for how these beverages might contribute to cancer risk generally, including its effects on weight gain, insulin resistance, chronic inflammation, and changes to the gut microbiome,” said Chan.

“Any or several of these could plausibly play a role in stomach cancer specifically,” he added.

Could fructose play a role?

The researchers also note an association between higher fructose intake and gastric cancer incidence. Evidence suggests that high-fructose corn syrup may play a role in chronic inflammation and tumor development. However, the study findings do not prove that fructose itself causes stomach cancer.

“Intriguing data suggest that fructose in particular may play a specific role in cancer development,” Chan said. “This may be due to insulin or inflammatory pathways, but also some metabolic pathways specific to cancer.”

The research team also add that certain lifestyle factors, such as dietary choices, smoking, and alcohol consumption likely play a role and it is difficult to account for these factors in observational research.

What does this mean for people who drink sugary beverages?

The study’s finding of a 2.45-fold higher risk may sound alarming, but it does not necessarily mean that someone who drinks soda occasionally is likely to develop stomach cancer.

Although the findings note more than twice the risk of developing stomach cancer, this is a measure of relative risk. This describes the likelihood of an outcome occurring in one group compared with another. This is different from absolute risk, which is the actual chance of experiencing a particular outcome.

While those who regularly consumed sugar-sweetened beverages had roughly a 145% higher relative risk of stomach cancer, there were 278 cases of gastric cancer among 112,284 participants during the study period, suggesting stomach cancer was relatively uncommon in this population.

Still, the findings add to evidence that frequent consumption of sugar-sweetened beverages may have adverse health consequences, such as obesity, type 2 diabetes, cardiovascular disease, and some cancers.

“Regularly drinking sugar-sweetened beverages appears to be associated with a meaningfully higher risk of stomach cancer,” Chan told MNT.

“While more research is needed to confirm this and understand why, cutting back on sugary drinks is a reasonable, low-risk step people can take in the meantime. Reducing consumption of these beverages is also associated with benefits in prevention of other chronic diseases, such as diabetes and obesity.”
— Andrew Chan, MD, MPH

Tips for reducing sugar-sweetened beverage intake can include swapping them for water or unsweetened varieties.

Alternatively, people can gradually taper these drinks by mixing soda with sparkling water. Individuals may also read the packaging label and choose a low sugar or sugar-free option, or avoid those containing added sugars such as high-fructose corn syrup.

What the research may be missing

It is important to consider the observational design of the study. Researchers observed participants’ existing dietary habits and then examined their health over time. They did not randomly assign people to drink sugary beverages or avoid them.

As a result, the findings show an association, rather than demonstrating that sugar-sweetened beverages directly cause stomach cancer.

Notably, the researchers had limited information on participants’ Helicobacter pylori infection status, an important established risk factor for stomach cancer. Data concerning H. pylori were available for only a small subset of participants, making it difficult to determine whether infection influenced the association.

Additionally, the study population was predominantly white, which limits how confidently the findings can be generalized to other groups. Dietary information was also based on participants’ reports, which can be affected by recall and reporting errors.

More research is still necessary to determine the association between sugar-sweetened beverages and stomach cancer, and whether there is a biological mechanism that could explain the relationship.

For now, the study adds to evidence suggesting that frequent consumption may increase the risk of health conditions and reducing consumption may be beneficial for several reasons.

• A recent study suggests that eating a vegan diet, even for a short time, may help reduce inflammation and slow biological aging. 
• The diet aids in these areas by altering DNA methylation patterns, which are chemical markers that regulate gene expression. 
• Although promising, the study findings are preliminary, and larger, longer-term studies are necessary to determine whether these changes could lead to meaningful health benefits.

Vegan dietary plans have gained popularity in recent years, with an increasing number of people opting to reduce or eliminate animal products from their diets. Concerns about animal welfare, the environmental impact of food production, and the potential health benefits likely influence this growing adoption.

As vegan options have become more widely available, following a vegan eating plan has also become more accessible and convenient. As a result, veganism has developed into a more mainstream dietary choice.

Now, a small randomized clinical trial suggests that eating a vegan diet for as little as 4 weeks may help reduce inflammation and even slow biological aging.

The findings, published in MedComm, indicate that healthy adults who followed a vegan diet for 4 weeks developed changes in DNA methylation, an epigenetic process that can influence gene activity. Some of the changes were associated with a less inflammatory immune profile and measures of biological aging.

However, the study involved only 48 healthy adults, and lasted for a month. As such, larger, longer-term studies are needed to determine whether the changes persist and translate into better health outcomes.

What did the study find?

Researchers from the University of California, San Diego, and the University of Freiburg analyzed blood samples from 48 healthy adults who first followed a standardized diet for a week. Participants were then randomly assigned to follow either a vegan diet or a meat-rich diet for a month.

The diets were designed to provide similar amounts of calories, allowing the researchers to investigate whether differences in food composition, rather than simply calorie intake or weight change, could account for the observed changes.

DNA methylation involves chemical modifications that do not alter underlying DNA, but can influence whether particular genes are more or less active. The researchers examined more than 800,000 DNA methylation sites across the genome before and after the dietary intervention.

They found several changes in the vegan group involving pathways related to immune function, metabolism, cell growth, insulin signaling, DNA repair, and cellular responses to stress.

As such, it suggests that adopting a vegan dietary plan may influence mechanisms that regulate gene activity.

“I find these findings interesting, but it is important we are careful with how we state the headline,” said Michelle Routhenstein, MS, RD, CDCES, CDN, a registered dietitian nutritionist who specializes in heart disease at EntirelyNourished, and who was not involved in this study.

“This study was a small, short term study in 48 healthy adults, and the researchers were looking at changes in DNA methylation, which is basically a chemical tagging system that helps control how genes are turned on and off. These changes can be influenced by diet, inflammation, activity, and aging. They are biological markers, not proof that someone is actually aging more slowly or will live longer.”
— Michelle Routhenstein, MS, RD

Similar previous research supports findings

“In 2023, we published the results of an 8-week study conducted in 22 pairs of identical twins. Our results were very similar to the recent study,” explained Christopher Gardner, PhD, the Rehnborg Farquhar Professor of Medicine at Stanford University, and Director of Nutrition Studies at the Stanford Prevention Research Center, who was also not involved in the study.

“We looked at chronological vs. biological aging with epigenetic clocks (similar to the recent study) and telomere length. In just 8 weeks, the twins randomized to these diets had aging measures that improved relative to their matched identical twins that were assigned a healthy omnivorous diet,” he continued.

Omnivores vs. vegans

“In our study, compared to the omnivorous study participants, the vegan participants experienced lower LDL-cholesterol, lower fasting insulin, lower weight, less aging (according to markers above), and had improved gut microbiome impacts.”
— Christopher Gardner, PhD

“We are not surprised by these recent findings, and are pleased to see that the types of findings we got in our study are being replicated in other studies. The replication makes the strength of the findings better solidified,” Gardner added.

Could a vegan diet cause a shift toward a less inflammatory state?

The DNA methylation patterns in those following a vegan dietary plan were associated with lower proportions of neutrophils and higher proportions of CD4 T cells.

Neutrophils are white blood cells that play an important role in defending the body against infection. However, excessive or prolonged inflammatory activity can contribute to tissue damage and chronic disease. CD4+ T cells help coordinate and regulate immune responses against disease and infection.

The methylation-based estimates also correspond with blood-cell measurements obtained during the original trial. This provides additional evidence that the detected changes reflect differences in immune cell composition.

However, this does not mean that a vegan eating plan necessarily prevents inflammation or inflammatory disease.

Instead, the findings suggest that changing dietary patterns may influence biological pathways involved in the body’s immune response.

Did the vegan diet actually make people biologically younger?

Unlike chronological age, which measures how many years a person has lived, biological age measures how the body is functioning. Researchers can estimate it using epigenetic clocks, or mathematical models based on DNA methylation patterns.

Two of the aging measures used in the study, PhenoAge and GrimAge, suggest that biological aging slowed in the vegan group during the 4-week intervention.

However, a third measure, Blood&Skin, produced a different result, showing age acceleration instead. This is important as different epigenetic clocks measure different aspects of aging and do not necessarily provide identical results.

Therefore, the findings should not be interpreted as a vegan eating plan reversing aging. Instead, they provide preliminary evidence that a short-term dietary intervention can affect molecular markers that researchers associate with biological aging.

What does this mean for people considering a vegan eating plan?

The findings support the role of nutrigenomics, which is the study of how diet and genes interact to affect a person’s health and risk of developing diseases.

A well-planned vegan diet can provide substantial amounts of vegetables, fruits, whole grains, legumes, nuts, and seeds.

However, simply removing animal products does not automatically make a dietary plan healthy. A vegan diet can also include highly processed foods that are high in added sugars, sodium, or saturated fats, and may require a person to to pay attention to nutrients that can be more difficult to obtain from plant foods, including vitamin B12.

“It is important to recognize that when someone replaces a meat-heavy diet, they may also be eating less saturated fat and processed meat, which has been associated with aging,” Routhenstein told Medical News Today.

“I would not interpret these findings as meaning that animal foods are inherently inflammatory. It is more likely that the overall shift toward more plant foods and less processed and meat-heavy foods is influencing several pathways involved in inflammation and metabolism.”

Diet quality matters

“[T]he quality of the diet matters within a vegan diet. A diet can technically be vegan while being high in refined carbohydrates, sugary foods, fried foods, and highly processed vegan products,” Routhenstein said.

“[Y]ou do not have to go fully vegan to support healthy aging and longevity. Increasing the amount and variety of plant foods in your diet can provide many of these benefits while still allowing you to include animal foods,” she added.

“A good quality vegan diet is typically composed of foods and food groups that are recommended, and avoids or minimizes foods that are of low/lower nutritional quality,” Gardner told MNT.

“The recent study looked at inflammation and aging. However, there are decades of studies that suggest a good quality vegan diet is associated with lower risk of heart disease, cancer, diabetes, obesity and stroke, and their risk factors,” he said.

Study limitations

While encouraging, the study has several important limitations.

It was a small study that only included 48 healthy adults. As such, it may not be representative for how different people may respond to a vegan eating plan. Additionally, the intervention only lasted 4 weeks, so it is unclear whether the DNA methylation changes would remain after returning to usual diets, or whether maintaining a vegan diet for longer would produce larger or different effects.

Furthermore, the researchers only measure methylation changes in blood. Epigenetic patterns can differ between tissues, so changes in blood do not mean that identical changes may occur in organs such as the liver, brain, muscle, or adipose tissue.

The study also only measured molecular markers rather than long-term clinical outcomes. This means that it does not demonstrate that a vegan eating plan can prevent cancer, cardiovascular disease, dementia, or other age-related conditions, nor does it establish that the diet extends lifespan.

While further research is necessary, the findings suggest that the relationship between diet and health may extend beyond calories, body weight, and conventional blood markers, potentially reaching into the mechanisms that help regulate how cells function.

• It is well known that being physically active benefits both your body and brain.
• However, the type of activity that is most beneficial for brain health is not yet entirely clear.
• A new study has found that when and why you move, rather than just how much you move could influence your risk of developing dementia.
• The study suggests that leisure activities, such as walking, cycling, running, swimming or playing sports, may decrease your risk of dementia, but physically demanding jobs could actually increase the risk.

According to the Centers for Disease Control and Prevention (CDC), physical activity is “one of the most important things you can do for your health”.

The CDC recommends that adults get at least 150 minutes of moderate-intensity physical activity, such as brisk walking, or 75 minutes of vigorous physical activity, such as running, each week, as well as doing muscle-strengthening activity at least twice a week.

This is a minimum — doing more exercise than this will give greater benefits.

Exercise benefits not only your physical health, but is good for your brain too. Several studies suggest that aerobic exercise — movement that increases your heart rate and increases blood flow — may improve cognitive performance, reduce the risk of developing dementia, and even alleviate some symptoms in people with dementia.

Now, a new systematic review suggests that when and why you exercise could impact your dementia risk. 

The review, which is published in Lancet Public Health, found that leisure-time exercise was associated with a decreased risk of dementia, whereas physically demanding work was linked to an increased risk of developing the condition.

Steven Allder, MD, a consultant neurologist at Re:Cognition Health, who was not involved in this research, told Medical News Today:

“I think the findings are certainly worth paying attention to, particularly because the analysis included more than four million people and followed participants for many years. The consistency of the results across a large number of studies makes the association interesting and potentially important.”

“However,“ Allder cautioned, we need to be careful not to confuse an association with cause and effect. Because this was an observational study, we cannot say that occupational physical activity causes dementia or that leisure exercise directly prevents it.”

Leisure activity linked to 24% lower dementia risk

The international team of researchers that conducted this review, led by scientists at the University of Southern California, analyzed data from 74 studies with more than 4.2 million participants from 30 countries.

The participants ranged in age from 45 to 93 years at the start of the median 10-year follow-up. During follow-up, researchers recorded all diagnoses of all-cause dementia, Alzheimer’s disease, and vascular dementia.

All 74 studies assessed physical activity by self-reported questionnaires or objective measurements, and included comparison with a reference group — active versus inactive, low- versus high-activity. Occupational physical activity was recorded only for those in work, rather than non-working or retired.

People who engaged in leisure-time physical activity had a 24% decreased risk of developing dementia compared with those who were least active. Occupational physical activity, in contrast, was associated with a 20% increased risk of dementia.

Allder told MNT that leisure time physical activity may protect the brain in several different ways: “Regular exercise improves cardiovascular health and blood flow, helps control blood pressure, blood sugar and cholesterol, and may support the brain’s ability to maintain healthy connections between nerve cells.”

“There is also something distinctive about leisure activity,” he continued. “We choose to do it. “

“Going for a walk with a friend, swimming, cycling or playing a sport can combine physical activity with social interaction, enjoyment and mental stimulation. These factors may reduce stress and social isolation, while helping to build what we think of as cognitive resilience, which is the brain’s ability to cope with age-related changes,” Allder suggested

“So, it may not simply be about the amount of movement, but also the physical, psychological and social benefits that come with enjoyable, voluntary exercise,” he told us.

Why physically demanding jobs may increase dementia risk

“It would be wrong to conclude that physically demanding work itself causes dementia,” Allder stressed.

The researchers found that higher levels of occupational physical activity were consistently associated with an increased risk of all-cause dementia in analyses adjusting for age, education and chronic disease.

They suggest that other factors involved in physically demanding jobs may play a role in increasing dementia risk. These factors could include heightened psychosocial stress, hazardous occupational exposures, and increased exposure to air and noise pollution, both of which have been linked to higher dementia risk.

Allder cautioned that the finding should be interpreted carefully, as the increased risk may reflect the context surrounding occupational activity.

“Someone in a physically demanding occupation may spend many hours standing, lifting, carrying or performing repetitive movements, often with limited control over the pace or intensity and not enough opportunity for recovery. Physically demanding jobs can also be associated with chronic stress, shift work, noise, air pollution and other workplace exposures,” he explained.

“There may also be a knock on effect,” he continued. “Someone who is physically exhausted after a demanding working day may have less time or energy for recreational exercise, social activities and other behaviours that support healthy ageing.”

Natan Feter, PhD, postdoctoral scholar and research associate at the University of Southern California, first author on the study, also advised caution when interpreting their results:

“We cannot completely rule out residual confounding — that is, the possibility that some of the association we observed is explained by factors we did not measure or fully account for. This is particularly important for occupational physical activity, because physically demanding jobs may cluster with other social, economic, environmental, and health-related disadvantages.”

“For this reason, our findings should not be interpreted as showing that physical activity at work itself causes dementia, but rather that the broader context in which that activity occurs may be important,” noted Feter.

How and when should you exercise to reap the most benefits?

“When promoting physical activity at the population level, we must ensure everyone has equal access to choice-led, safe, pleasant, and meaningful physical activity,” Feter told us.

The study authors note that rather than simply encouraging people to “move more,” dementia prevention efforts should recognize that not all physical activity occurs under the same conditions.

“For me,” Allder commented, “the most important message is that people should not be discouraged from being physically active, including those who have physically demanding jobs.”

“Instead, this research reminds us that physical activity is more complicated than simply counting steps or hours of movement. The way we move, the environment in which we do it, whether we have control over it, whether we can recover afterwards and whether it is enjoyable and socially engaging may all matter,” he told MNT.

“It also reinforces the importance of making recreational exercise accessible to everyone. Walking, cycling, swimming, dancing or simply being active with friends can all be valuable,” added Allder.

“Ultimately, dementia prevention is likely to involve a combination of factors, including regular exercise, cardiovascular health, good sleep, social and mental engagement and addressing other modifiable risk factors, rather than any single behaviour in isolation.”

– Steven Allder, MD

• Cardiometabolic health refers to how your cardiovascular and metabolic systems interact. 
• Past studies show that it’s possible to improve cardiometabolic health and reduce the risk of type 2 diabetes and cardiovascular disease by making healthy lifestyle choices, such as being physically active. 
• A new study found that shorter yet intensive exercises, such as sprint intervals, may be more effective at improving cardiometabolic health markers than moderate-intensity exercises, like consistent cycling. 

Over the last few years, researchers have been focusing on finding new ways people can improve their cardiometabolic health — the health of their cardiovascular and metabolic systems and how they interact. 

For example, how efficiently your blood vessels deliver oxygenated blood throughout your body can affect how well your mitochondria burn fuel and produce energy. A well-functioning cardiovascular system also affects the ability of hormones and blood sugar to reach their targets and of the body to remove waste. 

Past studies show that people with poor cardiometabolic health may have an increased risk of developing type 2 diabetes, chronic kidney disease, and steatotic liver disease. 

The good news is that you can improve your cardiometabolic health by making healthy lifestyle choices, such as eating a healthy diet, not smoking, limiting alcohol intake, getting enough quality sleep, managing stress, and being physically active. 

Now, a new study published in the journal Cell Reports Medicine adds to our understanding of cardiometabolic health and exercise.

Researchers found that more intensive exercises, such as sprint intervals, may be more effective at improving cardiometabolic health markers than moderate-intensity exercises, like consistent cycling. 

Comparing sprint intervals to moderate intensity cycling

In a clinical trial with 19 healthy young men, researchers evaluated the immediate blood protein response to either 90 minutes of moderate continuous cycling or six sets of 30-second all-out sprint intervals.

To assess long-term health implications, they then cross-referenced these exercise-activated proteins with medical records from over 53,000 UK Biobank participants, finding that many sprint-induced proteins linked directly to a lower risk of heart and metabolic disease.

“Both forms of exercise (sprint-interval and moderate intensity) are growing in popularity and are regularly used in clinical and general populations,” Paul Cohen, MD, PhD, Albert Resnick, MD, Associate Professor and head of the Laboratory of Molecular Metabolism at The Rockefeller University in New York City, and senior author of this study, told Medical News Today.

“It is important that we better understand the metabolic responses stimulated by different exercise intensities to help inform how we design and implement exercise programs,” he said. 

Sprinting changes 32 proteins linked to type 2 diabetes, obesity

At the study’s conclusion, researchers found that sprint interval training caused changes in more than 200 metabolites — small molecules produced or used during metabolism — and led to an immediate increase in the levels of proteins needed for blood vessel growth, tissue remodeling, and hormonal signaling.

“Exercise stimulates the release of proteins and metabolites into the circulation to communicate across diverse organs,” Luke Olsen, PhD, postdoctoral associate in the Laboratory of Molecular Metabolism at The Rockefeller University in New York City, and first author of this study, explained to MNT. “For example, a contracting muscle might secrete a protein into the circulation to notify the liver that it needs more fuel (sugar or fat). These fuels are then released by the liver and taken up by the muscle, permitting continued muscle contraction.”

“Such crosstalk is instrumental to coordinating the body’s response to exercise and, ultimately, driving its health benefits,” Olsen continued. “Our findings highlight just how extensive and rapid this communication can be following high intensity exercise.”

Additionally, scientists discovered that of the 33 proteins associated with a lower risk of cardiometabolic problems such as obesity and type 2 diabetes, sprinting altered 32, while only 3 were altered during moderate-intensity exercise.

“We know that high intensity exercise, such as sprinting, promotes body-wide adaptations that can be metabolically beneficial,” Cohen said. “However, what mediates these changes has remained largely unclear. Our data pinpoint specific proteins that could contribute to these beneficial effects and provide a potential link between high intensity exercise and improved cardiometabolic health.”

A few minutes of sprinting doesn’t replace benefits of regular exercise

MNT spoke with Socrates Kakoulides, MD, cardiologist and chief imaging officer of Baptist Health Heart & Vascular Care, part of Baptist Health South Florida, who was not involved in this study. 

Kakoulides commented that his first reaction to these findings was that this is a fascinating look at how strongly the body can respond to exercise intensity.

“We have known for a long time that physical activity is one of the most important things people can do to improve cardiovascular and metabolic health, but this study helps us better understand what may be happening at a molecular level,” he explained.

“What stood out to me was how quickly short bursts of very intense exercise changed proteins and metabolites circulating in the bloodstream. Those signals appear to affect communication between different tissues and organs and may help explain some of the cardiometabolic benefits we associate with vigorous exercise.”
— Socrates Kakoulides, MD

“At the same time, I would not want patients to interpret these findings as meaning that a few minutes of sprinting replaces the benefits of regular exercise,” Kakoulides continued.

“This study primarily examined molecular responses to different types and intensities of exercise. It gives us important clues about the biology, but we still need additional research to understand how these changes translate into long-term outcomes such as reducing the risk of heart disease, diabetes, or obesity,” he added.

How do these findings translate to real life? 

MNT also spoke with Joshua Scott, MD, primary care sports medicine physician and co-director of Non-operative Orthopedics and Sports Medicine at Cedars-Sinai Orthopedics and Sports Medicine in Los Angeles, who likewise was not involved in this study. 

Scott said that while sprinting may have triggered changes in many metabolites, leading to a surge in proteins involved in blood vessel growth, tissue remodeling, and hormone signaling, the question is how that translates into real-life scenarios that help our patients live a happier, healthier lifestyle. 

“I think the question is whether or not those translate to real-world changes,” he continued. “We know that some of the metabolites are associated with better cardiovascular health, type 2 diabetes, and metabolic disorders, but we really need to study that in multiple different individuals and translate that to longer life and a healthier lifestyle over time.” 

How can I change my exercise regimen if I can’t sprint?

Obviously, sprinting is not for everyone. Kakoulides said the most important message is that you do not have to sprint to benefit from exercise. 

“Moderate physical activity remains extremely valuable for cardiovascular and metabolic health,” he said.

Alternatives to sprinting

“For someone who is already exercising and has been medically cleared to increase the intensity, one practical approach may be to incorporate brief periods of greater effort into an activity they already enjoy. That could mean walking briskly or uphill for a short period and then returning to a comfortable pace, increasing resistance or speed briefly on a stationary bicycle, or adding faster intervals while swimming or using an elliptical machine.” 
— Socrates Kakoulides, MD

Scott agreed: “I think for those of us that are exercising on a regular basis, mixing things up and doing more higher intensity exercises, we know has some benefit even if you’re not able to sprint. Higher intensity exercises have been shown to be more helpful than doing just low to moderate intensity exercises, but obviously that needs to be done under the direction of a healthcare professional.” 

“Ultimately, the best exercise program is one that is safe, sustainable, and performed consistently,” Kakoulides added. “Adding intensity can be another tool, but it does not replace the importance of regular movement, aerobic exercise, and strength training.”

• Biological age has to do with how old someone’s cells are and might not be the same as the number of years since someone’s birth, also known as chronological age. 
• One study sought to explore how accelerated biological aging related to certain health outcomes in the long term. 
• The study found that having accelerated biological aging appears to increase the risk for cardiovascular disease and death among men and women.
• By contrast, accelerated biological aging in midlife was linked to a higher dementia risk in women only. 

Aging is unavoidable, but some people age at a faster rate than others. The term biological age refers to the age of someone’s cells, rather than how long it has been since someone was born, which is their chronological age.

A recent study including over 3,000 participants identified long-term risk from accelerated biological aging.

For all participants, accelerated biological age was linked to greater risk for death and cardiovascular disease. For women, there was also a higher risk for dementia.

The study was published in Scientific Reports. 

How does accelerated biological aging affect health?

The recent study sought to explore differences in outcomes between men and women when it comes to biological age, specifically focusing on long-term data.

Researchers utilized data from Framingham Offspring Study cohorts. They excluded some participants, such as those who lacked data on clinical biomarkers used to estimate biological age.

The research team considered three main outcomes in their analysis: cardiovascular disease, dementia, and all-cause mortality. 

They took into account measurements like total blood cholesterol, blood sugar, and Mini-Mental State Exam scores. They used different biomarkers depending on the situation. Covariates included a number of components, including diabetes, use of medications for blood pressure, and smoking status. 

Participants were placed in one of three categories when it came to biological age: accelerated, decelerated, or concordant.

Participants with a concordant biological age had a biological age that essentially matched their chronological age, while the other groups had an age that was higher or lower.

Most participants fell into the concordant biological age category and were middle-aged adults. For participants who had accelerated biological age, on average men were 4 years older than their chronological age, and women 2.5 years older.  

Biological aging rates linked to dementia risk, but only for women

The median follow-up time was 26 years for the samples examining dementia and mortality. The median follow-up time was 23 years for the sample examining cardiovascular disease.

During the follow-up, there were 713 cardiovascular disease events, 1,105 deaths, and 265 cases of dementia. 

Participants who had accelerated biological age were at a higher risk for cardiovascular disease. For men, there was a 1.6-fold higher risk, and for women there was a 1.8-fold higher risk compared to participants who had decelerated biological age.

Both men and women with accelerated biological age also had a 2-fold greater mortality risk in comparison to those with decelerated biological age.

For men, accelerated biological age did not appear to increase risk for dementia in a statistically significant way. For women, however, there was an increased risk for dementia.

Sensitivity analyses confirmed that women with accelerated biological age and even concordant biological age were at a higher risk for dementia compared to those with decelerated biological age.

How strong are these findings?

While these findings are striking, it is important to note that this was an observational study, meaning it cannot prove causal relationships, and that there is a possibility of residual confounding.  

The concept of biological aging comes with its own limits, with study authors noting that it “serves as a proxy measure for the aging process.”

Furthermore, there is no standard way to calculate biological age, which could lead to major differences in this realm of research.

In this study, biological age is an estimation that researchers calculated by factoring in a number of biomarkers. The authors note that additional biomarkers that they lacked data on could have “been more relevant to the aging process.”

Moreover, many participants from the Framingham Offspring study were white and of European descent, which limits generalizability. 

Speaking to Medical News Today, Salim Hayek, MD, a professor of cardiovascular medicine at The University of Texas Medical Branch (UTMB), who was not involved in the current study, highlighted that: 

“One limitation deserves attention, and to their credit the authors are candid about it. When they added biological age to a model that already included chronological age, smoking, blood pressure, diabetes, lipids and BMI, prediction barely improved. The change in the c-statistic ran from essentially zero to about 0.01. So the measure tracks risk, but it isn’t telling you much beyond what the individual risk factors already say.” 

Future research ought to explore a number of factors, including the differences observed when it came to the risk for dementia. It can also examine what contributes to accelerated biological aging.

Beverly Pennington, DNP, APRN, FNP-C, a geriatrics health nurse practitioner at UTMB, likewise not involved in the research, told us: “I do like the study, and I think this is a great way to look at accelerated biological age (ABA), but I would want to know what factors were associated that caused the ABA.“

In Pennington’s opinion, these likely include “items such as education, substance abuse, and environmental factors.”  

Starting point for a larger conversation about modifiable risk factors

This research does not necessarily point to a need to implement major changes in clinical practice just yet. However, it could help people address certain areas of health.

Hayek noted that these findings may be a good starting point for people to have some important conversations with their healthcare providers.

“In the near term, this isn’t a test to order […] Where I think it earns its keep is in the conversation,” he told us.

“Telling a 55-year-old man that his body looks 61 lands differently from reading him a list of six mildly abnormal labs. If that framing gets someone to control his blood pressure or quit smoking, it has done more than a better c-statistic would,” added Hayek.

“But the treatment doesn’t change. There is no therapy for accelerated aging; you treat the components, and the components are the same ones we’ve been treating for 40 years,” he pointed out.

The study authors also suggest that looking at biological age could help “identify individuals at higher risk of adverse outcomes not captured by a single biomarker.” 

It may also encourage a push towards standards for calculating biological age, since this is not something that has truly been established yet.

Cheng-Han Chen, MD, a board-certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center in Laguna Hills, CA, who was not involved in the research, said that “one day, we may have a standardized and clinically validated definition of biological age that could complement traditional measures of health and disease risk.“

“Such a measure could potentially help clinicians identify individuals who appear to be aging biologically faster than expected and who may be at greater risk for cardiovascular disease or other age-related conditions,“ noted Chen.

“It could also potentially help us evaluate whether interventions such as exercise, improving diet, controlling blood pressure and cholesterol, maintaining a healthy weight, or stopping smoking are influencing the underlying processes of biological aging. However, we are not yet at the point where biological age should be used as a routine clinical tool. More research is needed to establish standardized measurements and determine whether changing a person’s biological-age measure actually translates into better health outcomes.”

– Cheng-Han Chen, MD

• About 32 million people globally live with Alzheimer’s disease. 
• People who have Alzheimer’s disease are at increased risk for several health issues, including atrial fibrillation (AFib). 
• Past studies show that anticoagulant medications may help lower a person’s risk of developing dementia.
• A new study says treatment with newer blood-thinning medications, or new oral anticoagulants (NOAC), may help slow the cognitive decline rate of people with both Alzheimer’s disease and AFib. 

An estimated 32 million people around the world are living with a type of dementia called Alzheimer’s disease. 

People who have Alzheimer’s disease are at increased risk for several health issues, including pneumonia, depression and anxiety, urinary tract infections (UTIs), and heart health conditions like stroke and atrial fibrillation (AFib).

AFib is a heart rhythm disorder commonly treated with an anticoagulant, or blood-thinning medication. Past studies show that anticoagulants may help lower a person’s risk of developing dementia.

Now a new study published in the European Heart Journal suggests that treatment with new oral anticoagulants (NOAC) may help slow the cognitive decline rate of people with both Alzheimer’s disease and AFib. 

NOAC vs warfarin: How do they affect brain health?

For this study, researchers analyzed medical data for more than 7,300 participants from the SveDem (Swedish Register for Cognitive Disorders/Dementia) database. Selected study participants had both AFib and Alzheimer’s disease. 

Participants were broken down into three groups: those treated with NOAC, those treated with the anticoagulant warfarin, and those not treated with an anticoagulant at all. 

“Studies have found that about 15–20% of people with Alzheimer’s disease also have atrial fibrillation,” Maria Eriksdotter, MD, PhD, professor in the Department of Neurobiology, Geriatrics, Health Sciences, and Society at the Karolinska Institutet, senior consultant in geriatric medicine at Karolinska University Hospital, and lead author of this study, told Medical News Today.

“Blood thinning medications are widely used to prevent strokes and blood clots. By improving blood flow and reducing small-scale damage to the brain, blood-thinning medications could potentially help preserve cognitive function,” Eriksdotter explained. 

“We therefore wanted to investigate whether people with both atrial fibrillation and Alzheimer’s disease who were treated with blood thinning medications experienced a different rate of cognitive decline compared with those who were not on blood thinning medications. In addition, we also compared the modern blood thinning drugs NOAC with the older drug warfarin.” 

– Maria Eriksdotter, MD, PhD

NOAC help slow cognitive decline rate in Alzheimer’s disease

At the study’s conclusion, researchers reported that participants treated with NOAC had a significantly slower cognitive function decline rate than those receiving warfarin or no anticoagulant drug. 

“This finding suggests that NOAC may offer benefits beyond their established role in preventing stroke and blood clots in people with atrial fibrillation,” Eriksdotter said.

“While the effect was modest, even small delays in cognitive deterioration over several years can be meaningful for patients and families. It also strengthens the indication to treat people with atrial fibrillation and Alzheimer’s disease with NOAC,” she told us. 

As for how NOAC may help potentially slow cognitive decline in people with Alzheimer’s disease and AFib, Eriksdotter said at present, they can only speculate about the mechanisms. 

“One leading hypothesis is that NOAC may help protect the brain by improving blood flow and reducing small-scale vascular damage,” she detailed. “Another possibility is that NOAC may provide more consistent protection against small blood clots and cerebrovascular events than older treatments.” 

“Since vascular disease and Alzheimer’s disease often coexist and can interact, better protection of the brain’s blood vessels could potentially help preserve cognitive function,” Eriksdotter added. “However, our study shows an association, not causation, and more research is needed to understand the biological processes involved.”

Association does not establish causation

MNT had the opportunity to speak with Craig Basman, MD, FACC, FSCAI, associate director of the Structural and Congenital Heart Program, and director of the Structural and Congenital Fellowship Program at Hackensack Meridian Hackensack University Medical Center in New Jersey, who was not involved in this study. 

Basman commented that finding NOAC — which are already the standard of care for stroke prevention in AFib — may offer a secondary, neuroprotective benefit in patients who already have Alzheimer’s is ”highly encouraging.”

“It underscores the vital role that optimal cardiovascular management plays in holistic patient health. However, my biggest concern with this study is that this implies association and does not establish causation,” he cautioned.

Given that this was a retrospective observational study, Basman said, the fundamental next step must be prospective, randomized controlled trials to definitively establish causation rather than correlation. 

“I would also like to see future studies incorporate advanced neuroimaging, such as longitudinal brain MRIs, to identify the exact mechanisms at play, specifically, verifying if NOAC measurably reduce the burden of cerebral microinfarcts or improve cerebral blood flow,” he added.

“Finally, analyzing the comparative efficacy of specific NOAC agents (e.g., apixaban versus rivaroxaban) will be highly relevant for cardiologists looking to tailor anti-coagulation strategies for this highly vulnerable patient population,” noted Basman.

Any slowing of cognitive decline meaningful

MNT also spoke with Dung Trinh, MD, an internist for MemorialCare Medical Group and chief medical officer of Healthy Brain Clinic in Irvine, CA, who said that even a modest slowing of cognitive decline can be meaningful for people with Alzheimer’s disease and their families.

“Cognitive decline affects far more than performance on a test,” Trinh, who was likewise not involved in this study, explained.

“It can affect independence, communication, relationships, and a person’s ability to manage everyday activities. There remains a tremendous need for treatments that can preserve cognitive and functional abilities for as long as possible,” he stressed.

“Approaches that may provide benefits while also treating other medical conditions are particularly interesting,” Trinh continued.

“In this study, the difference associated with NOAC use was relatively small, about 0.2 points per year on the Mini-Mental State Examination (MMSE), but even incremental differences may become meaningful over time and warrant further investigation, particularly if they can be achieved while also reducing the risk of stroke,” he noted. 

Trinh also emphasized, however, that while these findings are encouraging, they need to be interpreted with caution. 

“This was an observational study, so we cannot conclude that NOAC themselves caused the slower cognitive decline,” he explained. “I would not recommend changing anticoagulant therapy solely because of a potential cognitive benefit based on these findings.“

“Rather, the study adds to a growing body of research exploring the important relationship between cardiovascular health, cerebrovascular disease, and Alzheimer’s disease,” he concluded.

• Researchers at Oregon Health and Science University recently conducted a study on treating a virus similar to human immunodeficiency virus (HIV) in infant monkeys. 
• They tested a combination of three therapies that target the virus. 
• The virus did not return in any of the eight macaques that received all three treatments, even after treatment stopped. 

Around 120,000 children worldwide are diagnosed with HIV each year, who typically acquire it from their mothers during pregnancy, childbirth, or breastfeeding.

Certain treatments can prevent HIV from progressing to acquired immunodeficiency syndrome (AIDS). However, they do not eliminate the virus completely, so it can return if treatment stops.

As researchers continue searching for ways to prevent or cure HIV, scientists involved in a new study tested a combination of treatments in primates.

They found that starting a three-part treatment within 3 days of exposure may stop a similar virus from becoming permanently established.

The study is published in Nature Microbiology.

3-pronged approach against viral infection

The World Health Organization (WHO) describes HIV as “a virus that attacks the body’s immune system.” Without treatment, HIV can progress to AIDS.

HIV-related deaths have declined over the years, and improvements in treatments such as antiretroviral therapy (ART) have contributed to this.

While ART can suppress HIV and stop it from turning into AIDS, it does not eliminate the hidden reservoirs of the virus. These reservoirs allow the virus to remain inactive in the body and begin multiplying again if treatment stops.

The researchers studied 55 male and female infant rhesus macaques. When the monkeys were around 1 month old, the scientists exposed them to simian-human immunodeficiency virus (SHIV), a virus that causes illness similar to AIDS.

The team compared seven treatment approaches aimed at preventing the virus from forming permanent reservoirs. 

The approaches included ART, two broadly neutralizing antibodies (bNAbs), and leronlimab, an experimental monoclonal antibody. The researchers tested the therapies individually and in different combinations.

For the final experiment, they gave eight  of the monkeys all three therapies at 72 hours after being exposed to SHIV. At this point, the researchers could already detect the virus in the macaques’ blood. 

The monkeys received one dose of two bNAbs, 9 weekly doses of leronlimab, and daily ART for 27 weeks.

After treatment ended, the researchers monitored the monkeys to see whether the virus returned. They later depleted the animals’ CD8 T cells to make sure the virus was truly gone rather than being hidden or controlled by the immune system.

Triple therapy prevented viral rebound in primates

The study authors noted that previous research using ART alone or ART combined with bNAbs did not consistently prevent the virus from returning. 

The researchers saw similar results in this study. The individual and two-part treatments lowered virus levels, but it eventually returned.

The outcome was different when the researchers combined all three treatments.

All eight macaques in the triple-treatment group had detectable virus when they began receiving ART, bNAbs, and leronlimab. Not only did the treatment suppress the virus, but it also did not return after the researchers stopped ART at week 27.

Over 6 months of follow-up, the researchers found no viral DNA in the monkeys’ blood. When they later depleted the animals’ CD8 T cells, they still detected no viral rebound. 

At 84 weeks after exposure, the scientists still found no detectable SHIV in the tissue samples. While they cannot yet say whether the treatment will work in human newborns, the findings offer hope that HIV detected and treated shortly after infection could potentially be cleared.

Are the findings likely to apply to humans?

Jagdish Khubchandani, PhD, MPH, a public health professor at New Mexico State University, who was not involved in this research, told Medical News Today that he was excited about the study results, but said he remains “cautiously optimistic.”

“This is a multipronged approach that makes a lot of biological sense,” Khubchandani said, explaining that the therapies target different stages of early infection.

Khubchandani said the use of primates made him more optimistic about the results. He pointed out that primates “mirror our biology in numerous ways, have a history of testing for HIV, and what we know from primates about HIV has been highly valuable so far.”

However, Khubchandani said applying the findings to human newborns could prove difficult and that clinicians would need to identify babies who acquired HIV and begin treatment shortly after birth.

He noted that the researchers must also determine the appropriate dose, whether the treatment works when started beyond three days after exposure, and whether it is safe and effective in human newborns.

Jagmohan Batra, MD, a pediatric infectious disease specialist and medical director of Bickerstaff Family Center at Miller Children’s and Women’s Hospital Long Beach, likewise not involved in the study, also spoke with MNT. Batra said the findings are “very important.” 

“A single therapy may control viral replication or decrease the reservoir but does not seem to eliminate it,” said Batra. He noted that by targeting HIV in three different ways, the combination may have a better chance of preventing a permanent viral reservoir from forming.

Batra said the primate findings make it plausible that the treatment could also work in human newborns. However, he said that determining when a baby acquires HIV could complicate things.

“The longer the infection persists, there are likely more reservoirs established and in more tissue types,” he explained.

Batra said the approach might initially be most useful for babies at high risk of acquiring HIV during delivery while clinicians await their birth test results.

• A new paper indicates that reducing sodium and increasing potassium intake together can significantly support blood pressure.
• While past research focused on sodium intake alone, newer research shows that the sodium-to-potassium ratio is a stronger predictor of heart health.
• Experts recommend consuming whole foods rich in potassium, such as bananas, potatoes, and spinach, and also reducing sodium intake, to prevent and better manage high blood pressure.

Traditional advice for managing high blood pressure has favored lowering sodium intake; however, new evidence suggests that increasing potassium may significantly support this effort, and the potassium-to-sodium ratio may be a more accurate indicator of cardiovascular health.

A new report, published in The American Journal of Clinical Nutrition, makes a case for updating current hypertension-lowering guidelines, recommending that people increase their potassium intake while also reducing their sodium intake to most effectively manage blood pressure.

Considering that most Americans consume around 3,400 milligrams (mg) of sodium per day, which exceeds the 2,300 mg recommended by federal and health guidelines, this advice becomes more pertinent. Most of this intake, approximately 70%, is also from restaurants and processed foods.

Adding to the mix the fact that over 98% of U.S. adults fail to meet daily dietary recommendations for potassium as well, these statistics begin to explain why hypertension has earned the nickname of “silent killer.”

Often progressing over the years without any apparent symptoms, high blood pressure affects about 120 million people in the U.S.

Medical News Today spoke to three experts — Leonard Pianko, MD, board-certified cardiologist in Florida, Yaz Daaboul, MD, a cardiologist leading the Advanced Cardiac Imaging Program at Harrison Memorial Hospital in Cynthiana, Kentucky, and Jen Hernandez, RDN, CSR, LDN, board-certified renal dietitian — to discuss how increasing potassium intake can help better manage blood pressure and whether certain groups of people should be careful about their potassium intake.

Why potassium is important for blood pressure

Recent research has demonstrated that the sodium-to-potassium ratio is a more accurate predictor of cardiovascular outcomes than sodium alone. High sodium intake has also been linked to a greater risk of hypertension and cardiovascular disease.

“A 2025 meta-analysis found that adding about 2,000 mg of potassium per day could reduce systolic blood pressure by about 5 mmHg [millimeters of mercury] and diastolic blood pressure by about 3 mgHg in people with hypertension,” Hernandez said.

The way potassium helps achieve this balance is by counterbalancing the effects of sodium, helping to excrete excess sodium from the body and promoting relaxation of blood vessels.

Pianko said that while the current standard favors a low sodium diet to help lower blood pressure, the conversation about adding potassium to diet is not new.

“Potassium is a vital mineral to maintain homeostasis, and too high or too low levels can be deleterious to your health. This report emphasizes how sodium and potassium work together to regulate fluid balance and blood pressure and how balanced eating, such as the DASH eating plan, is effective in lowering blood pressure,” he explained.

Will only increasing potassium help lower pressure?

Hernandez reiterated that increasing potassium without decreasing sodium can still help with high blood pressure. The 2025 American Heart Association/American College of Cardiology clinical practice guidelines state that a moderate increase in potassium alone can lower blood pressure by approximately 6/4 mmHg on average, she said.

“However, the most powerful way to reduce and control blood pressure is a combination of increasing potassium while sticking to a low sodium diet,” Hernandez stressed.

“The balance is key. A patient should never assume that diet alone will reduce blood pressure completely. Dietary changes complement medication,” Pianko said.

When asked how people can tell if they need to increase their potassium intake, Hernandez offered the following advice:

“A good starting point when considering if you should increase your potassium or not is to start with a food journal. There are some great apps and online journals available that can provide an estimate of your potassium intake”

“Taking this information to your physician or dietitian is a great place to start the conversation as well as set specific realistic goals on how much potassium to aim for daily, as well as ideas on how to reach your daily potassium goal,” she said.

How fast can people expect to see results?

Increasing potassium intake is unlikely to have immediate effects and may take many weeks to show results.

“The response is very individual. Some respond within a week, and others need more time to see a change in blood pressure. Some factors that influence response include medications, genetics, and age,” Pianko said.

Daaboul said this timeline can range from a few days to a week. He explained:

“Early on, the lowering of the sodium will reduce the blood pressure by reducing the total body volume in the body. Eventually, the heart and the kidneys flush the sodium out of the body (mainly through the urine), resulting in the drop in blood pressure that we see early on. Then over time, within the first 1–2 weeks, the potassium effect kicks in, whereby potassium helps relax the blood vessels and maintain the progressive decline of the blood pressure until it stabilizes in a few weeks.”

“Note, however, that the blood pressure numbers should be monitored throughout, and if the final blood pressure numbers (despite the diet interventions) do not result in reaching the blood pressure goal over time, then it would be best to consult your doctor on combining the diet with other strategies to reduce blood pressure, such as adding an exercise regimen or prescription medications,” he added.

• Climbing stairs regularly was associated with reduced incidence of cardiovascular disease, including heart attacks and stroke, a new review has found.
• Those who frequently took the stairs were less likely to die from cardiovascular disease and all causes than those who climbed stairs less often.
• As physical inactivity can increase the risk of cardiovascular disease, stair-climbing, for as little as 6 flights of stairs, could be a simple and accessible way for people to add more exercise to their routines.

New research could help people who have to decide between using an elevator and taking the stairs. A study reports that regularly climbing stairs could significantly reduce the risk of dying from cardiovascular disease.

Researchers from the University of East Anglia (UEA) and Norfolk and Norwich University Hospital in the United Kingdom carried out the study, published in the American Journal of Cardiovascular Drugs.

Their findings are of particular note, given the rising prevalence of cardiovascular disease.

“Cardiovascular disease is the leading cause of death worldwide, with cases nearly doubling between 1990 and 2019,” explained Prof. Vassilios Vassiliou, one of the study authors from UEA, in a press release.

“[Cardiovascular disease] is largely preventable through a healthy lifestyle — including regular physical activity, a heart-healthy diet, not smoking, maintaining a healthy weight, and managing blood pressure, cholesterol, and diabetes.”
— Prof. Vassilios Vassiliou, study author

This rise in cardiovascular disease, including coronary artery disease and stroke, represents a total of 523 million cases worldwide, according to the study authors.

What did the researchers set out to investigate?

As physical activity is a known risk factor for cardiovascular disease, and previous research has linked it to prevention, the researchers were keen to investigate a form of exercise that might help adults meet physical activity recommendations.

“Taking the stairs is a practical and often overlooked way to build physical activity into daily life,” said Prof. Vassiliou in the press release. “We wanted to better understand how this everyday activity could have life-saving potential.”

Stair-climbing is a form of vigorous physical activity. Previous research has indicated that adding stair-climbing to a weekly routine can lead to improvements in cardiorespiratory fitness, among other health benefits.

“With more than a quarter of adults worldwide failing to meet recommended activity levels, choosing to take the stairs offers a realistic, scalable intervention,” said Prof. Vassiliou.

As a result, the researchers set out to see how stair-climbing might affect the incidence of cardiovascular disease — including heart attacks, stroke, and heart failure — and deaths from cardiovascular disease.

What did the study find?

The researchers conducted a systematic review and meta-analysis of 9 studies involving 480,479 participants with a median follow-up of 14 years.

The pool of study participants was:

• ages 35 to 84 years old
• included people with a history of heart problems as well as otherwise healthy people
• 53% female

“After pooling results from over 450,000 participants, we found a consistent association between stair-climbing and lower risk of both cardiovascular death and overall mortality,” said Sophie Paddock, one of the study authors from UEA, in the press release.

Specifically, the review found that people who often climbed stairs had a 39% lower risk of dying from heart-related issues and 24% less likely to die from any cause compared with those who did not climb stairs often.

A specific sub-analysis included in the review suggested that around 6 flights (or ~60–70 steps per day) was when participants saw a sweet-spot reduction in cardiovascular risk. The researchers also reported that people who regularly climbed stairs were less likely to develop cardiovascular disease.

“Some of the studies we looked at showed that the more stairs climbed, the greater the health benefits,” said Paddock. “But even small changes had a measurable impact.”

Short bursts of stair climbing offer cardiovascular benefits

Medical News Today asked Paddock what was already known about people who frequently took the stairs.

“We know that habitual stair-climbing may co-occur with other health-seeking behaviors, so those that tend to take the stairs may well have overall higher physical activity levels or fitness levels compared to those that don’t,” she explained.

MNT also spoke to Paul Drury, MD, a board certified cardiologist and associate medical director of electrophysiology at MemorialCare Saddleback Medical Center in Laguna Hills, CA, who was not involved with the study. Drury was not surprised by the findings.

“Even one- to two-minute bursts of movement performed several times throughout the day can add up and may be associated with a lower risk of cardiovascular events and death,” he said.

“Climbing stairs is a practical example of this type of higher-intensity activity, so these findings are consistent with the broader evidence supporting the benefits of incorporating movement into daily life,” he added.

Potential limitations

The researchers noted a few limitations in the studies they analyzed for their review, suggesting that further research will be useful in supporting their conclusions.

One key issue was that many of the studies in the review relied on self-reports, meaning that what participants reported may not accurately reflect what happened.

Another shortcoming was that many of the studies measured stair-climbing in different ways. Some looked only at stair-climbing at home and excluded any that occurred in public or at work. Others investigated participants’ ability to climb stairs without difficulty rather than how much they climbed. This inconsistency makes the overall picture less clear.

“It is important not to interpret this as proving that stair-climbing itself prevents heart disease,” said Opel Baker, MBChB, general practitioner at the Mayfield Clinic, who was not involved in the study, in an interview with MNT.

“Much of the evidence is observational, so people who climb stairs regularly may also be healthier or more physically active in other ways. The findings therefore support, rather than fundamentally change, our knowledge of the relationship between physical activity and cardiovascular health.”
— Opel Baker, MBChB

The researchers suggest that future research will be needed to determine exactly what amounts and forms of stair-climbing are best for improving cardiovascular health.

“None of the studies included in our analysis utilized wearable trackers,” Paddock told MNT. “This represents an exciting opportunity for further research into this area as it will provide a more objective measure of stair-climbing and other physical activity behaviors rather than relying on self-reported data.”

‘Even brief periods of activity can be meaningful’

Although there are some limitations in what the review can confirm, it is another piece of evidence showing how beneficial taking the stairs can be.

“Unlike going to the gym or doing a workout, climbing the stairs is something you can easily fit into your day at home, at work, or when you’re out,” said Paddock.

“[Climbing stairs is] a good option for people who don’t have much time or easy access to exercise. So if you have the choice of taking the stairs or the elevator, go for the stairs as it will help your heart.”
— Sophie Paddock, study author

The present research was unable to determine an ideal amount of stair-climbing to achieve specific cardiovascular benefits. Still, the researchers state that any additional physical activity is likely to be useful.

“Even brief bursts of physical activity have beneficial health impacts, and short bouts of stair-climbing should be an achievable target to integrate into daily routines,” said Paddock.

The researchers note, however, that stair-climbing is not an exercise suitable for everyone. Due to the additional pressure it places on the leg joints, it may not be appropriate for people with osteoarthritis, musculoskeletal disorders of the legs, or impaired mobility.

Alternatives to stairs

“For people unable to climb stairs, there are plenty of alternatives. Brisk walking, cycling, swimming, water-based exercise, rowing, and adapted seated exercises can all raise the heart rate and provide cardiovascular benefits. Strength exercises such as sit-to-stands can also help replicate the muscular demands of stair-climbing.”
— Opel Baker, MBChB

Otherwise, the researchers believe that taking the stairs could play a role in the ongoing issue of cardiovascular disease in public health.

“Encouraging people to take the stairs in workplaces, public buildings, and homes could form part of a wider strategy to reduce cardiovascular disease at the population level,” suggested Prof. Vassiliou.

“I view this study as a reminder that cardiovascular exercise does not have to come exclusively from a structured workout,” said Drury. “The important message is to find safe ways to move more and sit less. Even brief periods of activity can be a meaningful part of an overall strategy for protecting cardiovascular health.”

• A recent mouse study suggests that polyethylene, a major source of microplastics that was thought to be biologically inert, may increase the risk of liver disease or worsen an existing liver condition.
• The research found that exposure to polyethylene affected liver metabolism in mice by altering genes involved in tissue repair and damage response.
• However, these findings do not yet confirm that polyethylene directly causes liver damage in humans.
• To minimize microplastic exposure, experts recommend avoiding heating food in plastic containers, using glass or stainless steel for food storage, among many other steps.

Microplastics are tiny plastic particles smaller than 5 millimeters (mm). As they can enter the body through food and drink, primarily via environmental contamination or by direct shedding from plastic packaging, researchers are concerned about their potential effects on human health.

A recent study published in Science Advances suggests that polyethylene, the most widely produced plastic worldwide, could affect liver health by increasing the risk of a type of liver disease called metabolic dysfunction-associated steatotic liver disease (MASLD) or worsening an existing condition.

However, because this was a mouse study, it does not yet establish that exposure to polyethylene can directly lead to liver disease in humans.

“Polyethylene is one of the most widely produced and used plastics, especially in food packaging (such as freezer bags, plastic wraps, and paper milk carton coatings, as well as disposable bottles, beverage cups, and squeezable containers), yet its effects remain understudied. Therefore, we chose to investigate how polyethylene may impact metabolism, a key function of the liver,” explained Adi Joshi, PhD, study author, in an interview with Medical News Today.

Polyethylene increases liver damage risk in mice

The study authors started their investigation on the possible effects of polyethylene by feeding mice either a control diet or a diet designed to induce metabolic dysfunction-associated steatohepatitis (MASH). The MASH diet was high in fat, fructose, and cholesterol.

The researchers orally administered polyethylene to the mice every day for 8 weeks. They then performed various analyses, such as spatial transcriptomics, which measures gene activity.

They found that both groups experienced liver problems as a result of exposure to polyethylene. In particular, the researchers noted changes in peroxisome proliferator-activated receptor alpha (PPARα), a nuclear receptor that regulates annexin A2 (ANXA2).

The study authors note that ANXA2 is involved in tissue recovery and damage response. Changes to this gene could impair typical liver function.

How significant are these findings from a human health perspective?

While this particular animal study has identified polyethylene as a possible risk factor for liver disease, causation in humans is not yet confirmed.

“The findings suggest that polyethylene microplastics may affect liver metabolism and potentially contribute to fatty liver changes in mice, but we cannot assume the same effect occurs in humans,” said Opel Baker, MBChB, general practitioner at the Mayfield Clinic, who was not involved in the study, in an interview with MNT.

“More human research is needed before we can say that microplastics are a cause of fatty liver disease,” Baker added.

The study did find that polyethylene exacerbated liver injury in those following the MASH diet.

“Those who have a more Western-style diet, including foods like burgers and sodas, may have a greater chance of progressing to fatty liver disease if they are also exposed to polyethylene,” said Joshi in the press release.

Limiting foods that could increase the risk of liver problems could help reduce this risk, though further human-based research is necessary to determine the role of microplastics.

Joshi discussed areas for further exploration with MNT.

“The next steps are to investigate whether polyethylene contributes to later stages of liver disease, such as fibrosis; to explore the comprehensive molecular mechanisms involved in the body’s response to microplastic exposure; and to determine whether targeting specific pathways could help mitigate polyethylene’s harmful effects on the liver.”
— Adi Joshi, PhD, study author

“Additionally, investigating the direct causal relationship between microplastics and liver disease in humans will be a critical next step,” he said.

How can a person avoid polyethylene and other microplastics?

As Baker explained, “It is impossible to eliminate exposure [to microplastics] completely, so I would focus on simple, practical measures rather than becoming anxious about it.”

To minimize exposure to polyethylene and other microplastics where possible, Baker suggests that people:

• Avoid heating food in plastic containers
• Use glass or stainless steel for storing food where possible
• Reduce reliance on single-use plastics
• Avoid keeping very hot food or drinks in plastic

Ultimately, Baker advised that, “Most importantly, there is currently no need for a specific ‘detox’ or treatment to remove microplastics from the body.”

How to further reduce liver disease risk

While the recent animal study suggests that polyethylene may contribute to the development of liver disease, it does not confirm that avoiding microplastics can help reduce the risk in humans.

However, there are still steps a person can take to help manage some common risk factors.

“For now, the best way to protect your liver remains focusing on the fundamentals: maintaining a healthy weight, eating a balanced diet, exercising regularly, managing conditions such as diabetes, and limiting alcohol,” Baker advised.

“Further human research will help us understand whether microplastics have a meaningful role in liver disease,” he added.

• Estrogen levels decrease during menopause, and this may increase the risk for Alzheimer’s disease. 
• Experts are interested in understanding how the use of menopausal hormonal therapy affects Alzheimer’s disease risk.
• One retrospective study identified that estrogen-only menopausal hormonal therapy may help to protect against outcomes related to Alzheimer’s disease and dementia.

Menopause is the complete end of experiencing menstrual periods, and it can increase the risk for certain health problems, such as stroke. A recent study published in Neurology, the medical journal of the American Academy of Neurology, notes that estrogen levels drop during menopause, and that this could lead to a higher risk for Alzheimer’s disease.

This study found that estrogen-only menopausal hormonal therapy was associated with better Alzheimer’s disease and dementia outcomes.

In the study, women who used estrogen-only menopausal hormonal therapy were less likely to show increased Alzheimer’s disease pathology, had lower chances of memory decline symptoms, and had lower chances of having a dementia diagnosis.

However, much more research is required to fully determine the possible protective impact of estrogen-only menopausal hormonal therapy.

How menopausal hormonal therapy affects dementia risk

The data on how menopausal hormonal therapy affects dementia is mixed, with many factors at play. The current research chose to focus exclusively on estrogen-only menopausal hormonal therapy and how this relates to aspects of Alzheimer’s disease and dementia.

Researchers collected data from the National Alzheimer’s Coordinating Center (NACC) and the Alzheimer’s Disease Neuroimaging Initiative (ADNI).

From this first data set, they examined data from 258 participants who used estrogen-only menopausal hormone therapy and 2,701 participants who did not. From the second data set, there were 110 participants who used estrogen-only menopausal hormonal therapy and 1,948 participants who didn’t.

This definition of estrogen-only menopausal hormonal therapy did not include topical use of estrogen. Researchers excluded participants who reported taking combinations of estrogen and progestin. A majority of participants were white, and the average age was between 71 and 72 years.

For some participants, researchers were able to look at data from brain autopsies, allowing them to look at several components related to Alzheimer’s disease pathology, like amyloid deposits.

Estrogen-only therapy linked to lower risk

Based on autopsy data, researchers found that participants using estrogen-only menopausal hormonal therapy had a lower chance of increased scores for Alzheimer’s disease pathology.

Estrogen-only menopausal hormonal therapy was also linked to better outcomes in other brain areas, like lower chances of infarcts, which are areas of tissue death because of a lack of blood supply.

Researchers also found evidence that amyloid load was better for estrogen-only menopausal hormonal therapy users, which indicated better Alzheimer’s disease pathology compared to non-users.

Among the NACC dataset, researchers found that estrogen-only users had a lower chance of having a clinical diagnosis of dementia and a lower chance of experiencing clinical decline.

In the ADNI group, estrogen-only menopausal hormonal therapy was linked to better immediate memory and learning. A subgroup analysis of participants in the ADNI group who did not have dementia found that estrogen-only therapy was linked to better verbal memory.

In addition to these outcomes, researchers also performed several exploratory analyses in subgroups, such as based on the type of estrogen-only menopausal hormonal therapy.

What about those with genetic Alzheimer’s risk?

The researchers found that non-APOEe4 carriers who also used estrogen-only menopausal hormonal therapy had a lower chance of experiencing Alzheimer’s disease neuropathology.

The researchers did not observe this result in APOE e4 carriers. The APOEe4 gene can increase the risk for Alzheimer’s disease. In both carriers and non-carriers, estrogen-only use was linked to less serious clinical diagnoses and better clinical dementia rating global scores.

There were some differences when it came to the type of estrogen used. For example, conjugated estrogen users (people taking a blend of estrogen hormones) saw a lower chance of experiencing increased Alzheimer’s disease neuropathology, while the risk for those using estradiol was similar to that of non-estrogen users.

Finally, starting estrogen-only menopausal hormonal therapy prior to age sixty was linked to a lower risk for Alzheimer’s disease neuropathology, but this link didn’t reach a level of statistical significance.

Study author Jennifer Bruno, PhD, Instructor of Psychiatry and Behavioral Sciences at the Stanford University School of Medicine, explained the following regarding the study’s findings:

“We found that, on autopsy, women who had used estrogen-only hormone therapy had 35% lower odds of showing the hallmark brain changes of Alzheimer’s disease: amyloid plaques, tau tangles, and neuritic plaques, compared to women who had not used hormone therapy.”

“These autopsy findings were supported by blood and spinal fluid biomarkers collected while women were still living, which also pointed to lower levels of amyloid accumulation in the brain,” she continued.

“In addition, estrogen-only hormone therapy users had lower odds of receiving a clinical dementia diagnosis and showed better performance on memory tests. Importantly, these associations held after we accounted for key risk factors including age, genetics, education, race, and hypertension,” she added.

Study limitations

When it comes to limitations, it’s important to note that this study doesn’t establish any causality. It only shows associations. Second, there is a reliance on participant reporting, such as the self-report of estrogen-only menopausal hormonal therapy, sex, and age.

A majority of the participants were white, limiting generalizability to other groups. There’s also limited generalizability because estrogen-only therapy is currently only appropriate for women who have had hysterectomies.

The average age of participants also doesn’t relate to current practices of menopausal hormonal therapy, where doctors may prescribe estrogen-progesterone therapy to women in the period prior to menopause, perimenopause.

Confounding is possible from multiple factors. Researchers note that the results could have been confounded “by improved pre-existing health status of the MHT [menopausal hormonal therapy] group.”

This research also only focused on estrogen-only therapy, so it cannot speak to the use of other hormones or hormone combinations. There was only autopsy data for a subgroup of participants, and some subgroup analyses were also limited, such as looking at the different types of estrogen therapy.  

Researchers were limited by the datasets they used, which included missing and sparse data. They were not able to confirm exactly when participants started hormone therapy. The authors note that the results cannot be generalized “to represent associations between life-time estrogen exposure and dementia outcomes” because they lacked data on how long estrogen-only menopausal hormonal therapy was used or on its use before the start of the study.

They also lacked data on topical estrogen use in the NACC data set. The sample size in the ADNI data was also small, so the researchers note that the findings in this group are exploratory. Other secondary outcomes were also exploratory. Finally, funding came from several sources.  

Does estrogen have a protective effect against dementia?

This data suggests a possible protective effect of estrogen-only menopausal hormonal therapy, but there’s a major need for more research before major clinical changes can occur.

Dung Trinh, MD, internist of MemorialCare Medical Group and Chief Medical Officer of Healthy Brain Clinic in Irvine, CA, who was not involved in the study, noted the following:

“The findings do not support prescribing menopausal hormone therapy specifically to prevent Alzheimer’s disease or dementia, since randomized trials have not established such a benefit. Instead, the study highlights the importance of taking a more individualized, life-course approach to women’s brain health.”

“Factors such as age at menopause, type and timing of hormone therapy, APOE status, vascular risk, and whether menopause was premature or surgical may eventually help clinicians better understand cognitive risk and personalize care, but more evidence is needed before these factors change routine Alzheimer’s prevention recommendations,” Trinh explained.

Additionally, despite the possible protective effects of estrogen-only therapy, it’s not something that’s always appropriate.

“Our findings are most directly relevant to women who have had a hysterectomy by age 60 (roughly 1 out of 3 women), since estrogen-only therapy is appropriate only for women without a uterus. For women with an intact uterus, combined estrogen-plus-progestin therapy is the standard approach,” Bruno noted.

“For the subset of women who have had a hysterectomy, our results suggest that estrogen-only hormone therapy may have a protective association with Alzheimer’s-related brain changes. These findings do not change current clinical recommendations, but they do add an important new line of evidence: neuropathological data from autopsied brains,” she added.

• On Monday, August 10, 2026, President Donald Trump signed an executive order recommending separate measles, mumps and rubella vaccinations.
• The executive order also recommended limiting core vaccinations to 11, and stopping vaccinations for hepatitis B, COVID-19 and influenza in young children.
• Public health experts, researchers and clinicians disagree with his premise, pointing out that decades of studies have shown there is no foundation for his claims of a link between combined shots and autism.
• They also highlight the added risks of infection, missed vaccinations, and increased costs, of getting individual vaccinations in separate appointments rather than receiving them in one shot.

With the United States almost certain to lose its measles elimination status for the first time since 2000 following a surge in infections this year, President Donald Trump this week signed an executive order advocating that measles, mumps and rubella vaccinations should be given as three separate shots, rather than the combined MMR vaccine.

In a long press conference, President Trump reiterated the disproved claim of a link between vaccines and autism, and recommended that 1-year-olds receive their childhood vaccinations in five separate medical appointments.

Health professionals have united in opposing the proposal, with the American Academy of Pediatrics disputing the recommendations. 

And the Republican chair of the Senate health committee, Louisiana senator Bill Cassidy, who is a medical doctor, said on social media, as reported by The BMJ: “This executive order is wrong. The President does not have the expertise to make these changes.”

Jennifer M. Walsh, DNP, CPNP-PC, CNE, Assistant Professor at George Washington University School of Nursing, practicing Primary Care Pediatric Nurse Practitioner and Certified Nurse Educator, is one of many speaking out against the recommendations.

Walsh told Medical News Today:

“There is absolutely no benefit to giving the measles, mumps, and rubella vaccines separately versus the combined MMR. But there are risks to dividing it up — risks to children being unprotected by delaying recommended vaccination, financial risk to families due to the need for multiple visits/time off work/missed work due to multiple side effects necessitating time off from work/daycare, and increased financial and workload burden to the health care system necessitating multiple visits. There is also the risk of trauma to the child by repeated, unnecessary visits to the provider’s office to complete the recommended series.”

Experts criticize reiteration of disproved link to autism

President Trump once again repeated the claim that vaccines, particularly the combined MMR vaccine, are linked to an increased risk of autism, despite many decades of research finding absolutely no evidence for this.

The link was first purported in a 1998 study which has since been retracted as it was found to be based on fake, fraudulent data from just 12 children.

Many studies since have found absolutely no evidence of an association between MMR and autism, but misinformation lingers and has contributed to a drop off in uptake of the vaccines and a huge rise in cases of these preventable infections. 

Further evidence against a link continues to accumulate. A study just published in the Pediatric Infectious Disease Journal, which followed 2,560,035 U.S. children from birth to 8 years old, and controlled for bias, found “no association between MMR vaccination before 24 months and childhood autism.”

“The false connection between vaccines and autism has been a decades-long misinformation assault on families. Pediatric providers are experts at discussing this with parents — we do it each and every day. It honestly leaves us flabbergasted that politicians are deliberately spreading misinformation and ignoring decades of research that has proven repeatedly that there is no link.  The false narrative serves no purpose but to fearmonger and put children at increased risk of vaccine-preventable infections.”

– Jennifer M. Walsh, DNP, CPNP-PC, CNE

Several other experts have made their views clear. In a reaction shared with the Science Media Centre, David Salisbury, FMedSci, Associate Fellow in the Programme for Global Health at the Royal Institute of International Affairs, Chatham House, in the U.K. was forthright.

“There is not a shred of evidence that the provision of single vaccines would prevent autism,“ said Salisbury. “There is a wealth of evidence that has failed to find a link between vaccines, especially MMR, and autism.“

“When Wakefield [author of the retracted study claiming a link] demanded the provision of single vaccines in the U.K. in the late 1990s and early 2000s, the manufacturers made clear that they would not provide them, not least because they were no longer licensed,“ he pointed out.

“Twenty-five years later, the situation in the U.S is the same. Single vaccines are not licensed,” Salisbury emphasized, expressing surprise that the President did not appear to be aware of this.

Other vaccine recommendations: What to know

The executive order also stated that hepatitis B, COVID-19, and influenza vaccinations were no longer recommended for all children, falling into the “shared clinical decision-making” category, a move that Walsh said had “absolute risks.”

“Hepatitis B is a preventable infection that can cause liver disease, cancer, and liver failure. Since the routine recommendation for hepatitis B vaccination starting at birth, we have seen millions of children protected against chronic infection and cancer,” she explained. 

“Yearly flu vaccination, starting at 6 months of age, has proven to significantly decrease outpatient visits, ER visits, hospitalizations, and even death in children. COVID vaccination is recommended for all children ages 6–23 months, as well as any children with underlying health issues, due their increased risk of complications.”

And Sir Andrew Pollard, Director of the Oxford Vaccine Group and Ashall Professor of Infection and Immunity, Pandemic Sciences Institute and Department of Paediatrics, University of Oxford, U.K. told the Science Media Centre:

“The U.S. administration’s decision to reduce the number of vaccines recommended for children, deprioritising jabs with a proven track record of effectiveness against serious diseases, and questioning the proven safety of vaccines in the process, undermines public confidence in the cornerstone of child health in the country.“

“Changes in vaccination programmes can be appropriate when disease risk changes or new evidence emerges, but such changes should be driven by scientific evidence developed by individuals with the necessary expertise and not by whim, because the lives of children are at stake,” Pollard continued. 

What should parents do?

Speaking to MNT, Jagdish Khubchandani, PhD, a Professor of Public Health at New Mexico State University, reiterated that “separate measles, mumps, or rubella vaccines are currently unavailable in the U.S. and may need testing or FDA approval when they have to be made available.“

“ Further, many practitioners may see this as a burden to invite parents/children to the office three times instead of one — e.g., scheduling issues, timing, transport, etc,” Khubchandani pointed out.

“In practice, the executive order may not change much, and the CDC vaccination schedule has not changed either,” he told MNT. “Even if approved, the proposed changes could take months to years.”

Despite some states having already changed school entry requirements, which “leaves their population at increased risk of disease and death,” Walsh reassured that many states will continue to follow medical evidence on childhood vaccinations.

“In the U.S., childhood vaccination recommendations are provided by the American Academy of Pediatrics. States can determine which vaccinations may be required for school entry. Many states have already insisted that they will continue to follow the AAP recommendations, since those are based on scientific evidence,” she told us.

“In the meantime, parents should continue seeking guidance from their child’s doctor and avoid paying attention to all the buzz around this topic. Nothing has changed or will change, at least for the rest of this year.”

– Jagdish Khubchandani, PhD

• Ovarian cancer, doctors explain, can be hard to treat as it may go undiagnosed for a long time. That also makes the cancer more likely to spread through the body.
• Researchers from The Wistar Institute at the University of Pennsylvania wanted to know what, exactly, makes it easier for ovarian cancer to spread, particularly in cases where it has already been subjected to chemotherapy.
• Through experiments in animal models they found that one particular nutrient — namely, fructose — can help boost the signalling of cancer cells, thus facilitating metastasis.

In 2026 alone, an estimated 21,010 people will have received a new diagnosis of ovarian cancer in the United States. This type of cancer has a 52% relative 5-year survival rate, which doctors and other medical experts are working hard to improve.

One of the most common types of treatment for ovarian cancer is chemotherapy but this does not result in the cancerous cells clearing up in every case, which can mean that the cancer may end up spreading further throughout the body, a phenomenon known as metastasis.

Recently, researchers from The Wistar Institute at the University of Pennsylvania, PA, set out to gain a better understanding of the mechanisms behind ovarian cancer metastasis.

“Chemotherapy remains one of the best treatment strategies for many cancers, including ovarian cancer. Unfortunately, some cancer cells can survive chemotherapy, and those cells release factors that influence cancer progression,” Katherine Aird, PhD, Professor and Co-Leader in the Molecular and Cellular Oncogenesis Program at the Ellen and Ronald Caplan Cancer Center, The Wistar Institute, told Medical News Today.

Aird is the senior author of a new preclinical study, which looked at how ovarian cancer cells that escape chemotherapy are able to spread throughout the body.

The study’s findings, which appear in Nature Aging, point the finger at a seemingly surprising culprit: fructose.

Why chemotherapy doesn’t always stop ovarian cancer from spreading

Cancers affecting the female reproductive system, such as ovarian cancer, “frequently present with vague or no symptoms in its early stages, such as bloating, pelvic pain, and feeling full quickly, which can be mistaken for other common conditions,” said Ami Vaidya, MD, Co-Chief of the Division of Gynecologic Oncology at the Hackensack University Medical Center, who was not involved in the study.

Thus, Vaidya noted, “most cases are diagnosed at an advanced stage when the cancer has already spread.”

Moreover, according to Nathan Goodyear, MD, an integrative medicine physician, board-certified in obstetrics and gynecology, co-founder of Williams Cancer Institute, who was likewise not involved in this study:

“Ovarian cancer is uniquely challenging because it is often biologically primed for metastasis long before it is clinically detected. Moreover, metastasis occurs far earlier in high-grade serous ovarian cancer than previously thought possible. Once metastatic, these disseminated tumor cells can persist in dormant or slow-proliferative states, hiding below the surface of detection of current lab and imaging modalities.”

In their recent study paper, the researchers explain that chemotherapy commonly induces a response called “cellular senescence” in cancer cells.

When a cell becomes senescent, it becomes, in some sense, stable, as it stops dividing further. However, the cell remains “alive.”

The question that then arises is: If senescent cancer cells stop dividing, how, then, is the cancer still able to spread throughout the body?

Past research has suggested that the spread may not always be a result of straightforward cellular division.

Instead, senescent cancer cells that have survived chemotherapy are able to secrete chemical messengers that then induce certain responses in the cells around them, thus allowing the cancer to continue spreading.

How fructose may help ovarian cancer spread

With this premise in mind, the researcher team at The Wistar Institute collected ovarian cancer cells that had been exposed to chemotherapy and survived. They were then able to further collect the signaling molecules released by those cells and expose other cancer cells to them, to see how they would respond.

Using animal models, the researchers were able to confirm that, just by being exposed to those signaling molecules, the cancer cells increased their ability to spread.

Notably, the researchers also found that senescent cancer cells that had survived chemotherapy released fructose, and that it was this nutrient that played a key role in “telling” other cancer cells to multiply.

“We discovered that cells surviving chemotherapy release fructose, the same sugar found in fruits and high-fructose corn syrup,” Aird told MNT.

She explained that:

“This fructose can be processed by cancer cells in a way that makes them more capable of spreading by decreasing the cellular glue that holds cancers together.”
— Katherine Aird, PhD

That “cellular glue,” as it turns out, is cholesterol. According to the researchers’ analyses, the “messaging” fructose lowers cholesterol production when it reaches other cancer cells.

This lack of cholesterol is what assists those cancer cells in spreading faster: Essentially, cholesterol holds clusters of cells together. When the cholesterol is lacking, the cells are able to detach and spread.

Could a high-sugar diet play a role?

The team also found something else, namely “that a high fructose diet alone increased cancer spread,” Aird told us.

High levels of dietary fructose — from sugary beverages, for example — appeared to speed up the spread of cancer in the absence of chemotherapy.

While the researchers have not confirmed to what extent dietary choices can influence the spread of ovarian cancer, this finding does seem to encourage caution and adherence to healthy, less sugary diet types.

“There are many potential implications to our work, although […] this is a preclinical study, and none of our findings have yet been confirmed in humans,” noted Aird.

“The first implication,” she said, “is that chemotherapy can have negative consequences. This doesn’t mean we should stop giving patients chemo, but instead that we need to learn more about these negative effects so that we can prevent them.”

“The second is that a high fructose diet could lead to worse cancer outcomes. Finally, we identified that fructose is processed in cancer cells in a way that leads to decreased cholesterol. This could have potential implications for patients on statins, drugs that lower cholesterol.”
— Katherine Aird, PhD

“All of these need to be further studied before we can make an definitive claims for ovarian cancer patient care,” cautioned the study author.

Is our understanding of fructose changing?

Goodyear further commented on how this study changes experts’ perspective on fructose and its potential role in health. “In this study, the authors showed that fructose sits at the crossroads between chemotherapy-induced senescence and metastasis,” he told us.

“Most are familiar with fructose as a component of the rapid rise of ultraprocessed foods post-1970s, driven by high-fructose corn syrup (HFCS),” said Goodyear. “Yet here, fructose is not the microbiome reprogrammer, the immune modulator, or simply ‘fructose bad’.”

“This study reframes fructose as the fuel that drives metastatic dissemination via chemotherapy-induced senescent cell metabolic reprogramming that allows neighboring cancer cells to exploit [other] cancer cells,” he emphasized.

“Our reaction should be a great pause. If chemotherapy induces the means to exploit fructose to enable metastasis and the success of metastasis, then increased availability of the fructose substrate in combination would pose a significant metastatic risk. Of note, a common thought is that diet does not matter when it comes to support of conventional cancer treatment. Yet, most chemotherapy practices supply ultraprocessed foods, in candy bars, baked goods, and soft drinks, increasing the metabolic driver in a reprogrammed environment which can exploit their availability. The authors of this study directly refute these outdated claims based on mechanisms.”
— Nathan Goodyear, MD

Shifting the outlook on chemotherapy for ovarian cancer

“The findings in the recent study represent a significant paradigm shift in understanding cancer metastasis,” said Vaidya, who also qualified the findings on the role of fructose in cancer metastasis as “the most striking discovery.”

According to her, this study reveals important new avenues for exploration in the context of ovarian cancer therapy, but there is still a long way to go in terms of validating the findings:

“This crucial connection between chemo-resistance and metastasis opens up promising new avenues for therapeutic strategies, potentially including dietary interventions or drugs that target this specific fructose-cholesterol pathway. While the researchers suggest this mechanism could be relevant for other abdominal cancers and raise questions about the interplay with common medications like statins, it is important to remember that these are preclinical findings that require further validation in human studies before clinical applications can be considered.”
— Ami Vaidya, MD

Goodyear likewise told MNT that “this study is important because it shifts thinking away from chemotherapy as simply a tumor-killing therapy to chemotherapy as a treatment that also changes the biological function of surviving cells.”

In his view, “one of the most important discoveries in this study is that metabolism — not genetics — is the principal driver of metabolic-reprogrammed metastasis.”

Going forward, Aird and her colleagues would like “to find a way to decrease fructose production by the cells that survive chemotherapy,” as she explained to MNT.

“Excitingly, there is an FDA-approved drug used in diabetic patients that may be able to do this. We are currently performing additional preclinical studies to examine this possibility,” Aird told us.

“We are also interested to identify other nutrients that are released by cells the survive chemotherapy. We think that this could inform additional studies on the negative consequences of chemotherapy. Finally, we hope to collaborate with physicians to understand whether dietary intake is associated with patient outcomes. This is our ‘pie in the sky’ goal, but one that I believe would be the most impactful. We could take knowledge found from these studies back into the lab to understand at a cellular and molecular level how diet influences cancer.”
— Katherine Aird, PhD

Expert advice on ovarian cancer and metastasis prevention

“Ultimately, while this [recent] discovery represents a significant scientific step forward that may lead to more effective treatments down the road, patients should continue to rely on their oncology team for all current health and treatment decisions,” Vaidya advised.

“Regarding ovarian cancer prevention, while there is no guaranteed method, risk can be significantly lowered through factors like using oral contraceptives, pregnancy, and maintaining a healthy lifestyle,” she noted.

“For high-risk individuals, especially those with genetic mutations like BRCA, genetic counseling and risk-reducing surgery are the most effective options,” said the oncologist.

“[M]aintenance of a healthy body weight, routine physical activity, smoking cessation, and adherence to dietary
patterns rich in whole-food vegetables, fruits, legumes, whole grains, and healthy fats while limiting, better yet eliminating, ultra-processed foods” can also help with prevention, added Goodyear.

“Since no reliable routine screening test exists, preventing metastasis after a diagnosis becomes the central goal of treatment. This is primarily achieved through a comprehensive and aggressive approach combining cytoreductive (debulking) surgery to remove as much cancerous tissue as possible, followed by systemic treatments like chemotherapy and targeted therapies, such as PARP inhibitors, to eliminate remaining cells and prevent recurrence.”
— Ami Vaidya, MD

“Ultimately, diligent, long-term surveillance after treatment is critical to monitor for and manage any potential spread of the disease,” she emphasized.

• Researchers continue to examine how GLP-1 medications may affect aspects of a person’s health outside of type 2 diabetes treatment and weight loss. 
• Past studies show that GLP-1 drugs may help lower a person’s risk for cardiovascular disease.  
• A new study found that adding tirzepatide to standard care for people with both type 2 diabetes and heart disease may help lower their risk for a major cardiovascular event.

As the use of glucagon-like peptide-1 (GLP-1) receptor agonist medications continues to rise, researchers are examining how these medications might affect other aspects of a person’s health outside of type 2 diabetes treatment and weight loss. 

Past studies show that GLP-1 drugs may help lower the risk for or treat conditions like kidney disease, metabolic syndrome, liver disease, sleep apnea, alcohol use disorder, Alzheimer’s disease, and cardiovascular disease.

Now, a new study published in the journal The BMJ reports further evidence of a link between GLP-1 medications and heart health benefits. 

The researchers found that adding the GLP-1 medication tirzepatide — the active ingredient in Mounjaro and Zepbound — to standard care for people with both type 2 diabetes and heart disease may help lower their risk for a major cardiovascular event, such as a stroke or heart attack.

Tirzepatide vs sitagliptin for MACE reduction

For this study, researchers analyzed clinical practice data from almost 53,000 people with both type 2 diabetes and heart disease. 

Study participants were split into two groups — one group started taking tirzepatide and the second group took the diabetes medication sitagliptin — and scientists measured any reduction in major adverse cardiovascular events (MACE), which include heart attack, stroke, and death from any cause.

“GLP-1–based medications were initially developed to improve glucose control, but their effects appear to extend well beyond blood sugar and weight loss,” Nils Krüger, MD, MPH, a physician data scientist in the Division of Pharmacoepidemiology and Pharmacoeconomics in the Department of Medicine at Brigham and Women’s Hospital in Boston, lead author of this study, told Medical News Today. 

“Cardiovascular disease remains the leading source of illness and death globally, so it is important to understand whether these medications can also reduce heart attacks, strokes, heart failure, and mortality,” Krüger continued.

“Studying these broader effects helps clinicians and patients make treatment decisions based on the full range of potential benefits and risks rather than on metabolic outcomes alone,” he said. 

Taking tirzepatide lowers heart attack risk by a third

At the study’s conclusion, researchers found that after one year, participants in the tirzepatide group had a 2.9% MACE risk, compared with 4.4% in the sitagliptin group.

Scientists also estimated that for every 70 study participants who started tirzepatide, one case of MACE could be prevented.

“These findings translate the relative effect into a measure that is tangible for clinicians and patients,” Krüger said.

“The 1.4-percentage-point absolute difference means that, among patients similar to those in our study, treating approximately 70 people with tirzepatide rather than the cardiovascular-neutral comparator for one year would be associated with one fewer major cardiovascular event.” 
— Nils Krüger, MD, MPH

Additionally, researchers discovered that tirzepatide use was linked to a 33% lower risk of having a heart attack, when compared to sitagliptin. 

“The reduction in myocardial infarction is important because heart attack is one of the most serious and clinically consequential complications of diabetes and established cardiovascular disease,” Krüger explained. “The finding also suggests that the overall reduction in major cardiovascular events was not driven solely by mortality.” 

How does tirzepatide help lower MACE risk?

Krüger said the mechanisms behind tirzepatide possibly helping lower MACE risk are likely multifactorial. 

“Tirzepatide improves glucose control, reduces body weight, and may favorably influence blood pressure, lipids, inflammation, and other cardiometabolic risk factors. In our study, the cardiovascular event curves began to separate relatively early, before substantial weight loss would generally be expected, raising the possibility that vascular or anti-inflammatory effects may also contribute.”
— Nils Krüger, MD, MPH

“The lower risks of serious infections and infection-related mortality suggest that non-atherosclerotic pathways may be involved as well, although the exact mechanisms require further investigation,” Krüger added. 

Krüger said their next steps in this research are to examine whether these benefits persist over longer follow-up and can be replicated in other populations and healthcare systems. 

“We also want to better understand the mechanisms underlying the reductions in infection-related events, and to determine how tirzepatide compares directly with other cardiometabolic therapies, including other incretin-based treatments and SGLT2 inhibitors,” he added.  

More evidence of GLP-1’s cardiometabolic benefits

MNT spoke with Cheng-Han Chen, MD, a board certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center in Laguna Hills, CA, who commented that this study adds to a rapidly expanding body of evidence highlighting the cardiometabolic benefits of GLP-1 receptor agonists. 

“Beyond their established role in managing type 2 diabetes, these medications are increasingly associated with improved cardiovascular outcomes,” Chen, who was not involved in this study, explained. “GLP-1 receptor agonists have emerged as one of the most impactful therapeutic classes in recent years.”

“A growing number of studies demonstrate benefits across a spectrum of cardiometabolic conditions, suggesting these agents could play a meaningful role in lowering the overall burden of cardiovascular disease at a population level,” he added. 

Still need to know how GLP-1s will affect overall long-term health

MNT also spoke with Sanjeev Kumar Gulati, MD, FACC, executive deputy director of Baptist Health Heart & Vascular Care and system chief of cardiovascular medicine at Baptist Health South Florida, who likewise was not involved in this study. 

Gulati said that while these findings are encouraging and consistent with the growing amount of evidence suggesting that tirzepatide provides benefits beyond just blood sugar management and weight loss, the most important question is how they affect overall health and long-term outcomes. 

“As evidence continues to emerge regarding heart health, kidney protection, weight management, and other potential benefits, ongoing research will help us optimize care and ensure that the right patients receive the greatest benefit from these therapies,” he continued.

“I would like to see longer-term studies that help determine whether the cardiovascular benefits observed with tirzepatide are sustained over many years and whether they extend to broader patient populations, including those without established cardiovascular disease. Randomized studies will be important for us to have a better understanding of the potential benefits of tirzepatide.”
— Sanjeev Kumar Gulati, MD, FACC

• Metabolic dysfunction-associated liver disease (MASLD) is a common liver condition that requires careful management.
• Research is ongoing about what food choices are most helpful for managing MASLD.
• One exploratory randomized controlled trial in participants with MASLD found that eating tomatoes daily helped to decrease fat buildup in the liver. 

Metabolic dysfunction-associated liver disease (MASLD) includes a range of liver problems, but a main feature is hepatic steatosis, which is fat buildup in the liver.

For a diagnosis of MASLD, people also need to have at least one cardiometabolic risk factor like obesity or high blood pressure.

Diet and lifestyle changes can be helpful for people who have MASLD, and experts are interested in also understanding what specific food choices may be most helpful. 

A study published in Nutrients explored whether consuming tomatoes was helpful for individuals with MASLD.

Researchers found that participants who ate raw tomatoes and tomato sauce daily saw a greater decrease in hepatic steatosis than the control group.

While there is still a lot more research needed in this area, the results suggest a possible benefit for people with MASLD consuming more tomatoes in their diets.

Tomatoes and MASLD

The authors of this study wanted to see how tomatoes, a common food in the Mediterranean diet, affected liver steatosis.

This study enrolled of 79 adult participants who had MASLD. Researchers excluded certain participants, such as those who consumed over a certain amount of alcohol or had a body mass index of over 30, which indicates obesity. 

Researchers divided participants into two groups. One group followed a tomato-free control diet. The other ate 200 grams of raw tomatoes and fifty grams of tomato sauce each day.

All tomato products came from the same producer. Other than the intervention, researchers told participants to continue their normal lifestyles.

The tomato intervention lasted for 6 weeks. Researchers assessed a number of health indicators, including body composition, hepatic steatosis, liver stiffness, and cholesterol levels.

Researchers found that hepatic steatosis actually declined in both groups. However, there was a greater decrease for those in the intervention group.

Further evaluation indicated that hepatic steatosis was similar at baseline between the two groups. When it came to other measurements like liver stiffness, researchers did not find any major changes.

They also didn’t find any significant differences between the groups when it came to components like lipids, liver enzymes, and body mass index after the 6-week intervention time.

The authors suggest that their findings indicate that “tomato consumption may reduce hepatic fat accumulation independently of major changes in body weight, total and abdominal adiposity.”

Study limitations and continued research

The intervention time only lasted for 6 weeks, so any long-term benefits are not something this study can speak to. The research also only included adults aged 65 and younger, so it’s unclear how results may differ in older adults.

Most of the participants were men, so more balanced groups may be valuable in future research too. Additionally, excluding participants who had a body mass index of over 30 could have also limited the findings.

Endocrinologist and obesity specialist Randa Abdelmasih MD, DipABOM, from the University of Texas Medical Branch (UTMB), who was not involved in this study, told Medical News Today:

“The study demonstrates a modest reduction in hepatic steatosis over only six weeks in a highly selected population of adults with MASLD and BMI [body mass index] of 30 kg/m² [kilograms per square meter] or more. Most patients we see in clinical practice have obesity (BMI over 30 kg/m²), type 2 diabetes, or more advanced metabolic disease, so the generalizability of these findings is limited.”

Jonathan Jennings, MS, MD, a board-certified internist with Medical Offices of Manhattan, likewise not involved in this study, expressed a similar sentiment about the limitations of its findings.

“The inclusion criteria required only one cardiometabolic risk factor, and it could be any risk factor. I am concerned that not all risks are equal, and people with multiple factors are at higher risk than those with a single risk factor,“ Jennings told us.

“Type 2 diabetes is more likely to lead to MASLD than high blood pressure but the study evaluates them as equal risk factors,” he pointed out.

Researchers note that the reduction in liver fat could have been related to other factors, like how participating in a dietary intervention study may affect participants. Researchers were also limited by how they had to rely on dietary counseling and participants’ reports of actually following the intervention.

Abdelmasih noted that since the intervention combined raw tomatoes and tomato sauce, it’s “difficult to determine which component or combination was responsible for the observed effect.”

Additionally, researchers did not measure circulating amounts of lycopene and carotenoids, which are components that may be responsible for the possible impact of tomatoes on liver health.

Limited clinical application

The authors note that their study was exploratory, so it mainly helps to provide information for future research. They encourage that the findings need confirmation with bigger and more long-term research and encourage that people should interpret the findings as hypothesis-generating.

It’s also unclear how helpful the findings are in clinical practice since other factors remained unchanged.

Abdelmasih noted:

“The study showed improvement in liver fat but no significant improvements in liver stiffness, fibrosis scores, liver enzymes, insulin resistance, inflammatory markers, lipid profile, or body composition. Therefore, while the imaging findings are interesting, we cannot conclude that tomato consumption meaningfully alters disease progression or improves clinically relevant outcomes.”

Further clinical implications

While this study can only show so much, it does indicate a possible health benefit of eating tomatoes for people who have MASLD and a possible strategy that could help with fat buildup in the liver.

Tomatoes may bring other benefits as well. For example, they may offer cardiovascular benefits and even have anti-cancer properties.

People should work with their doctors and other health experts to create a dietary plan that addresses health concerns, rather than hyper-focusing on specific foods.

Jennings noted that:

“The study’s conclusions are hopeful but careful discussion with a healthcare provider is still needed before engaging in any radical dietary adjustments. Tomatoes and tomato-based products may be problematic for individuals with gastroesophageal reflux disease (GERD). Many tomato-based foods are also calorically dense and may worsen insulin resistance in certain individuals.”

It’s also important to look at the findings in the broader context as well.

According to Abdelmasih: “Dietary interventions should be viewed within the broader context of treating the underlying metabolic disease. For patients with obesity, sustained weight loss of approximately 10% or more remains the intervention with the strongest evidence for improving steatohepatitis and fibrosis.“

“While tomatoes can certainly be part of a healthy Mediterranean diet, they should not distract from therapies that have demonstrated meaningful improvements in liver and cardiometabolic outcomes,” she concluded.

• Arginine is an amino acid that supports multiple metabolic and immune functions.
• A new study in mouse models linked low arginine with reduced production of a protein that helps the immune system detect threats.
• Arginine supplementation reduced colon tumors and improved flu and COVID-19 outcomes in mice.

A new study led by Rockefeller University researchers found that arginine levels may affect how the immune system recognizes cancer cells and virus-infected cells.

The researchers tested arginine supplementation in mice and learned that as arginine levels increased, cancer tumors decreased and viral infection outcomes improved. 

Since arginine is relatively inexpensive, the scientists hope it could provide a low-cost addition to existing treatments if human trials confirm the findings.

The study appears in the journal Cell.

How arginine may influence the immune system

Arginine is an amino acid found in protein-rich foods such as meat, fish, dairy products, nuts, and legumes.

According to the National Human Genome Research Institute, amino acids serve as the “building blocks for proteins.” Arginine also supports immune function, blood flow, wound healing, and other processes.

The body produces arginine and obtains it through food. However, cancer and viral infections such as COVID-19 can reduce its availability. These conditions may activate immune cells that produce arginase, an enzyme that breaks down arginine. 

The researchers behind the new study wanted to determine whether these changes could directly affect the body’s immune response to cancer and viral infections.

First, they analyzed existing data on amino acid levels in cancer tissue and in lung tissue from mice with influenza or SARS-CoV-2 infections. Their analysis identified arginine as one of the most consistently depleted amino acids across these conditions.

Next, the researchers restricted arginine in human and mouse colorectal cancer cells. They also tested human cell lines from melanoma and breast, stomach, and pancreatic cancers.

The team measured levels of a protein called major histocompatibility complex class I (MHC-I), which helps the immune system identify infected or abnormal cells.

The researchers measured how much antigen the cancer cells displayed and how effectively CD8 T cells killed them. They also examined how arginine affected protein production.

Next, the team tested supplemented, standard, and restricted arginine diets in a mouse model of colorectal cancer.

In separate experiments, the researchers infected mice with influenza or a mouse-adapted form of SARS-CoV-2. They monitored weight loss, survival, viral levels, and lung damage.

Arginine improved cancer and viral infection outcomes in mice

Arginine restriction reduced MHC-I levels in human and mouse colorectal cancer cells. The researchers found similar effects in several other cancer cell lines.

In mice, arginine supplementation reduced colon tumors and improved outcomes from influenza and SARS-CoV-2, the virus that causes COVID-19.

Cancer cells with less arginine displayed fewer antigens. As a result, CD8 T cells identified and killed fewer cancer cells.

When the researchers restored arginine after 24 hours of restriction, MHC-I levels recovered within hours. The researchers found that low arginine levels caused ribosomes to stall during MHC-I production. 

In the colorectal cancer experiments, mice that received additional dietary arginine developed fewer and smaller tumors, while mice that consumed less arginine developed more tumors.

Arginine supplementation also reduced weight loss and mortality in mice with influenza. The researchers observed benefits even when they started supplementation 1 day after infection. 

In mice with SARS-CoV-2, supplementation reduced weight loss, viral levels, and lung damage. 

Study author Sohail Tavazoie, MD, PhD, spoke with Medical News Today about the study. 

“The amount of arginine that we have supplemented is equivalent to about 10 grams of arginine per day,” Tavazoie said. 

His team hopes to test supplementation in people with influenza who face a high risk of severe illness. 

The NIH reports that doses of 9 to 30 grams (g) may cause gastrointestinal discomfort and slightly lower blood pressure. Human trials are needed to determine whether the arginine dose Tavazoie mentioned safely and effectively improves outcomes.

Should you take arginine supplements to boost the immune system?

Anton Bilchik, MD, PhD, a surgical oncologist, chief of medicine, and Director of the Gastrointestinal and Hepatobiliary Program at Providence Saint John’s Cancer Institute, who was not involved in this research, also spoke with MNT about the study. 

“The study highlights an intriguing and potentially important role for arginine, an inexpensive and widely available amino acid,” said Bilchik.

Bilchik said most healthy people can generally tolerate 10 g daily, but the dose may pose risks for people with kidney or liver disease. He advised consulting a healthcare professional before using arginine to boost immunity.

“Patients should avoid self-prescribing supplements like arginine with the expectation of boosting immunity or improving cancer outcomes until more definitive human data are available,” he advised.

Jagdish Khubchandani, PhD, MPH, a public health professor at New Mexico State University, likewise not involved in the study, agreed that arginine could plausibly improve MHC-I production.

However, Khubchandani emphasized that researchers conducted the study in highly controlled animal models and focused on specific antiviral and antitumor conditions. 

“Unless there is a human trial, the findings have little value,” he said, noting that researchers still need to establish who might benefit and under what circumstances.

He stressed that people with cardiovascular, kidney, or liver disease and pregnant people should not take this amount without medical guidance.

“We have too many diet fads and supplements that are mostly useless,” Khubchandani cautioned, adding that human testing should come next.

• Previous research suggests that people can manage metabolic syndrome by making healthy lifestyle choices, such as being physically active. 
• A new study compared 10 types of exercise, including yoga, resistance training, and tai chi, to determine which was most effective for treating metabolic syndrome. 
• The researchers found that the most effective type of exercise varies and depends on the specific areas of metabolic syndrome that people are looking to improve. 

Researchers estimate that between 25-31% of the world’s population lives with metabolic syndrome — a group of risk factors that can potentially increase a person’s risk for heart disease and type 2 diabetes. 

Previous research suggests that people can manage metabolic syndrome by making healthy lifestyle choices. Additionally, healthy lifestyle choices such as following a healthy diet, not smoking, managing stress, getting enough sleep, losing weight, and being physically active have been shown to reduce the risk of metabolic syndrome.

Now, a new study published in the journal iScience says that no single type of exercise is best for treating metabolic syndrome. 

Instead, scientists say, the most effective solution is to find exercises that treat the specific areas of metabolic syndrome you’re looking to improve. 

How 10 exercises impact core metabolic syndrome markers

For this study, researchers analyzed health data from six major medical databases for almost 3,000 participants from previous studies. 

Scientists focused on 10 specific exercises: 

1. combined aerobic and resistance training
2. resistance training on its own
3. low-intensity exercise training 
4. moderate-intensity exercise training
5. moderate-to-vigorous intensity exercise training
6. high-volume high-intensity interval training (HV-HIIT)
7. low-volume HIIT (LV-HIIT)
8. HIIT combined with resistance training
9. yoga
10. traditional Chinese exercise.

Researchers examined how these different types of exercises impacted core markers of metabolic syndrome, including:

• blood pressure
• blood sugar levels
• body mass index (BMI)
• body fat percentage
• cholesterol levels
• waist size

“Since ‘exercise is medicine’ was introduced, exercise has become widely accepted as an important way to improve health,” Yaqi Xue, PhD, a researcher in the College of Physical Education and Sports at Beijing Normal University in China and corresponding author of this study, told Medical News Today. “However, metabolic syndrome is not a single health problem.” 

“It includes several related conditions, such as high blood pressure, high blood sugar, abnormal blood lipids, and abdominal obesity,” Xue continued. “Different types of exercise may affect these conditions in different ways, but there is still limited evidence to help clinicians choose the most suitable exercise for each problem.” 

No single exercise improves all aspects of metabolic syndrome at once

At the study’s conclusion, researchers found that no single exercise improved all aspects of metabolic syndrome at once. Instead, different exercises worked better for certain metabolic syndrome issues.

The researchers found that: 

• Combined aerobic and resistance training was the most effective at improving BMI, waist circumference, low-density lipoprotein (LDL) or “bad” cholesterol, and fasting blood glucose levels. 
• HV-HIIT was most effective for helping reduce body fat percentage 
• LV-HIIT was most effective at improving total cholesterol, triglycerides, and diastolic blood pressure.
• Traditional Chinese exercises helped increase high-density lipoprotein (HDL) or “good” cholesterol levels and reduce systolic blood pressure.

“Our study suggests that no single type of exercise works best for every component of metabolic syndrome. Exercise should be introduced gradually and selected according to the individual’s main metabolic problems, physical condition, and possible risks.” 
— Yaqi Xue, PhD

“Next, we hope to examine how different doses of exercise affect these outcomes and use this information to support more precise exercise prescriptions,” Xue said.

Moving toward highly personalized exercise prescriptions

MNT spoke with Craig Basman, MD, FACC, FSCAI, associate director of the Structural & Congenital Heart Program at Hackensack University Medical Center in New Jersey, about this study, who commented that it’s a highly practical and refreshing piece of research.

“In cardiology, we frequently tell patients with metabolic syndrome they need to ‘exercise more,’ but metabolic syndrome is a complex cluster of conditions — obesity, high blood pressure, elevated blood sugar, and abnormal cholesterol,” Basman, who was not involved in this study, explained.

“This study confirms that not all exercise affects these specific risks equally, giving us an evidence-based roadmap to move away from a generic, one-size-fits-all recommendation toward highly personalized exercise prescriptions.”
— Craig Basman, MD, FACC, FSCAI

MNT also spoke with Mir Ali, MD, a bariatric surgeon, bariatric medicine specialist, and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, who agreed. 

“[This] is in line with my own experience — there’s no one exercise that’s perfect for everybody,” Ali, who likewise was not involved in this study, explained. “And so whatever exercise regimen, they have to individualize it depending on the patient, their age, their mobility level, the underlying factors that we’re trying to address. So it’s a good study at a lot of different controlled trials.”

What exercises are best for which metabolic syndrome symptom? 

To help people figure out the best workouts for them when tackling certain aspects of metabolic syndrome, Basman said this study’s biggest takeaway is to tailor your workout to your specific health data. 

Once you know your primary metabolic risk factors from your primary care doctor or cardiologist, he explained, you can choose the most effective modality:

• For weight, waist size, and blood sugar, a combination of aerobic and resistance training (AT + RT) is your best approach
• For reducing body fat percentage, High-volume high-intensity interval training (HV-HIIT) yields the best results
• For high blood pressure and low “good” HDL cholesterol, traditional Chinese exercises, like tai chi and qigong, actually showed the most significant benefits
• For high triglyceride and total cholesterol levels, low-volume HIIT is the most effective.

Ali added that regular exercise is key. “I advise my patients to just be consistent with exercise, being able to find something that can be done at least five days a week for 30 minutes,” he said. “That’s most effective if you’re consistent.” 

“Metabolic syndrome drastically increases a person’s risk of severe cardiovascular events, including heart attacks, heart failure, and strokes. Clinically, it often leads to polypharmacy, where patients end up on a cascade of medications for blood pressure, cholesterol, and blood sugar.” 
— Craig Basman, MD, FACC, FSCAI

“Finding accessible, lifestyle-driven therapies is crucial because it empowers patients and targets the root causes — such as visceral fat and insulin resistance — simultaneously and without the side effects of multiple medications,” Basman added. 

• If detected early, colorectal cancer is a curable disease, with about 90% of those diagnosed with stage 1 cancer surviving 5 years from diagnosis.
• However, later stage, or metastatic colorectal cancer has much poorer outlook.
• Studies have shown that vitamin D supplements may help treat metastic colorectal cancer.
• A new phase 3 trial, testing high dose vitamin D3, has found that it is no better than lower doses in improving survival rates, but may benefit people whose primary tumor is in the left colon.

Early stage colorectal cancer can usually be treated with surgery, with or without chemotherapy, and has a 5-year survival rate of about 90%.

But when colorectal cancer has spread, or metastasized beyond the bowel, only around 14% of people with this diagnosis survive longer than 5 years from diagnosis.

Early research has shown that vitamin D3 supplementation, alongside chemotherapy, may help prevent the disease from progressing, and enhance survival rates from metastatic colorectal cancer.

Following these encouraging results, the SOLARIS randomized clinical trial, published in JAMA, tested whether higher doses of vitamin D3 would improve progression-free survival in these patients.

Although the higher dose enhanced survival in people with tumors on the left colon, overall there was no significant difference in survival between those on the higher and lower D3 doses.

Kimmie Ng, MD, MPH, professor of medicine at Harvard Medical School, Associate Chief of the Division of Gastrointestinal Oncology at the Dana-Farber Cancer Institute in Boston, MA, lead author of the study, told Medical News Today:

“Unfortunately, the primary results of the study did not show statistically significant differences in progression-free survival between patients randomized to high-dose vitamin D compared to low-dose vitamin D. There were also no statistically significant differences in the response rates of these patients’ cancers or in overall survival.”

The importance of negative findings

The study may not have found a benefit of high-dose vitamin D3, but Ketan Thanki, MD, a board-certified colorectal surgeon who specializes in benign and malignant disease of the colon, rectum, and anus with the MemorialCare Todd Cancer Institute at Long Beach Medical Center in Long Beach, CA, and was not involved in this study, welcomed its publication.

“Studies with ‘negative’ results are equally important as, if not more important than, studies with ‘positive’ results. This is because without negative results, the medical literature becomes skewed toward positive findings, leading to overestimation of how promising treatments are, wasting of resources on dead end hypotheses, and potentially repetition of experiments already answered in unpublished files,” Thanki told MNT.

“A negative trial like SOLARIS can close an open question, redirect resources, and tell us something true about biology,” he added.

Treating late-stage bowel cancer

In the double-blind, multicenter, phase 3 clinical trial, 455 patients with metastatic colorectal cancer were randomly allocated to receive either high-dose or standard dose vitamin D3 every 14 days alongside the standard chemotherapy treatment for their disease.

“My first thought upon reading this paper was that current standard of care does not include routine supplementation, even at low dose, of vitamin D3 for patients undergoing chemotherapy for metastatic colorectal cancer. As a result, are we missing an effect of any degree of supplementation — whether low or high — by comparing low dose to high dose and not including an arm that includes no supplementation at all, unless a patient is already deficient at baseline or high risk for bone loss during chemotherapy?”

– Ketan Thanki, MD

Following withdrawal of some patients whose disease had progressed, the 212 patients in the high-dose group received 8,000 international units/day (IU/d) of vitamin D3 as a loading dose at the start, followed by 4,000 IU/d for subsequent 14-day cycles, and 209 patients in the standard dose group received 400 IU/d throughout the trial.

At entrance to the trial, patients had a median age of 59 years, and a median body mass index (BMI) of 27.1. Women made up 39.8% of the group. 

In the high dose group, 38.2% had their primary tumor in the left colon, 35.1% in the right colon and 21.5% in the rectum. For the standard-dose group, 39.8% had the primary tumor in the left colon, 33.6% in the right colon, and 20.4% in the rectum.

The researchers followed up participants until the primary end point, which was progression-free survival — time from randomization to first occurrence of documented disease progression, or death. Throughout the trial researchers monitored participants’ plasma vitamin D levels.

No overall survival difference between high and standard vitamin D doses

Median progression-free survival in the high dose group was 11.8 months, and in the standard dose group, 10.3 months. In the high-dose group, 120 people died, and in the standard dose group, there were 112 deaths. 

There was no significant difference between the 2 groups for either progression-free survival, or overall survival rates.

However, high-dose vitamin D3 did appear to benefit one group of patients, as Ng explained: “In a subgroup of patients who have left-sided primary colorectal tumors, there did seem to be a benefit favoring those who were randomized to high-dose vitamin D, with significant improvements in progression-free survival compared to those patients with left-sided tumors who received low-dose vitamin D.” 

Those on the high-dose had a median 13.8 months of progression-free survival, whereas for those on the standard dose it was 10.2 months.

However, Ng cautioned that this finding was “hypothesis-generating and exploratory, and definitely requires further confirmation in future studies, but is intriguing given that we do know that left-sided colorectal tumors are different from right-sided colorectal tumors.”

Thanki agreed that the finding needed further research: “When you look at multiple subgroups, you increase the chance of finding a false positive result by chance alone. The overall trial was negative, which means any subgroup signal needs to be treated skeptically.”

However, he told MNT:

“This is a great starting point to ask a question if left and right colon cancers respond differently to D3 supplementation, but is by no means an answer that they do. We know that right and left-sided colon cancers have very different tumor biology, so it is not a stretch to suggest that they may, and perhaps further studies will demonstrate that D3 is beneficial for one and not the other.”

• Research suggests that avoiding three midlife risk factors — smoking, diabetes, and high blood pressure — may help delay dementia onset by up to 13 years.
• Other modifiable risk factors include high cholesterol, physical inactivity, hearing loss, depression, and social isolation.
• Experts recommend managing vascular health as early as possible to help protect cognitive health.

Avoiding smoking, not having diabetes, and having normal blood pressure may help protect against dementia for an additional 13 years.

This is according to new research published in Neurology Open Access. The NYU Langone Health researchers determined that avoiding midlife risk factors between the ages of 46 and 70 years could help delay the potential onset of dementia.

Dementia causes symptoms such as memory loss, confusion, and problems with communication. Alzheimer’s disease, the most common type of dementia, typically develops after the age of 65.

However, the recent study suggests that taking steps to manage certain risk factors could help protect against the development of dementia until later in life.

Avoiding risk factors could add 13 more years without dementia

In the new study, researchers analyzed data in the Atherosclerosis Risk in Communities (ARIC) study, a cohort study that began in 1987.

They examined the data of 12,409 participants. They assessed three risk factors, which the ARIC study consistently measured:

• high blood pressure (hypertension)
• smoking
• diabetes.

Participants were followed over a median of 26.3 years. In that time:

• 3,008 people developed dementia
• 5,238 people died without developing dementia.

Individuals with no risk factors for dementia had the lowest risk of developing the condition. In contrast, those with all three risk factors were 2.69 times more likely to develop dementia.

The study also found that taking care of vascular health in midlife could help protect against dementia for an additional 12.6 years. Diabetes, hypertension, and smoking are all risk factors for vascular disease.

Dung Trinh, MD, an internist at the MemorialCare Medical Group and Chief Medical Officer of Healthy Brain Clinic in Irvine, CA, spoke to Medical News Today about these findings.

“I find the results compelling because they reinforce the close connection between cardiovascular health and brain health during midlife,” Trinh, who was not involved in the study, said. “High blood pressure, diabetes, and smoking can damage blood vessels, increase inflammation, and reduce the brain’s resilience over time.”

However, Trinh also explained that: “This was an observational study, so it cannot prove that avoiding these conditions will give an individual exactly 13 additional dementia-free years. The figure compares people with none of the three risk factors with those who had all three, and ‘dementia-free survival’ reflects both the timing of dementia and overall longevity.”

Who benefits most from vascular health interventions?

The researchers identified certain demographic differences.

For example, Black people were more likely to develop dementia sooner than white participants.

People who carried the apolipoprotein E4 (APOE-e4) gene were also at risk of developing dementia earlier than people who did not carry the gene. The APOE-e4 gene is a known risk factor for cognitive decline.

The findings also suggested that women typically lived longer without dementia than men. Josef Coresh, MD, PhD, senior investigator of the study, discussed this with MNT.

“Much of that difference reflects lower mortality rather than lower dementia risk. With three risk factors, women averaged 18.1 dementia-free years versus 16.6 for men,” Coresh said.

“But because women survive into the ages where dementia risk is highest, their lifetime dementia risk is higher — about 40% versus 33% in our data. It’s the same pattern as our main finding: The added years are added at the oldest ages, which is the highest-risk period,” he explained.

What other dementia risk factors need to be considered?

Diabetes, hypertension, and smoking are not the only risk factors for dementia.

Coresh described other factors that are important to consider:

“The other five components of Life’s Essential 8 — physical activity, diet, sleep, body weight, cholesterol. Beyond that, the 2024 Lancet Commission identifies 14 modifiable factors accounting for about 45% of dementia, and several are late-life targets: hearing loss, vision, social isolation, depression. Education and cognitive engagement matter as well.”

Trinh explained that, while “nonmodifiable risk factors such as age, genetics, and family history” can increase the risk of dementia, there are numerous modifiable risk factors, or factors that are capable of being changed or prevented.

He advised that, “rather than focusing on one isolated behavior, the strongest prevention approach is to address a person’s combined vascular, lifestyle, sensory, social, and environmental risks across the life course.”

How to improve vascular health to reduce dementia risk

The study authors determined that better vascular health in midlife was linked with longer dementia-free survival.

While it may not be possible to completely prevent dementia, taking steps to improve vascular health could help reduce the risk or delay its onset.

Steps that may help include:

• getting enough regular physical activity or exercise
• working with a healthcare professional to manage conditions such as diabetes, hypertension, high cholesterol, depression and other mental health problems
• getting regular hearing checks and treating any hearing loss
• avoiding or quitting smoking
• avoiding or limiting alcohol consumption
• getting enough quality sleep
• staying mentally active, such as with brain exercises.

Coresh recommended aiming to manage risk factors “as early as possible.”

“Know your blood pressure and A1c by your 40s, and aim to prevent rather than only treat: physical activity, lower salt intake, and weight control keep blood pressure from rising in the first place,” he advised.

“Timing matters for diabetes in particular — diabetes diagnosed before 60 carries substantially more dementia risk than diabetes appearing at 65, so delaying onset has value beyond good control. And avoid smoking,” Coresh stressed.

Trinh added that “the central message should be one of opportunity rather than certainty or blame: Dementia risk can often be reduced, but it cannot be eliminated, and people who develop dementia should not be assumed to have caused their condition.”

He concluded:

“Healthy choices also depend on access to primary care, affordable medication, nutritious food, safe places to exercise, smoking-cessation services, and equitable treatment of vascular disease. It is also important to note that this study examined dementia broadly, not biologically confirmed Alzheimer’s disease specifically. Its greatest value is in showing that protecting the heart and blood vessels during midlife may help people preserve both longevity and cognitive health.”

• Recent trends and advice have been recommending increased protein intake, especially for certain groups of people.
• A recent study, however, suggests that consuming less protein could help extend life span and have many health benefits by improving metabolism and reducing cellular damage.
• The study specifically suggests that reducing the consumption of certain amino acids, such as isoleucine and methionine, aids healthy aging, rather than simply reducing the amount of protein consumed.

Evidence so far has supported caloric restriction for its purported longevity benefits, but reducing protein intake has not been widely explored.

Now, a new review, published in the journal Cell Press Blue, suggests that restricting overall dietary protein intake or specific essential amino acids could help people achieve improved health span and increased longevity, similar to that achieved through calorie restriction.

The review, combing over 350 scientific papers on animal and human trials, outlines how restricting dietary protein and specific essential amino acids such as isoleucine and methionine helps promote healthy aging and extends life span.

The review examined the effects of protein restriction on several organisms, including microbes, mice, other animals, and humans, using observational studies, randomized controlled trials, and cell culture experiments.

Researchers found that eating less protein had many health benefits.

Consuming less protein helped the body burn more calories, reduced body fat, and better managed insulin levels by increasing levels of Fibroblast Growth Factor 21 (FGF21), a hormone that helps protect against aging.

A low protein diet also inhibited mTORC1 and activated GCN2, which are two key nutrient sensors that regulate cell growth and stress response, effectively telling the body’s cells to slow down aging and more efficiently clear cellular “trash” through autophagy.

Eating less protein also reduced the number of senescent or aging cells. Senescent cells are often called “zombie” cells because they are damaged cells that stop dividing (mitosis) but refuse to die, driving inflammation in the background.

Another important effect scientists observed of a low protein diet was the improvements in mitochondria, the powerhouse of the cell, and decreased reactive oxygen species (ROS) damage to tissues. In animal studies, scientists also saw that lab animals lived longer and had lower age-related frailty when fed less protein.

However, the researchers emphasized that protein needs should be personalized according to physical activity and age.

How does eating less protein improve metabolism?

Medical News Today discussed the study findings with two experts — Kristin Kirkpatrick, MS, RDN, president of KAK Consulting and a dietitian at the Cleveland Clinic Department of Wellness & Preventive Medicine in Ohio, and Michelle Routhenstein, MS, RD, CDCES, CDN, a preventive cardiology dietitian at EntirelyNourished.

“This review suggests the benefit isn’t simply eating less protein — it’s how the body responds to lower levels of certain amino acids. Protein restriction appears to activate pathways involved in metabolic health and cellular repair, while reducing activity in pathways that may contribute to aging,” Kirkpatrick said.

“Eating less protein, especially certain amino acids, may help the body spend less time in a constant ‘build and grow’ state and more time in a ‘repair and clean up’ state. This may help improve how the body uses energy and reduce cellular stress, which may have longevity and metabolism-boosting effects,” Routhenstein explained.

The review specifically identifies three Essential Amino Acids (EAAs) — isoleucine, valine, and methionine — that may bring benefits when restricted in one’s diet. Reducing nonessential amino acids such as tyrosine and cysteine may also provide health benefits, according to the authors.

However, the review also stresses that reducing the intake of all amino acids may not be beneficial and lists three that may provide greater benefit when supplemented: glycine, serine, and proline.

“[T]he goal is not to avoid protein; it is about finding the right amount to support muscle strength while also promoting long-term metabolic health,” Routhenstein pointed out.

Why the study isn’t saying just ‘consume less protein’

“First, this study is really examining protein intake beyond muscle health and focusing on the biology on longevity, health span, healthy aging, etc.,” said Kirkpatrick, speaking to MNT.

“This study is not saying not to consume protein, it is looking more at aging biology and metabolic pathways rather than muscle preservation,” Routhenstein clarified.

“What [the study is] examining is more about reducing certain amino acids (isoleucine and methionine) for healthy aging and the importance of balancing the message that ‘more is better’ without looking at other lifestyle changes and/or specific types of protein,” Kirkpatrick explained.

“I [w]ant to make sure that my patients don’t look at this study and just blindly eat less protein but to look at this to balance what type of protein they are consuming and their personalized needs based on age, activity level, chronic disease risk or existing conditions.”
— Kristin Kirkpatrick, MS, RDN

Should everyone eat less protein?

“Higher protein intake is still important for maintaining muscle mass, strength, and recovery, especially with aging and exercise. However, this review suggests that lower protein intake or restriction of specific amino acids may activate longevity pathways, reduce chronic growth signaling, and improve metabolic health,” Routhenstein told MNT.

“The findings do not mean everyone should eat less protein, but highlight that optimal protein intake depends on individual goals, age, activity level, and health status,” she said.

Kirkpatrick underscored that current calls for higher protein intake have largely been driven by research showing health benefits linked to muscle maintenance, improved muscle recovery, increased strength, and a reduced risk of sarcopenia (muscle wasting) associated with aging.

“These recommendations remain well supported by human research, so just having less is not the message; it’s to look deeper into types of protein as well as other factors associated with aging,” she explained.

What the study may be overlooking

Although the study does promote that low protein intake can support metabolic health in early and middle age, it makes an important point: age matters.

The study notes that reduced protein intake may adversely affect certain groups. It states that adults older than age 65 can have protein insufficiency, be at risk of frailty, and experience sarcopenia, which means protein restriction could be contraindicated.

“If there is anything overlooked [in the study], perhaps it’s that this has the potential to underemphasize the well-studied role that protein plays in preserving muscle,” Kirkpatrick said.

“The study also does not fully account for the importance of maintaining muscle, resistance training, or the overall dietary pattern,” Routhenstein said.

This review also focuses on cellular longevity, which is the process of keeping individual cells in the body healthy and young at the molecular level.

The point of confusion and potential contention with previous research comes from the fact that most of them focus on functional longevity, which is about staying strong, mobile, and reducing frailty that comes with age.

And while functional longevity is important for operating independently and healthily throughout life, even in older age, cellular longevity is the driving factor.

Protein still very important for health

An important point the study makes is that it argues for restricting specific essential amino acids, rather than all proteins.

“The biggest surprise wasn’t that lower protein looked beneficial — it was that specific amino acids may matter more than total protein,” Kirkpatrick said, adding: “But we need more human studies to continue exploring this concept.”

The study also distinguishes between the type of protein consumed and its purported health benefits. The researchers emphasize that, compared with animal protein, plant protein has been associated with a lower risk of frailty.

“The biggest limitation is that much of the research comes from animal studies, and we still need more long-term human data,” Routhenstein said.

What all this research so far shows us is that our protein needs evolve and change over our life span:

“The takeaway I would discuss with my patients is that healthy aging has multiple goals—maintaining muscle, preserving metabolic health, reducing frailty, and supporting cognitive function. Protein is one piece of a larger puzzle related to health span but taking a step back and finding the best personalized approach for one’s individual needs is a key factor in living not only longer but better.”
— Kristin Kirkpatrick, MS, RDN

• Past studies show that an infant’s nutrition in the first days of life can affect their health later in life. 
• A new study found that infants exposed to less sugar in their first 1,000 days of life experienced lower risks of developing Alzheimer’s disease and dementia from any cause as adults. 
• Scientists also found that consuming less sugar during the first 1,000 days of life also led to a lower risk of depression and anxiety later in life. 

Past studies show that an infant’s nutrition during the first 1,000 days of life can affect their health later in life. 

A healthy, nourishing diet during the first years of life is important for establishing a healthy gut microbiome, building a strong immune system, and supporting brain development. 

Previous research has found that not being exposed to proper nutrition early in life can potentially increase a person’s risk for diseases such as type 2 diabetes, obesity, metabolic syndrome, and cardiovascular disease.

Now, a new study published in the journal npj Aging says that infants exposed to less sugar in their first 1,000 days of life experienced lower risks of developing Alzheimer’s disease and dementia from any cause as adults. 

Comparing nutrition during pre- and post-sugar rationing in the UK

For this study, researchers analyzed health data from more than 60,000 participants in the U.K. Biobank who were born between 1951 and 1956 to examine how the end of sugar rationing in 1953 in the U.K. affected health.  

“The first 1,000 days of life are a critical window for brain development, and early nutrition is known to have lasting effects on health,” Bing Zhang, PhD, a geriatric medicine researcher at Guangzhou First People’s Hospital and the senior author of this study, told Medical News Today. 

“The end of sugar rationing in the U.K. in 1953 created a unique natural experiment: individuals conceived during rationing consumed far less sugar in early life than those born shortly after. This allowed us to study the long-term cognitive effects of early sugar restriction while minimizing confounding by socioeconomic or behavioral factors that typically plague nutritional studies.” 
— Bing Zhang, PhD

Less sugar exposure lowers Alzheimer’s and depression risk

At the study’s conclusion, researchers found that adults exposed to sugar restriction during the first 1,000 days of their lives had a 46% lower Alzheimer’s disease risk and 27% lower risk of developing all-cause dementia. 

“This is, to our knowledge, the first human evidence that limiting sugar exposure in very early life is associated with substantial long-term protection against both neurodegenerative and psychiatric disorders.”
— Bing Zhang, PhD

“The risk reductions, especially for Alzheimer’s disease, are remarkably large. These findings highlight that dietary exposures during pregnancy and infancy may have lifelong impacts on brain health, and they reinforce the importance of current guidelines that recommend limiting added sugars early in life,” Zhang said.

Researchers also noted that participants exposed to sugar restriction also lowered their depression risk by 11% and anxiety risk by 20%. 

Lower sugar consumption in infancy may help slow brain aging

Additionally, scientists observed that participants who were exposed to sugar rationing after birth had brains that were, on average, 0.39 years younger than their chronological age. These participants also had larger volumes in certain brain regions, including the hippocampus and thalamus.

“These imaging findings offer a plausible biological explanation for the reduced dementia risk,” Zhang explained.

“A younger-appearing brain and larger volumes in areas such as the hippocampus — a region critical for memory and one of the earliest affected in Alzheimer’s — suggest enhanced brain structural integrity and greater cognitive reserve. This indicates that early-life sugar restriction may promote optimal brain development and slow brain aging decades later.”
— Bing Zhang, PhD

“Alzheimer’s disease is a major and growing global health challenge, yet disease-modifying treatments remain limited and cannot halt progression,” Zhang continued.

“Preventing or delaying dementia through modifiable risk factors is therefore a public health priority. Identifying novel protective strategies, especially those that can be implemented early in life, offers a realistic pathway to reducing the future burden of dementia as populations age,” he added.

Caution against over-interpreting findings

MNT spoke with Peter Gliebus, MD, chief of neurology and director of cognitive and behavioral neurology at Marcus Neuroscience Institute, part of Baptist Health South Florida, about this study, who commented that what makes this study interesting is that it takes advantage of a unique historical event, the end of sugar rationing in the U.K. in 1953. 

“Because exposure to sugar was largely determined by when someone was born, it helps reduce some of the biases that often affect nutrition studies,” Gliebus, who was not involved in this study, continued.

“At the same time, I would be careful not to over-interpret the headline finding of a 46% lower risk of Alzheimer’s disease. That result was based on a relatively small number of Alzheimer’s cases, and the participants are still not at the ages when Alzheimer’s becomes most common. The findings related to depression and anxiety appear somewhat stronger,” he said. 

Does restricting sugar in midlife affect dementia risk?

While this study cannot tell us whether or not lowering sugar in adulthood would produce the same benefit, Dung Trinh, MD, an internist for the MemorialCare Medical Group and chief medical officer of the Healthy Brain Clinic in Irvine, CA, who was not involved in this study, said that there still may be benefits for reducing sugar.

Reducing excessive added sugar later in life may still support brain health by lowering the risk of obesity, insulin resistance, diabetes, high blood pressure, and cardiovascular disease, all of which are associated with cognitive decline and dementia, Trinh said.

“The goal should not be to eliminate all sugar, especially from nutritious foods such as whole fruit, but to limit excessive added sugars as part of a broader lifestyle that includes exercise, healthy sleep, and good control of blood pressure, cholesterol, and diabetes.”
— Dung Trinh, MD

MNT also spoke with Rehan Aziz, MD, DFAPA, geriatric psychiatrist at Hackensack Meridian Jersey Shore University Medical Center, and associate professor of psychiatry and neurology at Hackensack Meridian School of Medicine in New Jersey, who likewise was not involved in this study. 

For the next steps in this research, Aziz said he would like to see whether sugar-restricted diets begun in midlife affect rates of late-life dementia, depression, and anxiety, since this study only speaks to the first 1,000 days and leaves the far more common question of adult intervention unanswered.

“I would also want to know whether some forms of sugar are more harmful than others, for example, added and liquid sugars versus those in whole foods, along with the threshold at which sugar or total carbohydrate intake becomes harmful, and the specific effects of high-fructose corn syrup and other ultra-processed carbohydrates, since those dominate the modern diet, on brain aging,” Aziz added. 

• The Food and Drug Administration (FDA) approved Lipfendra (enlicitide), a new oral treatment for high cholesterol (hypercholesterolemia) and heterozygous familial hypercholesterolemia, on July 16, 2026.
• Lipfendra is an oral PCSK9 inhibitor that helps lower low-density lipoprotein (LDL) cholesterol, commonly known as ‘bad cholesterol.’
• Medical News Today spoke to a cardiologist to find out how Lipfendra compares to statin treatment for high cholesterol, and answer other salient questions about this new treatment.

On July 16, 2026, the Food and Drug Administration (FDA) approved Lipfendra (enlicitide), the first ever oral PCSK9 inhibitor, for the treatment of high cholesterol (hypercholesterolemia) and heterozygous familial hypercholesterolemia.

Lipfendra comes in pill form, and should be taken daily in 20 milligram (mg) doses. It works by reducing blood levels of low-density lipoprotein (LDL) cholesterol, or “bad cholesterol.”

But how does this new treatment compare to statins, some of the most commonly used cholesterol-lowering drugs, and who is it the right choice for?

To answer these, and other salient questions, Medical News Today reached out to Rigved Tadwalkar, MD, FACC, a consultative cardiologist, and director of the Digital Transformation Pacific Heart Institute in Santa Monica, CA.

• Despite colorectal cancer being one of the most preventable and treatable cancers when detected early through routine screening, millions of eligible Americans remain overdue for screening.
• Existing screening methods, such as colonoscopy and stool-based tests, are highly effective, but many people avoid them because of preparation difficulties, discomfort, embarrassment, inconvenience, or fear of the results.
• The FDA approval of Freenome’s SimpleScreen CRC blood test provides a new screening option for average-risk adults, complementing current options.
• In clinical studies, the test detected roughly 8 in 10 colorectal cancers.

At present, colorectal cancer is the second leading cause of cancer-related deaths worldwide, and early-onset colorectal cancer is the leading cause of cancer-related death among males and females under age 50.

Current colorectal cancer screening guidelines advise that average-risk adults ages 45 years and older should undergo regular screening. However, despite this recommendation and colorectal cancer being one of the most preventable cancers through screening, an estimated 60 million eligible individuals in the U.S. do not participate.

For many years, experts have considered colonoscopies as the gold standard for colorectal cancer screening. Stool-based tests have also become increasingly popular because they can be completed at home. Yet, many eligible adults are reluctant to undergo screening.

People may consider screening a taboo or stigmatized topic. Potential barriers may include preparation, fear, discomfort, embarrassment, taking time off work, limited access to healthcare, cost concerns, lack of awareness of screening recommendations, and a tendency to delay preventive care when no symptoms are present.

Recognizing that no single screening method appeals to everyone, researchers have developed blood-based screening tests designed to make colorectal cancer screening more convenient. In 2024, the U.S. Food and Drug Administration (FDA) approved the Shield blood test. In July 2026, the FDA also approved Freenome’s SimpleScreen colorectal cancer blood-based screening test.

In the large PREEMPT CRC clinical study, which involved more than 48,000 participants, the SimpleScreen blood test correctly identified roughly 8 out of 10 colorectal cancers and produced negative results for about 9 out of 10 people without colorectal cancer or advanced precancerous lesions.

The approval offers another screening option, which some people may find significantly less intimidating than scheduling a colonoscopy or completing a stool test at home. This convenience may encourage previously unscreened people to participate, potentially leading to more cancers being detected earlier, when treatment is most effective.

Medical News Today spoke with Paul Limburg, MD, MPH, Chief Screening Medical Officer, Screening, Abbott Cancer Diagnostics, about how blood-based colorectal cancer screening works and compares to other options, if it can help close the screening gap, and how it fits into routine cancer screening.

• A new study suggests that older adults taking a daily multivitamin for 3 years reported significantly better functional health, including reductions in symptom burden and improvements in overall physical functioning.
• These functional health benefits may support daily activities and everyday independence, such as walking, climbing stairs, dressing, bathing, and completing household chores.
• Although cocoa extract supplementation did not significantly improve functional health, it was associated with benefits in participants with congestive heart failure.
• The findings have not yet been published in a peer-reviewed journal and, as such, are preliminary. Additionally, the researchers emphasize that multivitamins are not a substitute for a healthy diet and regular exercise.

Multivitamin supplementation describes a daily vitamin and mineral supplement that can help fill nutritional gaps in the diet. In older adults, this may be helpful because aging can make it harder for the body to absorb or get enough nutrients from food.

Good nutrition supports general well-being and cardiovascular function, including how well the heart and blood vessels work, supplying oxygen and nutrients throughout the body. However, there is limited evidence that multivitamins directly improve heart health or prevent cardiovascular disease in healthy older adults.

The COSMOS trial was a large, randomized, double-blind, placebo-controlled clinical trial designed to test whether taking either a commercially available daily multivitamin (Centrum Silver), or a daily cocoa flavanol supplement could reduce the risk of cancer, cardiovascular disease, and other age-related conditions in older adults.

Now, a secondary analysis of the COSMOS trial suggests that daily multivitamin-mineral supplementation modestly improved cardiovascular-related functional health in older adults over a 3-year period.

The study, presented at NUTRITION 2026, the annual meeting of the American Society for Nutrition, found that adults aged 60 years and older who took a daily multivitamin reported better functional health than those who received a placebo.

The improvements included measures of symptom burden and physical functioning, suggesting multivitamins may help preserve day-to-day independence as people age.

However, because the findings have not yet been published in a peer-reviewed journal, they should be considered preliminary.

Multivitamins linked to better functional health

The study analyzed data from more than 16,000 participants enrolled in the COcoa Supplement Multivitamins Outcomes Study (COSMOS), a large randomized clinical trial investigating the effects of daily multivitamins and cocoa extract supplements in older adults.

Participants were randomly assigned to receive either a daily multivitamin, a cocoa extract supplement, both supplements, or matching placebos.

After 3 years, researchers found that those taking a daily multivitamin had significantly better functional health scores than those taking a placebo, based on the Kansas City Cardiomyopathy Questionnaire, a validated tool that measures symptoms, physical limitations, and quality of life related to cardiovascular health.

Notably, the largest differences were seen in symptom burden and the clinical summary score, which combines measures of symptoms and physical function.

The benefits were primarily driven by reductions in symptom burden, including fatigue, shortness of breath, and swelling, rather than improvements in physical ability alone.

The researchers state that the study focused on outcomes that matter directly to older adults, noting that maintaining functional health may help older adults continue everyday activities.

“Multivitamin-mineral supplementation may help preserve functional health in older adults with heart failure, particularly by reducing symptom burden such as fatigue, edema, and shortness of breath,” Jennifer Wong, MD, a board-certified cardiologist and medical director of Non-Invasive Cardiology at MemorialCare Heart and Vascular Institute at Orange Coast Medical Center in Fountain Valley, CA, told Medical News Today.

“While these findings are encouraging, additional research is needed to determine whether these benefits translate into improved long-term clinical outcomes,” Wong, who was not involved in the study, further commented.

Could multivitamins support healthy aging?

The observed benefits from the secondary analysis suggest that multivitamins could reflect improvements in several aspects of health, including cognitive function, blood circulation, and physical stamina.

However, the current study was not designed to determine the biological mechanisms responsible for the effects.

The study authors emphasize that multivitamins should complement, rather than replace, established healthy lifestyle habits, such as healthy eating, regular physical activity, and social connection.

A daily multivitamin could offer a helpful, low-risk addition to a healthy lifestyle to support physical well-being as people age, but is not a substitute for a good dietary plan or exercise.

Could cocoa extract benefit heart health?

Unlike multivitamins, cocoa extract did not significantly improve functional health scores across the overall study population.

However, researchers observed a significant benefit among those living with congestive heart failure, suggesting this finding warrants further investigation.

“The finding that cocoa extract may help preserve symptom burden in people with heart failure is an encouraging signal,” Wong added. “However, larger, well-designed clinical trials are needed to determine whether cocoa extract provides meaningful and reproducible clinical benefits before it can be recommended as part of routine care.”

What do the findings mean?

Functional health refers to a person’s ability to perform routine daily activities independently. Health experts consider preserving this ability as an important component of healthy aging, as declines in physical function can reduce quality of life and increase the need for support.

The findings add to a growing body of research examining whether multivitamin supplements may provide benefits beyond correcting nutrient deficiencies.

For example, previous analyses from the COSMOS trial suggest that daily multivitamin use may support aspects of cognitive health in older adults. However, other evidence remains mixed, and some studies have found little or no benefit.

Because the current research has not yet undergone peer review, it is too early to conclude whether daily multivitamin use directly improves functional health in all older adults. Future analyses will help clarify the strength of the findings and whether they apply to broader populations.

“There are several potential mechanisms,” Wong noted. “Certain vitamins and minerals may help regulate blood pressure, improve blood vessel function, reduce inflammation, support healthy cholesterol levels, and prevent nutritional deficiencies such as anemia.”

“Together, these effects may contribute to better cardiovascular health and improved energy levels, which could help preserve physical function. Improved vascular health may also support cognitive function, although this relationship requires further study,” she added.

For anyone considering a new supplement, it is advisable to discuss it with a healthcare professional, particularly those with underlying medical conditions or who take prescription medications, as some vitamins and minerals can interact with certain treatments.

• Reducing intake of processed foods, red meats, salt and sugars, while increasing fresh fruit and vegetables, whole grains and pulses can help reduce the risk of health conditions such as overweight and obesity, type 2 diabetes, cardiovascular disease and some cancers.
• This type of diet is also good for the planet, as plant farming produces fewer gases that contribute to the climate crisis.
• Now, a study suggests that, for postmenopausal women, this type of diet can significantly reduce the risk of cardiovascular and coronary heart disease.
• Encouragingly, the researchers say that even small changes to diet can have significant health benefits.

Altering diet and lifestyle is one of the most effective ways to reduce the risk of many health conditions.

The Centers for Disease Control and Prevention (CDC) advise that a diet high in protein, dairy, vegetables, fruits, healthy fats, and whole grains, and low in added sugars and salt can help reduce the risk of heart disease, type 2 diabetes, and some cancers.

Together with exercise, it also supports bone health, muscles and immunity, while helping to maintain a healthy weight.

Now, a new study has found that one type of healthy diet — the Planetary Health Diet — may be particularly beneficial for older women.

In the study, whose finings were presented at NUTRITION 2026, the annual meeting of the American Society of Nutrition, researchers found that women whose diet most closely followed the Planetary Health Diet had a 28% lower risk of cardiovascular disease than those with a lower adherence to this type of diet.

These findings are yet to appear in a peer-reviewed journal.

Thomas M. Holland, MD, MS, a physician-scientist and assistant professor at the RUSH Institute for Healthy Aging, RUSH University, College of Health Sciences, Chicago, who was not involved in the study, told Medical News Today that:

“Research focused specifically on older women is particularly valuable because cardiovascular risk increases after menopause, as age-related changes in cholesterol, blood pressure, and metabolism accelerate vascular disease. Studies like this demonstrate that dietary modification remains a powerful tool for improving heart health, even later in life.”

“This is an interesting abstract and it is encouraging to see these results,” Eamon Laird, PhD, lecturer in Nutrition at the Atlantic Technological University Sligo and Adjunct Professor Trinity College Dublin, Ireland, likewise was not involved in the study, told MNT.

“However,” Laird noted, “I would add caution as it is only an abstract and would like to see the full detailed analysis before we fully embrace all the findings. Plus because this is an observational study, we cannot conclude that the diet itself caused the lower risk.”

How does the Planetary Health Diet differ from other healthy diets?

The Planetary Health Diet is a “science-based dietary pattern designed to promote human health and protect the planet, linking what we eat with how we sustain life on Earth.”

It has much in common with other healthy-eating plans, such as the Mediterranean and DASH diets, in that it is rich in plants.

The majority of the diet is made up of whole grains, fruits, vegetables, nuts, and legumes, with only moderate or small amounts of fish, dairy, and meat recommended.

Although the diet focuses on the benefits to people’s health, eating this way also supports cultural and regional variation and reduces the environmental impact from food production and supply.

Planetary Health Diet linked to lower cardiovascular disease risk

Researchers assessed the dietary intake of almost 67,000 postmenopausal women enrolled in the Women’s Health Initiative observational study. 

At enrolment, the women had a mean age of 63.2 years. Researchers followed them up for a median of 8.2 years, during which time they recorded 5,033 cardiovascular events.

All participants completed a semi-quantitative food frequency questionnaire, from which the researchers calculated their Planetary Health Diet scores, on a scale of 0 to 140.

Researchers divided the scores, which ranged from 35 to 123, into five groups, from least to greatest adherence, and 10-point increments.

The researchers adjusted for factors that might impact cardiovascular health, including sociodemographic characteristics, lifestyle behaviors (smoking status, alcohol intake, physical activity), energy intake, and body mass index.

Participants in the highest quintile had a 28% lower risk of cardiovascular disease, and a 34% lower risk of coronary heart disease, than those in the lowest quintile. They also had a 22% lower stroke risk, and a 31% lower risk of heart failure.

“These findings align with what we’ve consistently seen in other plant-forward dietary patterns, such as the Mediterranean and MIND diets, which have been associated with lower cardiovascular disease risk and better vascular health. The planetary health diet similarly emphasizes vegetables, fruits, legumes, whole grains, nuts, and healthy fats, providing fiber, antioxidants, and unsaturated fats that help reduce inflammation, improve blood vessel function, lower LDL cholesterol, and support healthy blood sugar regulation.”

— Thomas M. Holland, MD, MS

“In postmenopausal women, improvements in metabolic health may be particularly important because the decline in estrogen is associated with adverse changes in cholesterol, body fat distribution and vascular function,” Laird also added.

Even moderate adherence showed benefits

The researchers found that for every 10-point increase in adherence to the Planetary Health Diet, there was a reduction in cardiovascular disease and coronary heart disease risk. 

Holland welcomed this finding, saying that:

“One of the most encouraging findings from this study is that meaningful (statistically significant) reductions in cardiovascular risk were seen even with moderate adherence. This really reinforces the point that every healthy choice counts. Rather than trying to completely change your diet overnight, focus on sustainable habits like adding an extra serving of vegetables, choosing whole grains more often, or replacing one meat-based meal each week with beans or lentils.”

Small changes that could make a difference to your heart health

Laird suggested simple dietary changes that can help protect cardiovascular health and reduce environmental impact.

These include:

• fill half the plate with vegetables at every meal
• choose oily fish or legumes more often and reduce processed meats such as sausages or bacon
• choose whole grain bread, oats or brown rice instead of refined grains
• replace one or two meat-based meals each week with meals based on beans, lentils or chickpeas
• reduce food waste by planning meals and using leftovers.

Holland echoed this advice, adding that, “together, diet and exercise help stabilize blood sugar, lower LDL cholesterol, improve HDL cholesterol, reduce inflammation, and support healthier blood vessels, including the coronary arteries that supply the heart.“

“Consistently combining these healthy lifestyle habits remains one of the most effective ways to promote healthy aging, maintaining cognitive and physical functionality, and reduce the risk of cardiovascular disease,” he noted.

“Small, consistent changes practiced over time will more often produce much greater long-term health benefits than short-lived, dramatic, ‘fad’ diet changes.”

— Thomas M. Holland, MD, MS

• The use of GLP-1s, such as Ozempic and Wegovy, may increase the risk of hair loss, a new study has found.
• Non-scarring alopecia, a typically nonpermanent type of hair loss, was more common among GLP-1 users than among those who took SGLT-2 inhibitors or DPP-4 inhibitors for the treatment of type 2 diabetes.
• While the absolute risk of hair loss may be low, raising awareness can help people make informed decisions about their treatment plan.

A new large-scale study found that people with type 2 diabetes who are taking GLP-1 medications may have a higher risk of hair loss.

The research, published in The BMJ, compared the risk of alopecia, a form of hair loss, among adults who took either GLP-1 drugs, SGLT-2 inhibitors, or DPP-4 inhibitors for the treatment of diabetes.

Specifically, there was an increased risk of non-scarring alopecia, a typically temporary or reversible type of hair loss, which can include telogen effluvium and androgenetic alopecia.

While the researchers suggest that the absolute risk of hair loss with GLP-1 medications is low, understanding the potential for alopecia may help inform treatment decisions among patients.

GLP-1s linked to up to 68% higher hair loss risk

GLP-1 use in adults with type 2 diabetes was associated with a higher risk of clinically recorded non-scarring alopecia, a type of hair loss that does not permanently damage the hair follicles.

The researchers examined electronic health record data from the University of Pennsylvania Health System (Penn Medicine) between January 2019 and September 2024.

They looked at electronic health record data from 12,004 GLP-1 users and 15,221 SGLT-2 inhibitor users in the GLP-1 versus SGLT2i cohort. In the GLP-1 versuss DPP4i cohort, they focused on data from 11,964 GLP-1 users and 11,238 DPP-4 inhibitor users.

Compared with adults taking SGLT-2 inhibitors, those taking GLP-1 medication to treat diabetes had a 37% higher chance of experiencing hair loss.

GLP-1 users also had a 68% risk of hair loss compared with people treating diabetes with DPP-4 inhibitors.

The findings suggest that GLP-1s were associated with a higher risk of hair loss than two alternative diabetes treatments, but they do not establish the hair loss risk in people taking GLP-1s for non-diabetes purposes.

“The findings regarding the increased risk of alopecia compared to SGLT-2 inhibitors (37%) and DPP-4 inhibitors (68%) are notable, though not entirely surprising given that significant weight loss by any means can result in hair loss,” Mir Ali, MD, a bariatric surgeon, bariatric medicine specialist and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, told Medical News Today.

“The medication acts as a catalyst for weight loss, but the resulting physiological stress and hormonal changes are often the direct trigger for telogen effluvium,” Ali, who was not involved in the study, added.

Are rapid weight loss and nutritional deficiencies the cause?

As the latest research is an observational study, it cannot confirm whether any specific factor directly caused another. This means that it cannot determine that weight loss and nutritional deficiencies definitely led to hair loss.

However, the researchers did note a possible link. Telogen effluvium is already associated with weight loss, and the rapid weight loss associated with GLP-1 use could also lead to non-scarring alopecia.

In reducing calories, some people taking GLP-1 drugs may develop certain nutritional deficiencies, which can affect how hair grows. The study authors suggest that deficiencies in the following may contribute to hair loss:

• biotin
• iron
• zinc.

“My recommendation is to ensure patients maintain adequate protein intake and supplement appropriately with key micronutrients, especially iron, zinc, and biotin, while on these medications,” said Ali. “Routine monitoring should include checking basic nutritional labs if hair loss becomes a concern.”

Other factors that may contribute to hair loss in people taking GLP-1 medications include changes in thyroid function and altered absorption of oral drugs, such as thyroid hormone or sex hormone medications, due to delayed gastric emptying.

Could awareness inform patient decision making?

Around six or seven in every 1,000 people taking GLP-1 medications experienced hair loss each year, according to data cited in the study paper.

While the absolute risk of hair loss with GLP-1 drugs is low, it is necessary for people to be aware of the possibility so that they can weigh the benefits of the treatment against the risks and make an informed decision about their treatment plan.

Speaking to MNT, Manish Mittal, MD, hair transplant surgeon at Mittal Hair Clinic, who was not involved in this study, explained that “the vast majority of patients will never experience clinically significant hair loss, but the study reinforces that shedding can occur in a small proportion of people and is something clinicians should discuss before treatment.”

Thus, individuals taking GLP-1 medications for type 2 diabetes should be aware of all options available to them, which could include SGLT-2 inhibitors and DPP-4 inhibitors, depending on individual circumstances.

It is particularly important for people to be aware of the risk of hair loss in cases where they already have an increased risk of alopecia.

Ali further emphasized that the benefits of taking GLP-1s as prescribed usually outweigh the risks:

“For the vast majority of patients seeking treatment for obesity or diabetes, the metabolic benefits of GLP-1s significantly outweigh the risk of temporary, non-scarring hair loss, which usually resolves once weight stabilizes. Groups who might be more at risk for hair loss are those with pre-existing nutritional deficiencies or those experiencing very rapid, significant weight loss.”

“People who lose weight very rapidly, have pre-existing nutritional deficiencies, women with low iron stores, individuals recovering from bariatric surgery, or those with underlying androgenetic hair loss may notice shedding more readily because they already have reduced hair reserve,” Mittal added.

How to manage hair loss when taking GLP-1s

Working closely with a healthcare professional can help you manage hair loss or monitor for any changes when taking GLP-1 medications.

Opel Baker, MBChB, DipOccMed, MRCGP, a general practitioner at the Mayfield Clinic in Brigthon, United Kingdom, who was likewise not involved in the study, spoke to MNT about what a person can do if they have concerns about hair loss while taking a GLP-1.

“The most important advice is not to panic and not to discontinue treatment without medical advice. We encourage patients to lose weight at a sustainable pace rather than as quickly as possible, prioritize adequate protein intake, and attend regular follow-up appointments,” Baker said.

“If hair shedding develops, it’s sensible to assess dietary intake and, where clinically indicated, arrange blood tests to check for iron deficiency, thyroid disease, vitamin B12, or other contributing factors. Monitoring is straightforward and can form part of routine reviews,” he added.

Some general tips for managing non-scarring alopecia include:

• limiting the use of heated hair tools, such as hairdryers, as well as hair bleaching
• following a balanced diet favoring foods rich in rich in iron and protein
• stop smoking.

“Patients shouldn’t stop treatment because they’re worried about hair loss alone. Instead, they should focus on prevention,” explained Mittal.

He advised that:

“Maintaining adequate protein intake, avoiding excessive calorie restriction, and ensuring sufficient iron, zinc, and other micronutrients can make a significant difference. If someone notices increased shedding, particularly after 3 to 6 months, they should seek assessment early rather than assuming it’s permanent. A specialist can identify whether this is temporary telogen effluvium or an unrelated hair condition requiring different treatment.”

• Pancreatic cancer is a serious cancer type that can be difficult to catch early. 
• One potential target area is a protein called KRAS that can mutate in pancreatic cancer. 
• One study in people at risk for pancreatic cancer found that a vaccine that targeted KRAS was safe and produced a good immune response. 
• The results point to a way to prevent pancreatic cancer as research moves forward.

Pancreatic cancer accounts for 8% of cancer deaths in the United States, and it is challenging to catch pancreatic cancer early. Finding ways to treat and potentially prevent pancreatic cancer is a critical area of research.

One study evaluated a peptide vaccine in people who were at a high risk for pancreatic cancer. This vaccine targeted the mutated protein, KRAS, which is found in the most common pancreatic cancer, pancreatic ductal adenocarcinoma (PDAC).

The study, which appears in Cancer Discovery, found that using this vaccine to target KRAS mutations produced a long-term immune response. This discovery could lead to a full-fledged strategy to prevent pancreatic cancer. 

Why target the KRAS protein

This research explored a possible way to prevent PDAC, noting that one possible target is mutant KRAS.

Study author Elizabeth M. Jaffee, MD, Deputy Director of The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, explained to Medical News Today: 

“Pancreatic cancer takes 10 years or more to develop. It starts in normal pancreas cells with a mutation in the protein KRAS. KRAS normally regulates cell growth, division, and survival to maintain the health of organs like the pancreas. The mutation in this protein results in uncontrolled growth. But for pancreatic cancer to develop, additional mutations have to occur. Over 90% of pancreatic cancers start with this mutation, and the cancer remains dependent on this mutation.” 

Prior to this research the team had developed a vaccine targeting the six most common KRAS mutations present in PDAC, which they had tested in individuals who already had PDAC with favorable results. 

The current study focused on participants at risk for PDAC, such as those with a close relative with PDAC. All participants also had “radiographic evidence of a pancreatic abnormality,” the study paper details.

In all, researchers were able to work with 20 participants, and participants’ median age was 66.5 years old. 

Researchers gave participants 5 doses of the related vaccine, over several weeks, with the last booster dose happening on week 13. Participants tolerated the injections well, with only mild adverse events such as fatigue. 

The research team conducted a number of tests and analyses, including using information from particular blood cells from participants.

Vaccine leads to solid response against pancreatic cancer

The vaccine produced a solid T-cell response, a specific white blood cell type. This mutant KRAS-specific T-cell response occurred for 90% of participants. 

They did find that the T-cell response was greater against certain KRAS mutations than others, but 50% of participants still had a significant T-cell response against all six mutations.

Additional testing in particular blood cells found that the response against KRAS mutations was highest for a subtype of T cells called CD4+ T cells.  

Researchers followed up with participants for a median of 16.5 months. During this time, no participants experienced PDAC or had pancreatic lesions that required surgical intervention.

Three participants even saw a pancreatic cyst resolve and three others saw a decrease in cyst size. Compared to an unvaccinated cohort similar to the intervention group, the vaccinated group had greater cyst reduction and resolution. 

Long-term follow-up also suggested that the response of T-cells could be maintained and be useful in the long term. Additional testing at various timepoints further confirmed that the vaccine “can generate a durable repertoire of functional, [mutant]KRAS-specific T cells,” the researchers write.

Jaffee highlighted:  

“This study tested a vaccine that induces immunity against the KRAS mutation to eradicate the earliest changes in the pancreas cell that starts its journey to become a cancer. The goal is to stop this progression from happening. We tested it in healthy individuals who have either a family history or a genetic predisposition and had small cysts on their pancreas observed on MRI. We found that the vaccine induced immune responses against the mutations in KRAS and remained detectable for at least 2 years.”

What were the study limitations?

This study provides more information and hopes of preventing pancreatic cancer, but it still has limitations. For one, it only included 20 participants, so more data with a larger number of individuals will likely be helpful.

Certain follow-ups also included an even smaller number of participants, further indicating the need for more research. The trial type also carried limitations, such as how it was non-randomized. 

Researchers acknowledge that they also had a limited ability to see how the immune response correlated to cyst stability and cases of PDAC in the long term. They also note that the cyst resolutions that they did observe could actually be from technical limitations of the imaging they used.

They note that the most common lesions that are precursors to PDAC aren’t easy to find radiographically. Most of the cysts they observed were not these most common lesions. Further research and analysis of pancreatic cancer precursors will likely be helpful.

Not all participants received vaccines that targeted one particular KRAS mutation, although the T-cell response was still about the same for those who did and those who did not. There is also the possibility of skewed data on T-cell phenotypes, or what researchers were able to observe about the T-cells’ characteristics.  

The maximum amount of follow-up was 2 years, so additional long-term data may be helpful, as well as looking into the need for booster shots, since the immune response did experience declines.

Vaccine could expand prevention options

Overall, the findings indicate a possible pathway towards preventing pancreatic cancer, which would add to options when it comes to addressing this challenging cancer type.

Nilesh Vora, MD, a board-certified hematologist and medical oncologist and medical director of the MemorialCare Todd Cancer Institute at Long Beach Medical Center in Long Beach, CA, who was not involved in this study, noted that “this strategy introduces a potential shift from treatment to prevention.“

“Currently, most pancreatic cancer therapies focus on managing disease after diagnosis, often at advanced stages,“ said Vora. “A vaccine-based approach could expand our toolkit by offering a proactive option aimed at preventing cancer from developing in the first place, particularly in high-risk individuals. Over time, this could complement existing therapies and improve overall outcomes.”

Jaffee also emphasized that “this is the first study showing it is possible to induce an immune response against a cancer-causing protein at the earliest stages of cancer development.“

“We cannot say for sure that the resolution of cysts is directly related to the immune responses we test in the blood. The cysts are too small to biopsy,“ she cautioned.

“But these findings suggest we need to do further studies to try and prevent cancer. It is safe and may prevent cancer development and morbidity associated with treatment for advanced precancers which require surgery,” the study author concluded.

• A new study suggests that older females who limited their daily eating window to 8 to 9 hours showed significant improvements in some aspects of cognitive function compared with those who ate over a typical 12-hour period.
• While both study groups lost an average of 15 pounds over 6 months, only the time-restricted eating group experienced measurable cognitive improvements, suggesting the eating pattern itself may offer additional brain health benefits.
• Participants following time-restricted eating made fewer errors on memory and learning tests, although these improvements did not reach statistical significance. No differences were seen in multitasking or reaction time.
• However, the findings are from a small preliminary study, and the researchers plan to investigate the biological mechanisms behind the observed benefits and confirm the results in larger, more diverse populations.

Recent research from the World Health Organization (WHO) suggest that almost half of dementia cases globally could be delayed or even prevented.

Certain lifestyle choices, such as weight management and dietary choices, could potentially help lower the risk for dementia.

Time-restricted eating is a dietary approach where all daily food and calorie-containing drinks are consumed within a set time window each day, followed by a longer fasting period.

Previous research suggests that time-restricted eating may have a positive impact on cognitive function and mental health in older adults.

Although existing research has linked dietary and lifestyle habits with dementia risk, relatively few studies have explored whether changing eating patterns can directly influence cognitive health.

Now, a small clinical trial has found that limiting food intake to an 8 to 9-hour daily eating window may provide cognitive benefits for older women with overweight or obesity, beyond those achieved through weight loss alone. However, larger studies are necessary to confirm the results.

The findings come from a pilot clinical trial led by researchers at Rutgers University, presented at NUTRITION 2026, the annual meeting of the American Society for Nutrition. The study has not yet undergone peer review.

Time-restricted eating linked to better problem-solving, memory recall

The small trial enrolled 47 females aged 50 to 79 years who had overweight or obesity. All participants received counselling to reduce their daily calorie intake by approximately 500 calories.

Participants were then assigned to either a time-restricted eating or a standard eating group.

Those in the time-restricted eating group limited food intake to fewer than 9 hours per day, typically eating between 10:00 a.m. and 6:00 p.m., with an average eating window of 8.2 hours.

The standard eating group continued eating across a more typical 12-hour window, averaging 12.6 hours per day.

After 6 months, both groups lost a similar amount of weight, roughly 15 pounds (lb) or 6.8 kilograms (kg) on average. However, differences emerged when the researchers assessed cognitive performance.

Compared with those following the standard eating schedule, participants in the time-restricted eating group demonstrated significant improvements in spatial planning and problem-solving.

Researchers also observed a trend toward fewer errors on tests measuring memory and learning, although these differences did not reach statistical significance.

No meaningful differences were found between the groups in tests assessing multitasking ability or reaction time.

“The main takeaway is that when people eat may matter for cognitive health, not just how much they eat,” Dung Trinh, MD, Internist MemorialCare Medical Group and Chief Medical Officer of Healthy Brain Clinic in Irvine, CA, who was not involved in the study, told Medical News Today.

“In this study, women who combined calorie restriction with an 8- to 9-hour eating window showed greater improvement in spatial planning and problem-solving than women who followed calorie restriction alone,” Trinh explained.

“At the same time,” he cautioned, “this was a small, 6-month study, so the findings should be viewed as preliminary. We are not saying that time-restricted eating prevents dementia or treats Alzheimer’s disease. Rather, the results suggest that meal timing may be an important and modifiable lifestyle factor that deserves further study.”

“For healthcare professionals, the findings highlight the potential value of looking beyond calories and weight loss alone and considering the timing and consistency of food intake as part of a broader discussion about metabolic and cognitive health,” he suggested.

Does the timing of food intake matter more than the weight loss?

The researchers suggest that restricting eating to an 8 to 9-hour window may provide modest cognitive benefits that extend beyond those of weight loss alone. They propose that reducing the eating window may lead to improvements in spatial planning, problem-solving, and reducing errors related to memory and learning.

Global cases of Alzheimer’s disease and other forms of dementia are increasing due to aging populations, with age being the strongest known risk factor for dementia.

Research also highlights that obesity and abdominal fat increase the risk of cognitive decline and dementia, with studies highlighting abdominal obesity as a significant, independent risk factor for early-onset dementia in females.

“The results suggest that meal timing may have contributed benefits beyond weight loss, because both groups lost a similar amount of weight, but the group following time-restricted eating showed greater improvement in planning and problem-solving,” Trinh noted.

“However, we cannot yet say that timing matters more than weight loss,” he cautioned. “Weight loss itself can improve metabolic health and may support cognition.”

According to Trinh:

“The more likely explanation is that these factors work together. Shortening the eating window may improve the alignment between food intake and the body’s internal clock, reduce late-day eating, and create longer daily fasting periods, while weight loss may improve insulin sensitivity and other cardiometabolic risk factors.”

“An important next step is to determine whether the benefit comes primarily from eating within a shorter window, eating earlier in the day, fasting longer overnight, or some combination of these factors,” he added.

Why might time-restricted eating affect brain health?

Interventions that may help preserve cognitive function form an important area of research. While the current study was not designed to explain why the benefits occurred, the researchers believe several biological mechanisms could be involved.

They suggest that time-restricted eating may influence cognitive health through interactions between circadian rhythms, nutrient-sensing pathways, inflammation, and metabolic health. However, they note that further research is necessary.

Previous research has highlighted the possible role of chrononutrition, which describes the timing, frequency, and regularity of food intake in relation to circadian rhythm.

Aligning food intake with the circadian rhythm may support weight regulation and metabolic health, which, in turn, could influence brain health.

However, more evidence is necessary to establish whether these mechanisms explain the improvements seen in this study.

“Circadian alignment is especially promising because meal timing is one of the strongest signals the body uses to coordinate metabolism across the day,” Trinh highlighted. “Eating over a shorter and potentially earlier window may help synchronize glucose regulation, hormone release, sleep-wake patterns, and brain function.”

“That said, circadian biology, inflammation and metabolic health are closely connected. Poor circadian alignment can impair insulin sensitivity and promote inflammatory signaling, while improved metabolic health may support blood flow and energy use in the brain,” he explained.

“The most informative future studies will measure all three pathways together. This could include continuous glucose monitoring, inflammatory biomarkers, sleep and activity tracking, hormone rhythms and, eventually, brain imaging or Alzheimer’s-related biomarkers,” Trinh noted.

Important limitations

Although the results are encouraging, the researchers caution that the findings should be interpreted carefully.

The study involved a relatively small number of participants and only included females with overweight or obesity. Thus, it is unclear whether the findings would apply to males, younger adults, or people with different body weights or health conditions.

Additionally, the results have not yet undergone peer review or been published in a medical journal, so they should be considered preliminary and may change following peer review.

Larger, longer-term clinical trials will be necessary to determine whether time-restricted eating can meaningfully reduce the risk of dementia or help slow age-related cognitive decline.

• The 2026 ACC/AHA Dyslipidemia Guideline introduced significant changes in how cardiovascular risk will be assessed and lipid (cholesterol) levels will be managed.
• Among the key updates are a new risk calculator, the introduction of lipoprotein (A) testing, lower cholesterol targets, and calcium testing.
• A recent study found that 1 in 3 Americans without heart disease have higher LDL cholesterol levels than the 2026 guideline now recommends.
• Medical News Today spoke to three experts to discuss what this means for cholesterol management and how people should approach taking medications such as statins.

Earlier this year, the American College of Cardiology/American Heart Association released the 2026 Guideline on the Management of Dyslipidemia, replacing its last iteration, the 2018 AHA/ACC Guideline on the Management of Blood Cholesterol.

The updated guidelines reflected many shifts in how medical professionals now approach cholesterol and heart disease.

Recently, Mass General Brigham researchers found that almost one out of every three adults without heart disease in the United States have LDL, or “bad”, cholesterol levels above the goals set by the 2026 guideline.

For those who have already had a heart attack, stroke, or other cardiovascular event, this figure jumps to almost four in five.

The 2026 guideline recommends specific target goals before prescribing medication, such as keeping LDL cholesterol levels at under 55 milligrams per deciliter (mg/dL) for very high risk individuals, and at under 70 mg/dL or under 100 mg/dL depending on baseline primary risk.

However, it also strongly emphasized personalized targets.

Medical News Today spoke to three experts to discuss whether people should revise their cholesterol targets, what medications are available to lower LDL levels, and whether dietary supplements can help:

• Chandan K. Buttar, MD, a cardiovascular disease and internal medicine specialist in New Orleans, LA
• Wahaj Aman, MD, a cardiologist with Memorial Hermann and UTHealth Houston
• and Kyle Hoedebecke, MD, MBA, MPA, MS, FAAFP, CPE, clinical advisor of Alpas Wellness NOVA in Virginia.

What changed with the new guideline?

Experts said the main takeaway from the 2026 ACC/AHA guideline was the reintroduction of specific LDL-C targets, universal Lp(a) screening, and the inclusion of children to assess familial risk.

For example, the guideline now recommends that cholesterol screening start in childhood at ages 9–11, which then should be repeated at ages 19–21, and every 5 years in adults to track and spot lifelong risk early.

Aman pointed out that the updated guideline introduced a new risk calculator called PREVENT, which expands the age of screening from ages 30 to 79 years, up from the previous range of ages 40 to 75 years.

It also provides 10- and 30-year risk estimates for heart disease and considers kidney function as a risk factor.

He also listed two important changes. First, that every adult should be tested for lipoprotein(a), or Lp(a), at least once. Testing of first-degree family members is recommended when Lp(a) is elevated.

Second, that calcium score testing in men aged 40 years or older and women aged 45 years or older is recommended when the decision about lipid-lowering therapy is at intermediate risk.

A calcium score above 100 should have a goal LDL cholesterol of under 70. Above 1,000, the goal LDL is under 55.

“[R]ather than treating based on a single number — the LDL [cholesterol levels] — clinicians will now use an estimated total cardiovascular risk assessment. They will also look at ‘risk-enhancing’ factors — e.g. family history, chronic kidney disease, inflammatory conditions, high levels of lipoprotein[a] — and treat based on the patient’s risk level,” Hoedebecke said.

“Thus, two individuals with the exact same level of LDL may present vastly different risks of suffering a myocardial infarction [heart attack] or ischemic stroke due to the rest of their medical profile,” he added.

On the topic of testing and treatment, Aman said patients may benefit from discussing new, lower LDL cholesterol goals with their clinicians if they are at higher risk.

“Asking your clinician about individualized LDL targets is reasonable, especially if you have a family history of early heart attack, diabetes, multiple risk factors, or established heart disease,” he said.

Why do so many Americans remain untreated?

“One of the reasons why so many Americans continue to be under-treated is that high cholesterol is typically asymptomatic. Patients frequently do not experience physical discomfort until after years of exposure to high levels of blood cholesterol,” Hoedebecke said.

Buttar said the reasons why Americans remain untreated or undertreated were manifold.

“A lack of awareness of cardiovascular risk, concerns about or experience with side effects from statins, limited access to primary care or preventive cardiology, and inconsistent measurement and monitoring of risk factors,” she listed.

“One reason some patients discontinue their prescribed statins is due to myalgia or other musculoskeletal pain experienced while using the medication. However, actual statin intolerance appears to be less frequent than commonly believed,” Hoedebecke added.

“There is a myth that doctors get paid to prescribe statin medications, whereas statins are completely generic,” Aman also noted.

Aman further pointed out the racial disparities when it comes to statin use:

“One of the leading reasons is that many patients are never offered a statin. In the PALM registry, [t]hose never offered were more likely to be female, Black, or Hispanic. There is significant racial disparity when it comes to statin use. Statin use is significantly lower in Black (44.3%), Hispanic (33.7%), and Asian (49.2%) adults compared with White adults (58.3%),” he said.

• As the popularity of GLP-1 medications continues to increase, further research is examining the potential side effects. This may include possible eye issues and vision loss. However, there is currently conflicting information about how these drugs may affect vision.
• In a target trial emulation, GLP-1 use was associated with a small increase in the risk of nonarteritic anterior ischemic optic neuropathy (NAION), but the absolute risk was very low, making the event rare despite the relative increase.
• In a Swedish study, people starting GLP-1 drugs did not have a significantly higher risk of NAION than those starting SGLT2 inhibitors, suggesting that any increased risk is likely to be small.
• Taken together, both studies suggest that GLP-1s may be associated with a small increase in NAION risk, but the absolute risk appears very low, indicating it is unlikely to be a common clinical risk.

As the use of glucagon-like peptide-1 (GLP-1) agonists for type 2 diabetes and weight loss continues to grow, so too does the research examining their potential impact on other areas of health, including possible eye issues and vision loss.

Previous research has linked GLP-1 use to potentially-blinding eye conditions. Specifically, research highlights a possible association with semaglutide, the active ingredient in medications such as Ozempic.

Other studies suggest that other drugs containing semaglutide, such as Wegovy, are more likely to cause adverse events causing vision loss.

Most studies propose a link between GLP-1 use and the development of ischemic optic neuropathy (ION), an uncommon eye condition that can cause sudden, painless vision loss due to blood not flowing properly to the eye’s optic nerve.

Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common form of optic neuropathy in adults over the age of 50, and is often linked to GLP-1 use, despite the exact mechanism remaining unknown.

Now, two separate studies suggest that while GLP-1 receptor agonists may slightly increase the risk of vision loss, the side effect remains very rare, meaning the likelihood of it occurring in people taking these medications is low.

The United States and Swedish studies, both published in the Annals of Internal Medicine, found that people with type 2 diabetes who begin treatment with GLP-1s may have a slightly higher risk of developing NAION.

However, the study authors suggest that the condition remains rare and the overall benefits of these medications are unchanged.

What did the US study find?

Researchers from Rutgers University analyzed healthcare data from a large U.S. database of insurance claims from adults aged 18 to 65 with type 2 diabetes who started glucose-lowering medication.

Compared with people taking other diabetes medications, such as SGLT-2 inhibitors or DPP-4 inhibitors, those treated with GLP-1 drugs had a higher relative risk of ischemic optic neuropathy. However, the researchers stressed that the condition remained uncommon.

“We found that GLP-1 receptor agonist use was associated with a small increase in the 18-month risk of ischemic optic neuropathy compared with SGLT2 inhibitors and DPP-4 inhibitors,” U.S. study author Chintan Dave, PharmD, PhD, Associate Professor of Pharmacy and Epidemiology at the Rutgers Ernest Mario School of Pharmacy and Rutgers School of Public Health, explained to Medical News Today.

“The signal was concentrated among adults aged 50 to 65 years and men, who accounted for approximately 85% and 70% of events, respectively. The main takeaway is that clinicians and patients should be aware of this potential risk, particularly in these higher-risk groups, while recognizing that the absolute risk remained very low,” Dave detailed.

Over an 18-month period, the increase amounted to approximately three to four additional cases per 10,000 patients treated with GLP-1 medications.

“This corresponds to approximately one additional case for every 3,333 or 2,778 patients treated, respectively. Even among patients aged 50 to 65 years and men, who generally had a higher risk, the event remained rare,” the researcher told us.

The study authors add that although the condition is rare, it is clinically important because vision loss can occur suddenly and may be permanent.

“Sudden, painless changes in vision, particularly dimming or blurring in one eye, loss of part of the visual field, or sudden vision loss, should prompt urgent, same-day evaluation by an ophthalmologist or emergency department,” Dave emphasized.

What did the Swedish researchers find?

Researchers from the Karolinska Institutet analyzed nationwide healthcare data from adults aged 35 to 84 years with type 2 diabetes in Sweden between 2013 and 2024.

The study included more than 293,000 participants who started either a GLP-1 drug or an SGLT-2 inhibitor. After 1 year of follow-up, the risk of NAION was 0.04% among people taking a GLP-1 medicatio and 0.02% among those taking an SGLT-2 inhibitor.

Although this represents a higher relative risk among GLP-1 drug users, the study authors stressed that the adverse event remained rare in both groups.

“Patients and physicians should interpret these numbers as a demonstration that the risk of having NAION can increase with use of a GLP-1RA medication. The risk, however, is still quite low,” Benjamin Bert, MD, a board-certified ophthalmologist at MemorialCare Orange Coast Medical Center in Fountain Valley, CA, who was not involved in the study, told MNT.

“Relative risk showed that there was double the chance of having NAION in the GLP-1RA group compared to the SLGT-2 group, that sounds very dramatic, but when you look at the absolute numbers, an increase in 0.02% is quite low,” Bert pointed out.

Similar to the U.S. study, in practical terms, this corresponds to roughly four cases per 10,000 people taking a GLP-1 drug over 1 year, compared with 2 cases per 10,000 people taking an SGLT-2 inhibitor.

However, further research is still necessary to fully understand the association between GLP-1 use and NAION risk, and the role of confounding variables.

“In a large population study there is likely to be many confounding variables,” Bert added. “Those can become even more challenging when you are looking at a disease like NAION that is rare to begin with.”

“The overall results found that there was an increased risk of having NAION due to GLP-1RA use. However, it was a small increase and the authors felt that it could be due to the confounding variables they uncovered in this study.”

– Benjamin Bert, MD

Should people taking GLP-1 medications be concerned?

The researchers of both studies caution that the findings should be interpreted carefully and should not change current prescribing practices.

As the studies were observational, they cannot prove that GLP-1 medications directly caused the increase in risk. Instead, the authors suggest it may highlight underlying differences between those receiving GLP-1s and other diabetes medication.

For example, those taking GLP-1s may have more advanced or a higher burden of cardiovascular risk factors, both of which are independently associated with optic nerve disease.

For most people, the study authors conclude that the proven benefits of GLP-1 drugs for those with type 2 diabetes, such as improvements in blood glucose control, weight loss, and reductions in cardiovascular and kidney disease risk, outweigh this potential safety signal.

Although both studies suggest that GLP-1 use may be associated with a small increase in the risk of developing NAION, the condition remains very uncommon, and any potential increase in risk is likely to be small in absolute terms.

While the new findings contribute to an evolving and sometimes conflicting body of evidence linking GLP-1 use to vision loss, the authors conclude that they underscore the importance of continued monitoring as use of GLP-1 medications expands worldwide.

It is advisable for people taking diabetes medication to seek prompt medical attention if they experience sudden changes in vision, including painless vision loss or new blind spots.

• Modifiable cardiovascular risk factors, such as obesity, type 2 diabetes, and smoking, were associated with the buildup of high risk plaque in the major coronary arteries.
• Having a greater number of modifiable risk factors was associated with a greater number of high risk, or vulnerable, plaques.
• High risk plaques are more likely to trigger adverse cardiac events such as heart attacks.

A new study has shed new light on how certain cardiovascular risk factors might alter a person’s risk of adverse cardiac events, such as heart attacks, by noting an association between modifiable risk factors and the buildup of plaques in the coronary arteries.

Researchers from Mass General Brigham Heart and Vascular Institute set out to investigate the association between both modifiable and non-modifiable risk factors and the amount and types of plaques found across the three major coronary arteries.

Clinical practitioners have long been aware of factors that can influence people’s risk of developing cardiovascular disease.

These factors include modifiable ones, which people can change, such as high blood pressure, obesity, and cigarette smoking. They also include non-modifiable factors that people cannot alter, such as age, sex, and a family history of coronary artery disease.

While these risk factors are well-established, most research up until now has focused on looking at them individually, or within specific groups of patients.

The new study, published in JACC: Advances, took a different approach by looking at all of these risk factors together to see how the number of risk factors present might relate to plaque formation.

What did the researchers look at?

The researchers examined optical coherence tomography (OCT) imaging from 131 patients from the Massachusetts General Hospital registry who had not previously received treatment for blocked or narrowed coronary arteries.

OCT is an imaging technique using near-infrared light that can provide highly detailed cross-sectional images of blood vessels.

Each participant received OCT imaging of their three major coronary arteries. Across all of the patients, this imaging revealed a total of 534 plaques for the researchers to analyze.

The researchers then looked to see if there were any associations between the plaques present in the coronary arteries with the risk factors the participants had. They carried out separate analyses looking at modifiable risk factors, non-modifiable risk factors, and total risk factors.

What did the researchers discover?

The study authors found that as the number of risk factors increased, so too did the number of plaques visible in the OCT imaging.

They also observed a greater number of a particular type of plaque, known as thin-cap fibroatheroma. This type of plaque is known to be a high risk, or vulnerable, plaque type that is more likely than other types to trigger adverse cardiac events like heart attacks.

A greater number of risk factors was also associated with a higher number of another type of vulnerable plaque: lipid-rich plaques.

Among participants with at least 4 modifiable risk factors, 1 in 2 plaques were thin-cap fibroatheromas, and 4 in 5 were lipid-rich plaques.

“The higher the number of vulnerable, or rupture-prone plaques, the greater the chance that one of them will trigger an adverse event,” said senior author Ik-Kyung Jang, MD, in a press release.

Modifiable vs. non-modifiable risk factors

The researchers found that it was only an increased number of modifiable risk factors that was associated with a greater spread of these high risk plaques across all three major coronary arteries.

Non-modifiable risk factors were associated with more stable plaque types.

The modifiable risk factors recorded in the study were:

• high levels of low-density lipoprotein cholesterol
• high blood pressure
• diabetes mellitus
• obesity
• cigarette smoking

Medical News Today asked Dr. Jang why modifiable risk factors might be more associated with the buildup of vulnerable plaques than non-modifiable risk factors.

“We believe that the association between modifiable risk factors and plaque vulnerability is largely mediated by inflammation,” he said. “All five modifiable risk factors—dyslipidemia, hypertension, diabetes, obesity, and smoking—are known to promote vascular inflammation.

“In contrast, non-modifiable risk factors, such as age, sex, and family history, may primarily contribute to the gradual progression of atherosclerosis through pathways less directly driven by inflammation,” he added.

What comes next?

“The natural next step is to test, in a prospective study, whether aggressive management of modifiable risk factors can reduce plaque vulnerability,” Dr. Yang told MNT.

The researchers acknowledge that the limitations of this study mean that more research is needed before their findings can be generalized to a wider population.

The data they analyzed for the study came from a specific pool of hospital patients, who had yet to receive certain types of treatment and who were able to receive OCT imaging. As a result, the study authors say these present findings are only suitable for interpretation among a similar patient population.

In order to generalize these findings, the authors suggest that research involving larger groups of people that include people who have received treatment for blocked arteries will be required.

Until then, they conclude that their findings underline the importance of targeting modifiable risk factors to help prevent heart attacks.

“Our findings highlight the importance of early, intensive and sustained interventions to control the modifiable risk factors and prevent future events,” said Dr. Jang in the press release.

• A new perspective paper argues that official public health advice for protein intake and exercise may be outdated, as it focuses on preventing disease rather than maximizing long-term health.
• The research cited in the study suggests that protein intake can be increased to approximately twice the current standard recommendations, reaching up to 1 gram per pound of body weight.
• The researchers conclude that increasing protein intake will not only support muscle recovery but also aid strength gains and fat loss, and help preserve bone health.
• Medical News Today spoke to two experts to discuss the evidence so far and see how these recommendations can be applied in real life.

Are the so-called “gym bros” actually onto something when it comes to protein? And could we all benefit from consuming more protein in our diets?

A perspective paper published on June 16, 2026 in Frontiers in Nutrition makes the case for updating current official public health advice for protein intake and exercise.

In the paper, Chris Macdonald, PhD, fellow and lab director at Lucy Cavendish College, University of Cambridge, in the United Kingdom, draws attention to the fact that current recommendations focus on minimum intakes to prevent disease rather than on maximizing long-term health benefits.

An important point from the research compiled is that certain groups of people — namely, physically active adults, older adults, and pregnant people — may benefit from much higher protein intakes than are currently recommended.

The paper argues that our protein intake could be increased to about twice the current minimum recommendations, reaching up to 1 gram per pound (g/lb) of body weight.

For reference, the current guidelines recommend at baseline around 0.75 to 0.8 grams of protein per kilogram of body weight per day (g/kg/day), or roughly about 0.34 to 0.36 g/lb.

The paper also concludes that increasing protein intake offers wide-ranging benefits, including faster muscle recovery, better weight management and fat loss, and reduced risk of fractures.

It’s important to note, however, that federal or international dietary guidelines are designed for the general population and not specific groups, so change is often slow and requires decades of evidence. Nonetheless, the current guidelines could benefit from a review by public health officials.

To discuss how individuals should approach consuming protein and more, Medical News Today spoke to two experts:

• Michelle Routhenstein, MS, RD, CDCES, CDN, a preventive cardiology dietitian at EntirelyNourished,
• and Kristin Kirkpatrick, MS, RDN, president of KAK Consulting and a dietitian at the Cleveland Clinic Department of Wellness & Preventive Medicine in Ohio.

How protein intake can affect kidney, gut, and heart health

So, when it comes to protein, is there an upper safe limit? And will eating too much affect other systems in the body?

“For healthy adults with normal kidney function, protein intakes up to about 2 g/kg/day appear to be safe. However, there’s little evidence that routinely eating more than this provides additional health benefits, and very high intakes over the long term may increase the risk of digestive, kidney, or vascular issues,” Routhenstein said.

However, Routhenstein singled out a particular group of people who should watch their protein intake — people with chronic kidney disease. She recommended they follow individualized protein targets depending on their stage of disease and lab results.

“Excessive protein can place additional stress on the kidneys and may accelerate disease progression,” she added.

Why protein source matters to health

Kirkpatrick also touched on another important consideration: how people increase their protein intake.

“If higher protein comes primarily from processed meats and foods high in saturated fat, it may increase cardiovascular risk. The goal isn’t simply ‘more protein’, it’s choosing higher-quality protein sources within an overall well-planned heart-healthy diet,” she said.

Routhenstein explained that high intakes of animal protein, particularly red and processed meats, can increase levels of TMAO (trimethylamine N-oxide) in the body. She said high TMAO levels have been linked to cardiovascular risk.

On the gut health front, Routhenstein said animal-protein-heavy diets may also disrupt the microbiome by “shifting toward more gram-negative gut bacteria, which can contribute to inflammation and arterial stiffness.”

“From a gut health standpoint, problems are less about the protein itself and more about what might be missing. If someone is eating a high-protein diet that’s low in fiber, fruits, vegetables, legumes, and other plant foods, gut health can certainly suffer. But that can happen with any poorly balanced eating pattern,” Kirkpatrick said.

And what about exercise? Kirkpatrick said she wouldn’t take protein as a stand-alone factor in a longevity plan.

“Regular physical activity is one of the most important pillars of longevity. We have strong evidence showing benefits not just for cardiovascular health, but also for maintaining muscle, supporting brain health, reducing the risk of certain cancers, helping with weight management, improving mental health, and preserving independence as we age,” she said.

“Eating more protein without challenging your muscles may still have benefits, but combining adequate protein with regular resistance training and overall physical activity is where you really maximize the return. Any longevity plan that leaves out exercise is missing one of its most critical pieces.”

— Kristin Kirkpatrick, MS, RDN

• Past research shows there a micronutrient known as polyphenols may help slow down the aging process. 
• Polyphenols are found in a variety of foods, including coffee.
• A new study says that polyphenols and other compounds in coffee help activate a specific protein in the body known to help alleviate inflammation and protect against stress and chronic diseases, leading to healthier aging. 

Although aging is inevitable, research shows there are healthy choices people can make — such as not smoking, being physically active, and following a healthy diet — that may allow them to age slower and in a healthier way.

When it comes to diet, previous studies show that certain foods may help slow down the aging process due to the nutrients they contain.

One example is polyphenols — naturally-occurring micronutrients known to help lower damage to the body’s cells and lower inflammation. 

Polyphenols are found in a variety of foods, including berries, pomegranates, artichokes, spinach, dark chocolate, extra virgin olive oil, walnuts, green and black teas, and coffee. 

“Aging and associated age-dependent development of chronic diseases are facts of life, however, there are dietary and lifestyle choices that can slow this process,” Stephen Safe, PhD, a distinguished professor and Sid Kyle Endowed Chair in Veterinary Toxicology in the Department of Veterinary Physiology and Pharmacology in the College of Veterinary Medicine and Biomedical Sciences at Texas A&M University, explained to Medical News Today.

“For example, individuals that live in Blue Zones or drink coffee live longer and have decreased age-related health problems,” Safe told us.

Safe is the lead author of a new study published in Nutrients that helps to shed more light on how coffee may help provide aging benefits.

Researchers found that polyphenols and other compounds in coffee help activate a specific protein in the body known to help alleviate inflammation and protect against stress and chronic diseases, leading to healthier aging. 

Coffee’s polyphenols activate protective protein in the body 

Using multiple cellular models, scientists examined how certain polyphenols and other compounds in coffee might interact with a specific protein in the body called NR4A1. 

“NR4A1 was initially discovered as a gene that responds to various types of stress including oxidative and inflammatory stress,” Safe explained.

“In my [previous] review, it was clear that NR4A1 was involved in aging and mortality and levels of this gene in humans decreased [in] age. And in mice, animals with loss of NR4A1 had a shorter lifespan. It was also evident that NR4A1 protected mice from tissue/cell injury and compounds that bound NR4A1 further enhanced the protection. Therefore, we hypothesized that coffee components would bind NR4A1 and be protective.” 

– Stephen Safe, PhD

At the study’s conclusion, researchers found that various compounds in coffee — including polyphenols like caffeic acid — bind to and activate NR4A1, potentially reducing cellular damage and offering disease protection.

“The significance of this finding is that now we know at least one pathway (coffee-NR4A1) that explains some of the age-protective effects of coffee that have been observed in humans, and these results further support a protective role of NR4A1 in aging,” Safe explained.

“It also suggests that NR4A1 may be a target for developing pharmaceuticals and nutriceuticals that are health protective,” he told us.

Not yet proof that coffee is an anti-aging treatment

MNT had the opportunity to speak with Dung Trinh, MD, an  internist for MemorialCare Medical Group and chief medical officer of the Healthy Brain Clinic in Irvine, CA, about this study. 

Trinh — who was not involved in this research — commented his first reaction to these findings was one of cautious optimism. 

“The study offers an intriguing biological explanation for some of the health benefits that have long been associated with coffee,” he explained.

“At the same time, it is important to put the findings in context,“ he told us. “This was primarily a laboratory study using cell models — not a clinical trial showing that drinking coffee slows aging or prevents diseases such as Alzheimer’s. I view it as an important mechanistic clue and a strong reason to continue the research, rather than proof that coffee is an anti-aging treatment.” 

Trinh said while we can’t stop chronological aging, we may be able to influence how well the body ages. 

“The goal should not simply be to add years to life; it should be to add healthy, functional years,” he continued. “This is especially important as populations live longer. Delaying the onset of disability, cognitive decline, or chronic disease by even a few years could have a major impact on patients, families, caregivers, and healthcare systems.”

“Research into receptors such as NR4A1 may help scientists identify new prevention strategies, biomarkers, and therapeutic targets, although those possibilities still require rigorous human testing,” Trinh added. 

Ways to activate the NR4A1 protein

For those who may not want to drink coffee, MNT asked Trinh if there were any other ways to activate the NR4A1 protein for its potential health benefits. 

Trinh said that at this point, we do not have a clinically proven diet, supplement, or lifestyle prescription specifically designed to activate NR4A1 in people, and that distinction is important.

“The compounds that appeared most active in this study were not primarily caffeine,” he detailed. “They included plant-derived polyphenols such as caffeic acid, chlorogenic acid, and ferulic acid. Related compounds are found in a variety of fruits, vegetables, and other plant foods, and previous laboratory research has identified substances such as resveratrol, quercetin, and kaempferol as potential NR4A1 ligands.”

“However, we do not yet know whether consuming a particular food produces enough of these compounds in human tissues to generate a meaningful NR4A1 effect,” Trinh added. 

For those who do not drink coffee, Trinh said the most responsible advice remains to follow an overall healthy pattern:

• follow a diverse, plant-rich diet
• exercise regularly
• obtain adequate sleep
• avoid smoking
• manage blood pressure, cholesterol, and blood sugar.

“Those behaviors have much stronger human evidence behind them than attempting to target one receptor through a particular food or supplement,” he added.

• A new paper investigates how the slow accumulation of certain mutations in DNA affects human life span.
• Called somatic mutations, they begin accumulating in cells from birth. 
• The study shows that mutations in certain cell types, such as neurons, may be a key factor in defining a human’s maximum possible age.
• In line with the mathematical model scientists created, researchers calculated the maximum age a human could reach as up to around 190 years.

In the Bible, we learn that humans should expect to survive to the age of “three score years and ten,” or 70 years in modern parlance.

Today, the internet is awash with influencers claiming that their wellness “hacks” will extend your life span well beyond the boundaries we consider typical today. 

However, a new study, published in the journal NPJ Aging, might push the biblical limit back somewhat, while putting a lid on lofty influencer claims of eternal life.

According to the new paper, genetic changes that occur throughout our lives create “critical longevity bottlenecks.” The authors believe this places the upper limit of human life span at around 190. 

The mysterious inevitability of aging

Ask anyone from any culture to explain what “aging” is, and they will be able to give you some kind of answer. However, if you ask a scientist, the answer will be long, couched in caveats, and inconclusive.

Researchers are still trying to get to grips with this complex and inevitably terminal process.

In 2023, a paper published in Cell outlines 12 hallmarks of aging. They include an increased likelihood of genetic mutations as a cell divides, an inability to manage protein production and maintenance, and mitochondrial dysfunction.

Some of these 12 hallmarks are theoretically reversible. For instance, one sign of biological aging is a decrease in telomere length (the protective caps at the end of DNA sequences that prevent entanglement). 

Certain interventions can prevent telomere shortening, which should, in theory, extend life span. However, as the authors of the new paper explain, “actual longevity therapies are yet to appear.”

Death by somatic mutation

Somatic mutations are changes in the genetic code of any cell in the body, except germline cells (sperm and egg). They are an inevitable part of cell division and occur throughout our bodies and lives.

Sometimes, they are triggered by exposures, such as tobacco smoke or ultraviolet light, but other times, they just… happen.

Some somatic mutations are not too disruptive, and the cell can continue in its slightly altered form. Others cause enough trouble within the cell that it causes cell death. 

The idea that somatic mutations might be involved in the aging process dates back to the late 1950s. Scientists believe that, over the course of a life span, these mutations build and build, slowly impairing cellular functions, increasing disease risk, and helping to drive the aging process.

Medical News Today contacted Jordan Weiss. He’s an assistant professor in the assistant professor in the Division of Precision Medicine and Optimal Aging Institute at NYU Langone Health.

We asked Weiss, who was not involved in the study, why somatic mutations are so important in aging: 

“A person in their 80s carries thousands of somatic mutations in a typical cell. The body has no mechanism for going back and correcting damage that has already been written into a cell’s genome.”

“Over decades,” he continued, “that accumulated damage degrades how well a cell does its job, and in some cases sets the stage for cancer.”

Because cells with somatic mutations occur in every tissue of the body, and each mutation can be different, they are not a viable clinical target. Where would one start if they aimed to eliminate every single cell with a mutation? 

So, regardless of what anti-aging interventions you attempt and which hallmarks you reverse, somatic mutations will continue to wreak havoc.

With this in mind, the new paper sets out to calculate “how long humans would live if we cured most aging processes except somatic mutations.”

To investigate, the scientists developed a model in which they could calculate the general rate of somatic mutations in the different tissue types of the body. This approach allowed them to “estimate the limits to human lifespan when aging is driven purely by somatic mutagenesis.”

Is immortality a pipe dream?

Using their model, the scientists calculated that, if all hallmarks of aging are taken out of the equation (including somatic mutations), the median life span would be 1,759 years, and the maximum would be 29,921 years; a ripe old age indeed.

However, once somatic mutations are added back in, these advanced ages disappear, and immortality becomes even more unlikely. The authors write: 

“Our results suggest that even if all hallmarks of aging were eliminated except for somatic mutations, median human life span would reach only 146–194 years — roughly twice the current 79 years.”

MNT contacted Egle Pavyde, a pharmacist by training with a PhD in regenerative medicine and stem cell research. “We know that the longest-lived person in our history was a lady who died at the age of 122,” said Pavyde, who was not involved in the study. 

“This means that somatic mutations are a major driver of aging but can’t account for it all by themselves,” she said.

While these results might come as a disappointment to biohackers and optimizers aiming for immortality like Bryan Johnson, the scientists hope their novel approach might offer a starting point for investigating how individual biological processes contribute to aging. 

Potentially, it could help identify which mechanisms should be prioritized when exploring new ways to slow aging.

At-risk organs for aging: Heart and brain

Interestingly, the authors found that some of the tissues in our bodies are more resilient to somatic mutations than others. In particular, liver cells. According to their models, these cells would happily replace old cells and continue to thrive for 100,000 years or more.

At the other end of the spectrum, myocardial cells (from the middle layer of the heart wall) and neurons (brain cells) are much more susceptible to somatic mutations. This is because these cells are “terminally differentiated.” In other words, they no longer divide and multiply, so once their function is lost, it cannot be regenerated.

Once these cell types fail, the heart and brain fail, and that, of course, will cause death. The authors refer to these cell types as “critical lifespan bottlenecks.”

What does it all mean?

Taken together, the results of this study suggest that, even if we could overturn the other hallmarks of aging, avoid chronic diseases, and live an accident-free life, somatic mutations would eventually ruin our fun.

At the same time, they provide potential new targets for future scientists to aim at. If we could design a way to overturn or in some way manage somatic mutations, neurons and heart cells should be the main areas to focus on.

However, we should take the results with a pinch of salt.

“This study is only mathematical modeling, and not a real-life exercise,” Pavyde told MNT.  “It’s a theoretical extrapolation built on simplified assumptions. It models a hypothetical human with every other aging hallmark switched off (which is not biologically achievable).”

“It also relies on estimated mutation rates and cell-death thresholds from a limited set of tissues, and doesn’t capture how the various hallmarks of aging interact and compound one another,” she added.

How to fend off aging

While we wait for the key to immortality, we asked Pavyde how people can extend their lives without hi-tech interventions.

“Since the paper itself implies most of what limits us today comes from aging processes other than mutations, the practical levers remain the well-evidenced basics.” According to her, this includes:

“Don’t smoke, be physically active, eat a whole-food diet, prioritize sleep, maintain strong social connections, and keep up with disease prevention at all costs. This alone can add up to 10–20 years of additional healthy years.”

“To date,” she concluded, “there are no other interventions that can provide a greater effect.”

“If human life span is constrained by non-regenerative tissues,” Weiss added, “then safeguarding the heart and brain remains our highest-value strategy. The best advice is something you’ve already heard: sleep well, eat well, move around, manage stress, and do them consistently.”

• About 75% of processed foods contain a commercially used sweetener, including artificial and natural sweeteners and sugar alcohols. 
• Past studies have linked consumption of artificial sweeteners to several potential health issues, including disruption of the gut microbiome. 
• A new study found that certain commercially used sweeteners slow or halt the growth of beneficial gut bacteria, either on their own or when combined with certain compounds and medications.

Researchers estimate that about 75% of all processed foods include a commercially used sweetener, which includes artificial and natural sweeteners, as well as sugar alcohols.

Past studies have linked consuming artificial sweeteners to several potential health issues, including a higher risk of heart disease, stroke, type 2 diabetes, metabolic syndrome, cognitive decline, chronic kidney disease, and cancer. 

Previous research has also shown a potential negative impact of consuming artificial sweeteners on the gut microbiome. 

Now, a new study published in the journal Molecular Systems Biology reports that certain commercially used sweeteners — including artificial sweeteners — slow or stop the growth of beneficial gut bacteria, either on their own or through enhanced effects when combined with certain compounds and drugs. 

Testing 39 sweeteners on 25 types of gut bacteria

For this study, researchers used an in vitro model in which 25 different gut bacterial species were grown in a lab. These bacterial species included those that are helpful to the gut, those that are harmful, and those that stay neutral. 

Each bacterial species was then exposed to 39 common, commercially used sweeteners. The sweeteners included: 

• Artificial sweeteners such as aspartame (Equal/NutraSweet), saccharin (Sweet’N Low), and sucralose (Splenda) 
• Natural sweeteners such as mogroside V (monk fruit), stevioside (Stevia), and sucrose (common table sugar)
• Sugar alcohols like sorbitol, maltitol, erythritol (Truvia), and xylitol

“Sweeteners are widely used as sugar substitutes in various food and beverages,” Kiran Raosaheb Patil, PhD, professor of molecular systems biology in the MRC Toxicology Unit at the University of Cambridge, and co-lead author of this study, explained to Medical News Today.

“Previous studies and World Health Organization (WHO) guidance have shown links between sweeteners and health parameters. It is therefore important to investigate molecular mechanisms through which the sweeteners may be affecting physiological processes. Such molecular insights can guide better-informed decisions for sweetener usage.” 

75% of commercially used sweeteners change gut bacteria

At the study’s conclusion, researchers found that of the 39 commercially used sweeteners tested, about 75% altered the growth of at least one gut bacterial species. 

“We tested sweeteners and related compounds to assess which, if any, can impact gut bacterial growth,” Patil said.

“Our laboratory tests show that many sweetener compounds have the potential to alter the growth of certain gut bacteria. While we yet do not know how these results would translate in a human context, our results suggest that future cohort studies should consider the direct effect on growth and metabolism of gut bacteria,” he explained.

Sweeteners may interact with medications

Scientists also tested each sweetener in combination with common food compounds such as caffeine and vanillin (vanilla extract), as well as eight commonly used drugs to see how those combinations might impact gut bacteria. 

Researchers observed more than 100 interactions between the combinations. The most eye-catching, researchers say, was the combination of isosteviol — a compound derived from stevia —and the antidepressant duloxetine. This combo suppressed two gut bacteria that play important roles in maintaining a healthy digestive system.

“Isosteviol is a sweetener derivative and not a sweetener itself; it was included in the study to broaden the mechanistic scope from a chemical angle,” Patil explained. “Our study included Stevioside and Rebaudioside A, both stevia sweeteners, and Rubusoside, another steviol glycoside found in Chinese sweet tea.”

“Like isosteviol, these compounds showed synergistic interactions with duloxetine. Our data highlights that sweeteners may interact with medications, and such ‘mixture effects’ should be investigated in future clinical studies. These effects may not necessarily be harmful, but for now we simply do not know.”
— Kiran Raosaheb Patil, PhD

Human trials needed next

MNT spoke with Ashkan Farhadi, MD, a board certified gastroenterologist at MemorialCare Orange Coast Medical Center in Fountain Valley, CA, about this study. 

Farhadi, who was not involved in this research, commented that this is one of the most comprehensive studies on the effects of sweeteners, including artificial sweeteners, on the gut microbiome. 

“[The study] not only looked into the effects of that directly on the microbiome; it’s looking into the effects on other food ingredients and materials, and their combination of their effects. So it’s very interesting in that respect. And what it does for me is confirm that the reaction of the bacteria and the work they do can be affected by many things we are doing, including artificial sweeteners.” 
— Ashkan Farhadi, MD

Meanwhile, a representative from the International Sweeteners Association (ISA) told MNT that while the research helps expand our understanding of sweeteners, the study “should be regarded as a mechanistic screening study rather than evidence that low/no calorie sweeteners adversely affect the human gut microbiota or human health under normal patterns of consumption.”

In a press release, the ISA also pointed out that the experimental conditions used in the study likely do not reflect real-world consumption patterns and that the study was conducted in isolated bacterial cultures.

“[In vitro experiments] cannot replicate the complexity of the human gut ecosystem or account for factors such as host physiology, diet, and the diversity of the microbiota. Therefore, bacterial responses observed under these highly controlled conditions outside of the human body may not translate to meaningful changes in the human gut microbiota,” they said.

The next steps would be to test this in animals or humans.

“This study is an in vitro study on bacterial culture, and we need to have similar studies in an animal model or, even better, in humans to see if artificial sweeteners can adversely affect the growth or proliferation of good germs in the human gut, so we have more direct evidence to provide recommendations,” Farhadi added. 

How can I reduce the amount of sweeteners I consume? 

For readers who may want to start reducing the amount of commercially used sweeteners they consume, MNT asked Monique Richard, MS, RDN, LDN, a registered dietitian nutritionist and owner of Nutrition-In-Sight — who was likewise not involved in this study — for her top tips. 

“Rather than completely eliminating every questionable ingredient ‘cold-turkey,’ I encourage clients to gradually retrain their palate while building their knowledge base. Small, simple changes are often the most beneficial and sustainable long-term.” 
— Monique Richard, MS, RDN, LDN

“Often navigating these changes doesn’t require anything fancy or expensive, but is about identifying what you like, what you’re currently consuming — by reading, investigating, and observing daily intake through labels, ingredient lists, and logging — and exploring how that can be modified,” she detailed. 

Richard said some simple strategies may include:

• Choosing water infused with citrus, cucumber, berries, herbs, or sparkling water instead of artificially sweetened beverages.
• If using sweeteners in coffee or tea, decrease the amount gradually over several weeks rather than stopping abruptly.
• Let naturally sweet foods do more of the work — berries, peaches, roasted apples, cinnamon, vanilla, citrus zest, and spices add flavor without relying on high intensity sweeteners. 
• Using Mother Nature’s sweeteners, such as local honey, maple syrup, molasses, and date paste, to sweeten a beverage or recipe can also be an option, and often, a little can go a long way and add a depth of richness and palatability as well as trace minerals and phytochemical content to the food, beverage, or recipe. 

“One concept I often emphasize with clients is that the goal isn’t simply ‘less sugar,’ or elimination of ‘ultra-processed foods,’ but about increasing the plethora of plants that Mother Nature provides,” she explained. “As whole foods begin replacing ultra-processed options, sweetener intake often decreases naturally,”

“It is also not about villainizing or creating a righteous ‘clean eating’ judgment zone for you/your children/family/friends when looking at products,” Richard added. “It is about being informed, the broader dietary pattern and overall quality, adequacy, and enjoyment of fueling our life.” 

• Although the U.S. experiences seasonal cyclospora outbreaks, this year has seen thousands of CDC-confirmed cases across multiple states, far exceeding typical trends.
• While the FDA announced it had traced the cyclospora outbreak to iceberg lettuce sold by Taylor Farms de Mexico to Taco Bell and Walmart stores, it recently reported that the test was a false positive. 
• While cycloporasis is rarely fatal, it causes prolonged, “explosive” watery diarrhea, and symptoms can last for weeks without the necessary antibiotic treatment.
• Medical News Today spoke to seven health experts to discuss who’s more at risk, how to prevent infection, and how it’s treated.

On May 13, 2026, the first case of illness from the parasite cyclospora was reported to the U.S. Centers for Disease Control and Prevention (CDC) and the U.S. Food & Drug Administration (FDA). 

As of July 21, the CDC announced it has received reports of 4,173 laboratory-confirmed cases of cyclosporiasis in the U.S., with more than 7,400 suspected cases still needing analysis. According to the CDC, cases have been reported in 41 states, with Michigan and Ohio among the hardest-hit. 

On July 17, the FDA announced it had traced one possible cause of the cyclospora outbreak to iceberg lettuce sold by Taylor Farms de Mexico to Taco Bell restaurants and Walmart stores, prompting a voluntary recall by the company. 

However, on July 19, the FDA announced, after reviewing sample results from Taylor Farms de Mexico lettuce, that it should be considered a false positive. The FDA says there is currently no confirmed product sample that tests positive for cyclospora. 

With uncertainty as to where the cyclospora outbreak is coming from, how can you protect yourself from becoming sick? 

Medical News Today spoke with seven experts to learn what exactly cyclospora is, how it spreads, what to do if you think you’re infected, and how to protect yourself. 

How to get tested for cyclospora infection

If you suspect you or a family member has been infected by cyclospora, Carl J. Fichtenbaum, MD, Gregory W. Rouan, MD, Endowed Professor of Internal Medicine and vice chair of internal medicine and infectious diseases researcher in the College of Medicine at the University of Cincinnati, said you should contact your doctor. 

Who may be more at risk

“Testing requires specific tests to look for cyclospora in a fecal sample. Some people with immune-compromised conditions can have more severe cases resulting in the need for hospitalization, largely due to dehydration and low blood pressure.” 
— Carl J. Fichtenbaum, MD

“Early in the infection, (cyclospora) testing can be challenging because the parasite may not yet be easily detectable in stool samples, meaning repeat testing is sometimes needed to confirm the diagnosis,” added David Cutler, MD, a board certified family medicine physician at Providence Saint John’s Health Center in Santa Monica, CA.

And diagnosing cyclosporiasis itself can be challenging, Michalik said. 

“Many pathogens such as norovirus, rotavirus, Salmonella, and Escherichia coli (E. coli) can cause similar diarrheal symptoms, and not all clinics or urgent care centers have the specialized testing needed to detect this parasite,” Michalik explained to MNT.  “In many cases, testing must be sent to external laboratories, which can delay results.

Tips for protecting yourself from cyclospora

Cyclospora prevention largely comes down to food and water safety, Cutler said. 

“Cyclospora is resistant to many standard disinfecting methods, so simply rinsing produce may not fully eliminate the parasite,” he explained. ”However, thoroughly washing fresh fruits and vegetables and avoiding potentially contaminated food or water, especially when traveling to areas where the parasite is more common, can help reduce risk.”

Perera said that cyclosporiasis outbreaks occur every year in the United States during the spring and summer months, and that cases have been increasing nationwide.  

Foods that may be risky

“South Florida is historically one of the hardest hit areas, with fresh produce like berries, salad mixes, and fresh herbs being the most common source of infection. Be cautious with fresh herbs, leafy greens, and berries during the spring and summer months, when outbreaks are most common.” 
— Alexis Perera, MD

Patel advised readers to prioritize produce that can be easily washed, such as smooth-skinned items like apples and tomatoes. 

“If I were to avoid anything, it would be pre-washed lettuce, berries, and foods that have a lot of crevices for the parasite to hide,” he continued. “It is important to remember that cooking these items will lower the risk of infection. People can also eat canned or frozen produce that was likely processed before this outbreak.”

How to know you are washing your vegetables long enough

“After handling these vegetables and fruit, wash your hands with soap and water (while) singing the Happy Birthday song twice (30 seconds).”
— Carl J. Fichtenbaum, MD

While this year’s cyclospora outbreak has been larger than most, Swanson reminded readers that fruits and vegetables remain an important part of a balanced diet and need not be eliminated from your diet.  

“Thorough washing, good hand hygiene, and careful cooking techniques ensure you continue to safely enjoy nutritious meals,” she added.

• Both sleep disturbance and excess sleep have been linked to development of dementias, particularly Alzheimer’s disease.
• Now, a study has found that people with particularly long sleep duration are more likely to have more of a brain protein linked to Alzheimer’s.
• The study found that sleeping for more than 8.5 hours a night was associated with blood biomarkers of tau protein, suggesting that long sleep may indicate early neurodegeneration.

The earlier dementia — of which Alzheimer’s disease is the most common — is detected, the better the prognosis for the person diagnosed.

Although there is no cure, early diagnosis of Alzheimer’s can help to delay the progression of the disease, allow the use of disease-modifying treatments, such as lecanemab and donanemab where appropriate, and give patients and carers time to arrange appropriate care.

Several studies have linked sleep changes to the development of Alzheimer’s disease, and now a study has suggested a possible physiological mechanism underlying the link.

The new study, published in Alzheimer’s and Dementia, the journal of the Alzheimer’s Association, found that people who slept for an average of more than 8.5 hours a night had higher levels of the blood biomarker p-tau181, suggesting that long sleep may be an early sign of neurodegenerative changes.

Steven Allder, MD, a consultant neurologist at Re:Cognition Health, who was not involved in the study, told Medical News Today:

“This study strengthens growing evidence that changes in sleep may be linked to the earliest biological processes involved in Alzheimer’s disease, rather than simply being a consequence of aging. […] What is particularly interesting here is the association between longer sleep and higher levels of plasma phosphorylated tau (p-tau181), a biomarker that reflects Alzheimer’s pathology.”

Might sleep changes affect Alzheimer’s markers?

Researchers analysed data from 2,410 participants in the Framingham Heart Study (FHS), who had a mean age of 70, give or take 8.45 years, and 55.2% of whom were female.

All participants had self-reported sleep duration data and assay results for at least one of four blood-based biomarkers: p-tau181, total tau (t-tau), neurofilament light chain (NfL), or glial fibrillary acidic protein (GFAP).

To assess the sleep-biomarker relationship across the cognitive spectrum, they included individuals with mild cognitive impairment, dementia, and any history of stroke.

The participants reported typical sleep duration to technicians during clinic visits, where they also gave fasting blood samples for biomarker analysis.

Researchers took several factors that may affect sleep and biomarkers into account during analysis:

• age at time of clinical examination
• APOE e4 status — this gene increases risk of developing Alzheimer’s
• biological sex
• cohort of the FHS the participant was in
• self-reported obstructive sleep apnea
• depression status
• kidney function

They then performed statistical and sensitivity analyses to determine any links between sleep duration and blood biomarkers. 

Alzheimer’s biomarker linked to sleeping more than 8.5 hours a night

Of the cohort, 576 (23.9%) reported short sleep (up to and including 6 hours a night), 1,475 (61.2%) average sleep (6-9 hours), and 359 (14.9%) long sleep (more than 9 hours).

Those reporting longer sleep were older, and were more likely to have depression, use antidepressants and have dementia than average sleepers.

All biomarkers tended to increase with longer sleep duration, but the increase was significant only for p-tau181. 

P-tau181 had a J-shaped curve, with short sleepers having more than average sleepers. It then increased steadily with more than 8.5 hours sleep, and increased sharply for people reporting 10 or more hours of sleep.

“While the findings do not prove causation, they add to the evidence that alterations in sleep may be an early clinical sign of underlying neurodegeneration and reinforce the role of considering sleep as part of an overall assessment of brain health,” Allder commented.

The authors suggested that longer sleep duration could be a sign of disturbed sleep, and Allder agreed:

“Sleep duration alone tells us very little about sleep quality. Someone spending nine or ten hours in bed may actually experience fragmented or inefficient sleep, repeatedly waking throughout the night without necessarily being aware of it. We know that deep, restorative sleep plays an important role in clearing waste products, including amyloid proteins, from the brain via the glymphatic system. Fragmented sleep may impair restorative processes,” he told Medical News Today.

“However,” he added, “it is equally possible that early Alzheimer’s pathology itself disrupts the brain regions that regulate normal sleep, meaning disturbed sleep could be both a contributor to, and a consequence of, the disease.”

Long sleep could be a result, not a cause, of early Alzheimer’s changes

“A lot of people worry about whether their sleep habits are affecting their brain health,” corresponding author Vanessa M. Young, PhD, MS, a postdoctoral research fellow at the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at UT Health San Antonio, said in a press release.

“Because this is a snapshot in time rather than a long-term study, we cannot say that long sleep causes Alzheimer’s, but the findings suggest it may be worth monitoring, and that more sleep is not always better for brain health,” Young noted.

The observational study allowed researchers to identify a link, but not prove any causation between long sleep and p-tau181.

It is equally possible that the sleep changes are a result of early neurodegeneration, rather than a cause of it, as Allder explained.

According to him: “Many dementia specialists believe this is one of the most likely explanations. Alzheimer’s disease begins silently in the brain 15 to 20 years before symptoms appear, and the earliest pathological changes may affect areas involved in regulating the sleep–wake cycle. As a result, people may gradually begin sleeping for longer before they notice any memory problems.”

“To determine whether long sleep is a cause or an early symptom, researchers need prospective studies that recruit cognitively healthy individuals, measure Alzheimer’s biomarkers at baseline and then follow changes in sleep over many years,” he added.

“Dementia is influenced by a complex relationship of genetics, vascular health, lifestyle and aging. Sleep is one piece of that puzzle, and maintaining good sleep hygiene, alongside routine physical activity, cardiovascular risk reduction and cognitive stimulation, remains one of the most sensible strategies for promoting long-term brain health.”

– Steven Allder, MD

• About 95 million people around the world are affected by glaucoma.  
• Past studies show that consuming certain nutrients may help lower your glaucoma risk. 
• Researchers have been investigating how a type of vitamin B3 called nicotinamide might help lower glaucoma risk. 
• A new study found that nicotinamide may help lower the risk of primary open-angle glaucoma (POAG) in people with ocular hypertension.

Researchers estimate that about 95 million people around the world are affected by glaucoma, a group of eye diseases that can cause damage to the optic nerve, potentially leading to vision loss. 

Past studies show that consuming certain nutrients, such as omega-3 fatty acids, dietary nitrates, and vitamins A and C may help lower glaucoma risk. 

Additionally, researchers have been investigating how a type of vitamin B3 called nicotinamide might help lower glaucoma risk as well.

Now, a new study published in the journal JAMA Ophthalmology reports that nicotinamide may help lower the risk of primary open-angle glaucoma (POAG) in people with ocular hypertension, a known risk factor for developing glaucoma. 

Taking vitamin B3 lowers glaucoma risk by 66%

For this study, researchers analyzed electronic medical record data from 67 United States healthcare organizations, encompassing about 2,900 people with ocular hypertension but had not yet received a glaucoma diagnosis. 

Half of the participant group received nicotinamide supplementation, while the other control group did not. 

After an average of 3.7 years, 51 participants of the nicotinamide group received a diagnosis of POAG, compared to 132 participants in the control group.

At the study’s conclusion, researchers found there was a 66% lower risk of developing POAG in participants taking nicotinamide, as well as a 43% reduction in rates of topical intraocular pressure–lowering therapy prescription and 62% reduction in laser trabeculoplasty surgery for glaucoma.  

Nicotinamide for glaucoma: Reasons for caution

Currently, nicotinamide is not an approved treatment or prophylactic for glaucoma.

While this is not the first study to look at nicotinamide and glaucoma risk, there are still questions regarding the safety of nicotinamide supplementation. 

In March 2025, the American Glaucoma Society and the American Academy of Ophthalmology issued a joint statement regarding the safety of nicotinamide supplementation, as taking too much of nicotinamide can lead to liver damage. 

According to the joint statement, ongoing clinical trials are using what are considered high doses of nicotinamide at 3 grams (g) per day. Typical nicotinamide dosage is much lower, between 500 milligrams (mg) to 1,500 mg per day. 

Potential adverse effects of taking too much nicotinamide include gastrointestinal issues such as nausea and stomach pain, headaches, dizziness, and fatigue, and has the potential for more severe risk including liver toxicity, elevated blood sugar levels, and blood disorders. 

Don’t start a supplement without doctor approval

Medical News Today spoke with Benjamin Bert, MD, a board-certified ophthalmologist at MemorialCare Orange Coast Medical Center in Fountain Valley, CA — who was not involved in this study — about these research findings. 

Bert commented that while this study further supports that nicotinamide may be protective in regard to the development of glaucoma in high risk individuals, before starting any new supplements, it is important to discuss them with your physician. 

“Even when a treatment does not require a prescription, there are still risks involved, including interactions with other medications or supplements that you are taking,” he explained. “With nicotinamide there can be liver toxicities at higher doses, so liver function tests may need to be monitored if you are using a higher dose.” 

Ariana Levin, MD, an assistant professor in the Department of Ophthalmology at NYU Grossman School of Medicine — who was likewise not involved in this study — agreed. 

“I recommend that patients who want to take supplements should discuss these with their primary care physician to ensure they are taking a dose that is reasonable to take along with the rest of their prescription medications and in the context of their general health,” Levin explained to MNT.

“In general, supplements are not regulated in the same way prescription medications are, so patients need to be diligent in evaluating the product that they are buying from the shelf (or online),” she advised. 

Glaucoma prevention remains crucial

Since glaucoma causes irreversible damage, Levin said that finding new ways or preventing the disease is key.

“Ideally we prevent damage from occurring before a high-risk patient develops the disease, or at least prevent further damage while the disease is still mild,” she detailed. “Once a patient has glaucoma, they have that diagnosis for life. We can get glaucoma under control, but it isn’t a diagnosis that ‘goes away’.”

“This article is exciting because it focuses on early prevention,” Levin continued. “It also focuses on a potential therapy that doesn’t act by lowering eye pressure. Lowering eye pressure is the most important tool we have right now in treating glaucoma, but we need other tools as well.” 

As glaucoma is a blinding disease, Bert said any treatments that we can have to prevent the development, prevent the progression, or reduce the overall risk are highly beneficial. 

“A treatment that allows our bodies to continue to function the way that they are supposed to, as is the hypothesis with vitamin B3, then that would be especially beneficial. Glaucoma can be a difficult disease to control, so it is important that research continues to look at it from many different aspects to help continue to develop new treatments.” 

– Benjamin Bert, MD

For the next steps in this research, Bert said the biggest piece of information missing from this study was the dosage of nicotinamide that the study population was taking.

“The study categorized those that were taking any supplementation of vitamin B3 as having ‘exposure’ to nicotinamide,” he explained. “Thus, it would be highly beneficial to have additional studies explore the exact dosing that would be beneficial. Knowing a specific dosage would also allow for the appropriate recommendations for monitoring potential side effects.”