Category: 8. Health

On June 3, 2025, the European Parliament hosted a pivotal event that signalled a turning point in the fight against a silent but pervasive public health threat: Steatotic (Fatty) Liver Disease. Titled “Fatty Liver & NCDs: A European Policy Action”, the event brought together patient leaders, medical experts, policymakers, and public health advocates to call for a unified strategy to address liver health as part of Europe’s broader approach to non-communicable diseases (NCDs).

Organised by the European Liver Patients’ Association (ELPA), co-hosted by MEPs Michalis Hadjipantela (Cyprus, EPP) and Irena Joveva (Slovenia, Renew), and attended by several MEPs and assistants, the gathering underscored a growing cross-party consensus: liver disease is not a niche issue. It is a pan- European epidemic linked to cancer, obesity, type 2 diabetes, and cardiovascular conditions—and it demands coordinated, urgent political action. Both MEPs shared a strong message about how, as policymakers, they are responsible for strengthening health systems, promoting liver screening programs, and ensuring no patient is left behind.

The Patient Voice: Front and Centre

The first panel, “The Patient Perspective: Navigating Liver Disease Across Borders,” highlighted lived experiences across Europe and beyond. Representatives from Cyprus, Israel, Denmark, France, Finland, and Spain painted a vivid picture of the daily struggle faced by people affected by liver disease—and the system-wide gaps in care and recognition.

Marko Korenjak, ELPA President, opened the event by framing Steatotic (Fatty) Liver Disease as “a silent epidemic.” Steatotic (Fatty) liver disease (SLD) is one of the most widespread liver conditions in Europe, affecting up to 25% of the adult population. Closely tied to metabolic dysfunction, SLD often begins silently but progresses over time to cirrhosis and, increasingly, liver cancer. Liver cancer is now one of the fastest-growing causes of cancer-related deaths in Europe. He pointedly asked why, despite clear links to major NCDs, liver disease remains marginal in national and EU-level health strategies. This theme was echoed throughout the discussion. Patients aren’t just calling for awareness—they are demanding structural change.

Bridging Silos: An Alliance of Associations

The true innovation of the event lay in its second panel, “Advocacy in Action.” Here, an unprecedented alliance took the stage: the European Liver Patients’ Association (ELPA), the European Coalition for People living with Obesity (ECPO), the International Diabetes Federation Europe (IDFE), and the Global Heart Hub (GHH). Their message was unified and unambiguous: to tackle Steatotic (Fatty) Liver Disease, Europe must abandon siloed disease strategies and adopt integrated approaches that address shared root causes. This is why patient associations were also joined by the European Public Health Alliance (EPHA) and the European Association for the Study of the Liver (EASL) representative.

This patient representative alliance formally launched a Call to Action—first drafted in Lisbon in November 2024 under the initiative Bridging the Gaps—marking a new era in cross-disease advocacy. For the first time, patient associations from different disease areas co-authored a policy vision, elevating liver disease to its rightful place in the NCD agenda.

David Kelly of the Global Heart Hub summarised the spirit of the Call: “This document isn’t just a list of demands. It’s a declaration of unity from communities that share risk factors and solutions. It shows the power of working together.”

Linking Disease to Systems: Public Health over Personal Blame

Much of the discussion focused on breaking the persistent narrative that liver disease is solely the result of poor lifestyle choices. Professor Shira Zelber- Sagi of EASL emphasised the role of commercial and social determinants of health. “This is not just about individuals. It’s about how we build our food systems, cities, and social protections,” she urged governments to act on upstream factors that drive disease.

Alessandro Gallina of EPHA echoed this call, criticising the EU’s limited public health focus during the current legislative term. “We need to respond to NCDs with integrated, system-wide policies,” he stated. “The narrative must shift to systemic responsibility and political will.” He also added the fundamental importance of fully implementing Europe’s Beating Cancer Plan since the link between cancer and many NCD risk factors, such as tobacco use, unhealthy diets, physical inactivity, and alcohol, is well-established.

The Future: Integration and Prevention

When asked about the obstacles to integrated care, Marko Korenjak didn’t hesitate: “The biggest challenge is the silo mentality. Ministries, budgets, disease areas—all fragmented. Integrated prevention means addressing common risk factors and giving patients a voice at every step.”

A consistent theme across all panellists was the need for integrated care. Elisabeth Dupont of IDFE advocated for diabetes screening programs that also test for liver disease, noting the high comorbidity rates. “Screening early allows us to intervene preventatively,” she said.

Vicki Mooney of ECPO highlighted stigma as a barrier to care for people living with obesity and liver disease. “Healthcare professionals often overlook liver symptoms in people with obesity. Worse, patients internalise stigma and delay seeking help. We must train providers to recognise and respect the full picture.”

Looking ahead, several speakers called for standardised EU-wide liver screening protocols, particularly for high-risk groups such as people living with obesity, type 2 diabetes, and cardiovascular disease. In addition, they pointed out how the European Commission consider integrating liver health into the next NCD framework and the forthcoming European Cardiovascular Health Plan.

Beyond the Event: Building a Movement

From the liver community, the call is loud and clear:

• Integrate liver disease into national and EU-level NCD plans.
• Implement and update the Europe’s Beating Cancer Plan.
• Include liver disease as a key component of the upcoming European Cardiovascular Health Plan.
• Develop screening strategies across primary care systems.
• Fund public health interventions that tackle the commercial determinants of health.
• Recognise and resource cross-disease patient alliances.

This was more than just a health event—it marked the beginning of a growing coalition driven by patients, grounded in science, and speaking directly to EU lawmakers. Building on this momentum, ELPA will organise a second event in early December 2025, in the European Parliament, continuing to place liver health at the heart of the broader conversation on chronic disease prevention and health system resilience.

As Marko Korenjak reflected on the Lisbon meeting where the Call to Action was born, he asked: “What happens when different communities realise they’re not alone in their fight? They form a movement. That’s what’s happening now.”

Click here to read ELPA’s Call to Action

The European Liver Patient Association (ELPA) is a member-based, non-profit organisation dedicated to promoting the interests of people affected by liver disease across Europe. ELPA represents liver patients regardless of their origin, lifestyle, or type of liver condition. Through advocacy, education, and collaboration with healthcare professionals, researchers, and policymakers, ELPA works to ensure that patient engagement is meaningful and patients’ voices are central to healthcare decisions. ELPA’s mission is to improve the quality of life for all liver patients by promoting equitable access to prevention, diagnosis, treatment, and care across the continent. For more visit https://elpa.eu/

 

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Eating a protein-rich diet can have several health benefits. If you struggle to get enough protein to meet your body’s needs, incorporating high-protein foods into snacks can help you reach your protein goal. We spoke with registered dietitians to find out why protein is so important—plus, which high-protein foods should make it into your snack rotation.

Benefits of Eating Protein-Rich Snacks

Protein is an essential macronutrient that is important for health and well-being. “Protein plays a key role in the body’s ability to build muscle, repair tissue, regulate hormones and perform other cellular functions like metabolism,” says Cayleigh McKenna, RD, nutrition consultant at Houston Family Nutrition.

Because protein is essential for building and maintaining muscle, physically active people should emphasize protein in their meals and snacks.

Adding protein to snacks can offer several benefits, including long-lasting energy and increased satiety. “Protein-rich snacks can help you feel fuller for longer, promoting a sense of nourishment and satisfaction,” says Andrea Hinojosa, M.S., RD, founder of Honest Health & Wellness. “Many high-protein snacks are also rich in other essential nutrients, contributing to overall health and well-being,” she adds. Eating protein with snacks may also balance blood sugar, improve heart health and reduce cravings later in the day.

The Best High-Protein Foods to Eat as Snacks

1. Greek Yogurt 

Creamy and refreshing, “Greek yogurt is high in protein and can be easily paired with honey and nuts for added flavor and texture,” says Hinojosa. Depending on the brand, you’ll snag about 20 grams of protein per 7-ounce serving.

You can also use Greek yogurt in place of sour cream and mayonnaise in dip recipes for a high-protein swap that’s lower in saturated fat. Strained Greek-style yogurt is also a great way to add protein to fruit smoothies. 

2. Hard-Boiled Eggs

One egg provides a satisfying 6 grams of protein. “They’re portable, easy to prepare and packed with high-quality protein,” says Hinojosa. Enjoy hard-boiled eggs with a handful of nuts or top with hot sauce. Hinojosa also recommends pairing eggs with kimchi to add digestive-friendly probiotics and a spicy kick.

3. Canned Tuna or Salmon

Canned fish is a quick high-protein option for snacks. You can even purchase “canned” fish in travel-friendly pouches, making them the perfect protein-rich snack when you’re on the go. Canned salmon has about 18 grams of protein per 3-ounce serving, while canned tuna has about 22 grams per serving. “They also provide omega-3 fatty acids, beneficial for heart health and brain function,” adds Hinojosa.

Try our Tuna Salad Spread, which combines canned tuna and Greek yogurt for a protein-packed snack. Spread it on whole-grain crackers or toast, or use raw veggies for dipping. 

4. String Cheese 

Another portable and easy option for snacking is string cheese. One stick has about 8 grams of protein. “For high-protein snacks, I love a turkey and cheese roll-up. I use a cheese stick and two slices of deli turkey or chicken and roll it up together. It’s really satisfying,” says Katie Drakeford, M.A., RD, owner of Drakeford Consulting. You can also enjoy string cheese with fresh fruit or a side of nuts.

5. Jerky

Jerky is a great high-protein snack option—and it’s especially handy if you can’t keep things cold. One serving of beef jerky (about 1 ounce) provides about 10 grams of protein, while turkey jerky has 11 grams per serving. Enjoy jerky with fresh fruit like an apple or banana, or with a handful of trail mix for an added boost of healthy fats. 

6. Deli Turkey

Deli turkey is another high-protein snack option. Just one slice of deli turkey has 6 grams of protein. Enjoy a couple of slices on crackers, layer a few slices with cheese on top of cucumber slices or make a grown-up snack box with turkey, cheese, grapes and crackers. 

7. Cottage Cheese

Until it became a social media darling, who knew there were so many ways to incorporate cottage cheese into meals and snacks? And it’s worth it to do so: 1 cup of low-fat cottage cheese has about 24 grams of protein. “A cup of cottage cheese with berries or pineapple is another go-to when looking to up protein intake,” says Drakeford. If you prefer a savory snack, try our Cottage Cheese Snack Jar.

Our Expert Take

Protein is an important part of a healthy diet. Including these dietitian-approved protein-rich snacks in your routine can provide long-lasting energy, increase feelings of fullness and balance blood sugar. Eating protein consistently throughout the day may also help regulate your appetite and reduce cravings.

A recent study has shed new light on how the ketogenic diet impacts men and women differently, especially when it comes to weight loss.

According to researchers, men consistently experience greater fat loss than women under identical keto protocols, with biological sex playing a significant role in how the body responds to this popular dietary approach.

In one 45-day clinical trial reviewed in the study, men on the keto diet lost an average of 11.63% of their body weight, compared to 8.95% in women following the same regimen. The findings point to complex physiological and hormonal differences that affect how men and women burn fat, store energy, and adapt to carb-restricted eating plans like keto.

The ketogenic diet, which is high in fats, moderate in protein, and extremely low in carbohydrates, puts the body into a state of ketosis.

In this state, the liver produces ketone bodies — byproducts of fat metabolism — which the brain and body use as a primary energy source in place of glucose.

This metabolic shift not only reduces fat stores but also suppresses appetite and regulates blood sugar. However, the new research highlights that sex-specific biology significantly influences how effective a ketogenic diet is for weight loss.

One of the key factors is fat distribution. Men typically store fat viscerally while women tend to store fat subcutaneously.

Visceral fat is more readily metabolised during ketosis, giving men a physiological edge when it comes to shedding pounds on a ketogenic diet.

Hormonal differences also play a crucial role. Testosterone enhances fat-burning processes by increasing beta-adrenergic receptor activity, while oestrogen — especially in premenopausal women — can hinder fat breakdown.

Moreover, the menstrual cycle introduces additional metabolic variability for women. During the luteal phase, elevated progesterone levels reduce insulin sensitivity and increase cravings for carbohydrates, making it harder for many women to maintain ketosis.

Another contributing factor is how each sex uses energy. Men are more likely to burn fat for energy, while women often store fat and rely on carbohydrates as a primary fuel source. These metabolic tendencies can make fat loss more challenging for women on a low-carb diet like keto.

Even at the microbiome level, differences emerge. The study found that men generally have higher levels of fat-metabolising gut bacteria, which may enhance the fat-burning effects of the diet.

Interestingly, the review also noted that a ketogenic diet can support muscle growth, but potentially at a cost for women.

Some studies have shown that keto may contribute to increased muscle fatigue in young, healthy females, possibly affecting workout performance and overall weight loss outcomes.

The researchers concluded that the ketogenic diet is most effective for men and postmenopausal women, with more limited success observed in premenopausal women.

They emphasised the need for personalised dietary approaches that take sex, hormones, genetics, and lifestyle factors into account.

The authors also called for more diverse clinical research to validate these findings across different populations, stating that personalised nutrition could be the key to more effective obesity treatment in the future.

Read more in the journal Frontiers in Nutrition.

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The study was published in Nature Communications. It revealed a tiny genetic difference in an immune protein called Fas Ligand (FasL) between humans and non-human primates. This genetic mutation makes the FasL protein vulnerable to being disabled by plasmin, a tumor-associated enzyme. This vulnerability seems unique to humans and is not found in non-human primates, such as chimpanzees.

“The evolutionary mutation in FasL may have contributed to the larger brain size in humans,” said Jogender Tushir-Singh, senior author for the study and an associate professor in the Department of Medical Microbiology and Immunology. “But in the context of cancer, it was an unfavorable tradeoff because the mutation gives certain tumors a way to disarm parts of our immune system.”

Tumor environment neutralizes key immune protein

FasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis. Activated immune cells, including CAR-T cells made from a patient’s immune system, use apoptosis to kill cancer cells.

The UC Davis team discovered that in human genes, a single evolutionary amino acid change — serine instead of proline at position 153 — makes FasL more susceptible to being cut and inactivated by plasmin.

Plasmin is a protease enzyme that is often elevated in aggressive solid tumors like triple negative breast cancer, colon cancer and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons — FasL — can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies.

The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumors. Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancer.

Plasmin inhibitors may enhance immunotherapy

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.

By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumors.

“Humans have a significantly higher rate of cancer than chimpanzees and other primates. There is a lot that we do not know and can still learn from primates and apply to improve human cancer immunotherapies,” said Tushir-Singh. “Regardless, this is a major step toward personalizing and enhancing immunotherapy for the plasmin-positive cancers that have been difficult to treat.”

A new groundbreaking study by researchers from University of Birmingham, UCL, Great Ormond Street Hospital and Birmingham Children’s Hospital has revealed important clues into what is driving disease in children with arthritis.

Cutting-edge techniques have allowed scientists for the first time to uncover the unique architecture of cells and signals inside the joint as inflammation takes hold.

The new study published in Science Translational Medicine looks at arthritis in children, caused by the immune system mistakenly attacking joints. Juvenile idiopathic arthritis affects more than 10,000 children in the UK. It causes swelling, stiffness and pain in the joints over years or decades, leading to damage of the joints and long-term disability. Whilst treatments are available to manage the condition, and in some cases achieve remission, there is no cure. It can take time to find which treatment works for each person. Treatments don’t work in the same way for every child, suggesting there are hidden differences between individuals that we are only beginning to understand.

Deepening the scientific and clinical community’s understanding of the condition is vital if more effective treatments are to be found, and undertaking biopsies in young children provides a new way forward. Working with families of children with arthritis opened the door to this study, as the families advocated for the potential of the study, agreeing that the procedure would be acceptable to families, especially compared to living with a chronic inflammatory disease.

In a world first, tiny tissue samples were collected from the joint lining when children were having medicine injected into the joint. These samples were then analysed with advanced imaging and gene-profiling technologies. The fine resolution maps of the joints revealed differences between children of different ages and cell changes in those with more severe disease. These unique cellular fingerprints may help researchers understand why some drugs work better for some children, and not others. The joints of children with arthritis looked significantly different to those with adults, demonstrating the need to understand arthritis in children better. 

We know how frustrating it can be for families and young people to find a drug that best works for their arthritis. Finding ways to better predict which medicines will be beneficial for a particular child would mean we were able to treat the disease more rapidly and effectively. To achieve this goal, we first needed to understand what cells make-up the lining of the joint where the inflammation occurs.

Equipped with that knowledge, we can now start to tackle the next challenge, determining how these cellular fingerprints within the joint tissue can help us predict which drug will work best, ensuring we give the right drug, to the right child, at the right stage of their disease.” 

Professor Adam Croft, Versus Arthritis Professor of Rheumatology at the University of Birmingham and chief investigator of the study

One of the children who took part in the study was Aurelia, from London, who was diagnosed with arthritis after injuring her knee while on holiday.

“Aurelia is a sporty child and loves art, drama, music and ballet. We noticed pain and swelling of her knee whilst on holiday. We thought perhaps she had injured it playing, but when this didn’t get better and she was struggling to walk, we realised something else was wrong. She was referred to the Rheumatology team at Great Ormond Street Hospital who diagnosed her with arthritis. This came as a bit of a shock given how active she is!

“They offered her a steroid injection in her knee under general anesthetic to alleviate the symptoms. The team asked if we were happy for her to take part in this research study and collect some tissue samples at the same time.

“We were keen for her to be involved, as there’s still a lot of unknowns with arthritis in children, and not all treatments can work. Given that she was already having an anaesthetic, and it wasn’t an additional operation for her, it was a great opportunity for researchers to take samples and to be better able to study the conditions. We hope the study will help other families with children in similar positions to us,” explained Aurelia’s mum, Emily.

Professor Lucy Wedderburn, University College London Great Ormond Street Institute of Child Health and Consultant of Paediatric Rheumatology at Great Ormond Street Hospital said:

“This study represents a real step change in our work with children and young people who live with arthritis, and has been a huge team effort. Rather than having to rely on blood tests which often do not tell us accurately what is happening in the joint, we can now directly analyse the joint lining, across different types of childhood arthritis and different ages. Our findings show that younger children have different types of immune cells invading their joints compared to older children. Samples from children with arthritis looked different to adult samples, with a different make up of immune cells, blood vessels and distinct connective tissue cells. This suggests that treatments may need to vary depending on age and shows why we can’t just extend studies from adult studies to understand arthritis in children.”

The study was funded by the Medical Research Council, Versus Arthritis, National Institute of Health and Care Research, Great Ormond Street Hospital Charity, amongst others, and delivered through the National Institute for Health and Care Research (NIHR) Birmingham Biomedical Research Centre (BRC).

Lucy Donaldson, Director of Research at Versus Arthritis said:

“People with arthritis should never be reduced to just their condition. Each person deserves to be treated holistically as an individual, including, of course, children and young people with arthritis.

“We are very proud to invest in truly innovative research like the MAPJAG study which is helping us to better understand the individual differences between young people with juvenile arthritis.

“The MAPJAG team’s findings clearly show that children and young people aren’t just small adults, but have a different “cellular fingerprint”. Importantly the team have also shown that this can change with age. The findings can give real hope to all those families that more can be done, sooner, to enable young people with arthritis to live the lives they choose.” 

A wider programme of work, made possible by a Medical Research Council partnership award known as Tissue Research in Childhood Arthritis (TRICIA), supports the infrastructure needed for multi-centre tissue research of the joint. In future, it is hoped that a larger study, involving more centres will allow researchers to dig deeper into the remaining questions about how best to tailor treatments for individual patients.

Instrumental to driving this research forward was Dr Eslam Al-Abadi, a study investigator from the Birmingham Women’s and Children’s Hospital NHS Foundation Trust, who sadly passed away before publication. His incredible efforts in seeking to improve the care of children with this disease are gratefully acknowledged.

Chronic inflammation occurs when the immune system is stuck in attack-mode, sending cell after cell to defend and repair the body for months or even years. Diseases associated with chronic inflammation, like arthritis or cancer or autoimmune disorders, weigh heavily on human health-and experts anticipate their incidence is on the rise. A new study by investigators from Mass General Brigham identified a protein called WSTF that could be targeted to block chronic inflammation. Crucially, this strategy would not interfere with acute inflammation, allowing the immune system to continue responding appropriately to short-term threats, such as viral or bacterial infection. Results are published in Nature.

Chronic inflammatory diseases cause a great deal of suffering and death, but we still have much to learn about what drives chronic inflammation and how to treat it. Our findings help us separate chronic and acute inflammation, as well as identify a new target for stopping chronic inflammation that results from aging and disease.”

Zhixun Dou, PhD, senior author of the Center for Regenerative Medicine and Krantz Family Center for Cancer Research at Massachusetts General Hospital

Using chronically inflamed human cells, the researchers found that WSTF interacts with other proteins inside cell nuclei, which prompts its excretion and degradation. Since WSTF is responsible for concealing pro-inflammatory genes, this nucleus-eviction reveals those genes and, in turn, amplifies inflammation. They confirmed that WSTF loss could promote inflammation in mouse models of aging and cancer. They also found, using human cells, that WSTF loss only occurred in chronic inflammation, not acute. Using these findings, the researchers designed a WSTF-restoring therapeutic to suppress chronic inflammation and observed preliminary success in mouse models of aging, metabolic dysfunction-associated steatohepatitis (MASH), and osteoarthritis.

The researchers went further to examine tissue samples from patients with MASH or osteoarthritis. They found that WSTF is lost in the livers of patients with MASH, but not in the livers of healthy donors. Using cells from the knees of osteoarthritis patients undergoing joint replacement surgery, they showed that WSTF-restoring therapeutic reduces chronic inflammation from the inflamed knee cells. These findings highlight the potential of developing new treatments targeting WSTF to combat chronic inflammatory diseases.

Further research is needed to validate the therapeutic potential of WSTF restoration in broader settings and to develop specific strategies to target WSTF. Additionally, the findings suggest other similar proteins may be involved in chronic inflammation, opening a promising new avenue for studying and treating inflammation in the future.

A study published in Cell Stem Cell reveals that some mutations in blood stem cells might help protect against late-onset Alzheimer’s disease.

A team led by researchers at Baylor College of Medicine discovered that both a mouse model and people carrying blood stem cells with mutations in the gene TET2, but not in the gene DNMT3A, had a lower risk for developing Alzheimer’s disease. Their study proposes a mechanism that can protect against the disease and opens new avenues for potential strategies to control the emergence and progression of this devastating condition.

“Our lab has long been studying blood stem cells, also called hematopoietic stem cells,” said lead author Dr. Katherine King, professor of pediatrics – infectious diseases and a member of the Center for Cell and Gene Therapy and the Dan L Duncan Comprehensive Cancer Center at Baylor. She also is part of Texas Children’s Hospital.

Hematopoietic stem cells live in the bone marrow and generate all the different types of blood cells the body needs to stay alive and healthy – red blood cells, immune cells and platelets. As people get older, blood stem cells can develop mutations, and this occurs in about 20% of 70-year-olds. Most of the time, these mutations don’t cause problems, but sometimes, a mutation drives the cells to divide more than others, forming a clone. This process is called clonal hematopoiesis and it has been linked to a higher risk for conditions such as cardiovascular disease, stroke, blood cancers like leukemia and chronic obstructive pulmonary disease. However, many questions remain regarding the connection between clonal hematopoiesis and Alzheimer’s disease.

“In the current study, we investigated the effect of the two genes most commonly mutated in clonal hematopoiesis, TET2 and DNMT3A, on Alzheimer’s disease,” said first author Dr. Katie A. Matatall, instructor in the King lab. “We also selected these mutations because they are involved in inflammation, which is known to be increased in Alzheimer’s disease.”

The researchers assessed the effect of clonal hematopoiesis on the prevalence of Alzheimer’s disease using human data stored in the UK Biobank. They also evaluated the role of mutations in genes Tet2 and Dnmt3a in a mouse model of Alzheimer’s disease.

The team discovered that the two mutations do not behave the same way. Clonal hematopoiesis with the TET2-mutant was associated with a 47% reduced risk of late-onset Alzheimer’s disease in humans, whereas other mutations of clonal hematopoiesis did not confer protection. In a mouse model, transplantation of Tet2-mutant bone marrow reduced cognitive decline and beta-amyloid plaque formation, effects not observed with Dnmt3a-mutant cells.

“Furthermore, we found that the protective effect seemed to be mediated by TET2-clonal stem cells circulating in the blood,” Matatall said. “Immune cells derived from these clones were able to migrate into the brain where they cleared beta-amyloid deposits, a hallmark of Alzheimer’s disease, more effectively than cells without the TET2 mutation. We think that it’s both the increased migration into the brain and the enhanced ability to clear Alzheimer’s-associated damage that drives the better outcomes.”

Until now clonal hematopoiesis has primarily been associated with promoting the progression of disease. This is the first time that these two mutations in blood stem cells have been shown to influence disease in different ways. The findings show that some clonal hematopoiesis promote disease while others, like TET2, may provide protection. We need to think about clonal hematopoiesis in a mutation-specific way and assess their risks and benefits.”

Dr. Katherine King, professor of pediatrics – infectious diseases, Baylor College of Medicine

The findings establish a novel experimental platform for understanding the role of clonal hematopoiesis in Alzheimer’s disease and may inform future approaches to mitigate the risks of central nervous system degenerative diseases.

Source:

Baylor College of Medicine

Journal reference:

Matatall, K. A., et al. (2025). TET2-mutant myeloid cells mitigate Alzheimer’s disease progression via CNS infiltration and enhanced phagocytosis in mice. Cell Stem Cell. doi.org/10.1016/j.stem.2025.06.006.

Adults with poor Life’s Essential 8 scores faced significantly higher atrial fibrillation risk, suggesting that heart-healthy habits could be key to preventing this common arrhythmia.

Study: Association of life’s essential 8 score with incidence of atrial fibrillation: The Framingham heart study. Image Credit: Magic mine / Shutterstock

In a recent study published in the American Journal of Preventive Cardiology, researchers in Boston, USA, investigated the relationship between the Life’s Essential 8 (LE8) score and the risk of atrial fibrillation (AF).

AF is the most common arrhythmia, whose prevalence and incidence are increasing worldwide. Thirty years ago, the Framingham Heart Study (FHS) established age, type 2 diabetes, hypertension, valvular heart disease, heart failure, and coronary heart disease as risk factors for AF. Since then, obesity, metabolic syndrome, excess alcohol intake, and obstructive sleep apnea have been identified as modifiable risk factors for AF pathogenesis.

LE8 is based on the Life’s Simple 7 (LS7), which was developed to define and measure cardiovascular health and promote positive health outcomes. LE8 is an update to LS7 that additionally includes a sleep health metric. Recent studies indicate an inverse relation between the LE8 score and health outcomes, such as fatty liver disease, cardiovascular disease (CVD), kidney disease, dementia, and CVD mortality.

About the study

The present study evaluated the associations between the LE8 score and AF risk. The study population included subjects from the FHS Omni 1 and Offspring cohorts. Individuals aged 45 years or older attending one or more index exam cycles were included in the current analyses. Participants were assigned a composite cardiovascular health score at their index exams based on their adherence to eight healthy lifestyle components.

These lifestyle components included diet, smoking habits, sleep duration, body mass index (BMI), fasting blood glucose, physical activity, cholesterol levels, and blood pressure. The LE8 score was the mean of the scores assigned to each component. The study’s outcome was incident AF, ascertained from electrocardiograms. Subjects were followed up from the date of the index exam until the next index exam, incident AF, death, or for 10 years.

Fine-Gray hazard models, which account for competing mortality risks, were used to evaluate the associations between LE8 and AF risk, adjusted for sex and age. In secondary analyses, separate models were developed for each LE8 component. In addition, the team investigated whether age modified the association between incident AF and LE8. The association between the LE8 score and the risk of all-cause mortality was also assessed.

Findings

The study included 3,161 participants aged 65 years, on average, who contributed 4,628 index exam cycles. Most participants were female (57%) and from the Offspring cohort (93%). The average LE8 score was 67.6 at the index exams. The LE8 score was ≥80 (ideal), <50 (poor), and 50–79 (intermediate) for 16%, 7%, and 76% of participants, respectively. Overall, 410 individuals had incident AF, and 424 deaths occurred over the follow-up.

The risk of incident AF was higher for individuals with poor LE8 scores compared to those with ideal scores. The incidence rate of AF per 1,000 person-years of follow-up was 17.2 for participants with poor LE8 scores, 7.9 for those with ideal scores, and 10.3 for those with intermediate scores. Notably, intermediate cardiovascular health showed no significant difference in AF risk compared to ideal health (sHR=0.95). Moreover, higher continuous scores were associated with a reduced risk of AF.

Subjects with poor scores on the BMI, blood pressure, and glucose components had a greater risk of AF than those with ideal scores on the respective components. There was no evidence that age modified the association between incident AF and LE8. Furthermore, participants with poor LE8 scores had an elevated risk of all-cause mortality relative to those with ideal scores. A more favorable score for physical activity, glucose, and smoking was associated with lower mortality risk.

Conclusions

In sum, the study assessed the risk of incident AF in two FHS cohorts using LE8 scores. AF incidence was 10.4 cases per 1,000 person-years, comparable to estimates from other studies. A poor LE8 score was associated with an increased risk of AF compared to an ideal score. Moreover, higher continuous scores were associated with lower risk of AF and all-cause mortality. Poor blood pressure, glucose, and BMI scores were also associated with a higher AF risk.

An intermediate LE8 score was not associated with the risk of AF. The analysis accounted for repeated participant contributions across exam cycles using statistical clustering methods. Notably, the sample predominantly comprised middle-aged and older adults of European descent (the Offspring cohort), which limits generalizability to younger individuals and other ethnic or racial groups. Recall or misclassification bias was also likely, as several LE8 components were assessed using self-reported data. Future analyses should focus on whether specific interventions or behaviors would augment CVD outcomes.