Cancer is rising in younger adults. Faster biological aging may help explain why

Younger generations may be aging faster on the inside, a biological shift researchers have linked to a higher risk of cancers diagnosed before age 55. Credit: Shutterstock

Cancer is strongly associated with age. The longer people live, the more opportunities their cells have to accumulate damage that can contribute to tumor growth. But cancer is increasingly being diagnosed in younger adults, and each newer generation appears to face a greater risk than the one before it.

That trend has prompted researchers to investigate a provocative possibility: Are younger generations accumulating biological damage more quickly, causing their bodies to age faster than expected?

A study led by researchers at Washington University School of Medicine in St. Louis offers evidence that this may be happening. The team found signs that younger generations are aging more rapidly on a biological level than older generations did at comparable ages.

Scientists are still working to understand what is driving these changes. The question is being investigated through international efforts involving research members of Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine, and Cancer Grand Challenges, a global initiative co-founded by the National Cancer Institute and Cancer Research U.K.

Importantly, the researchers also found that accelerated biological aging was associated with a greater risk of early-onset cancers among younger generations. In general, early-onset cancers are those diagnosed at age 55 or younger.

A Gap Between Biological Age and Actual Age

Chronological age simply measures how many years a person has been alive. Biological age, by contrast, reflects how old the body appears based on measurable changes in cells, organs, metabolism, and other physiological systems.

According to the researchers, cancer risk increased as the difference between biological age and chronological age grew. People from more recent generations tended to have larger gaps than those born earlier, suggesting their bodies appeared biologically older at the same chronological age.

That generational shift could help explain at least part of the rise in cancer among younger adults.

The team also found that aging did not appear to affect every organ system in the same way. Faster aging in specific parts of the body was associated with particular cancers. An immune system that appeared biologically older, for example, was linked to early-onset lung cancer. Older-appearing fat tissue was associated with early-onset colorectal cancer.

The findings were published in the journal Nature Medicine.

Researchers say measurements of accelerated aging could eventually help doctors identify younger people who face unusually high cancer risks, potentially allowing prevention or screening to begin earlier.

"Our ultimate goal is to decode how modern environments become biologically embedded to drive cancer risk, transforming prevention from broad recommendations to personalized interventions," said Yin Cao, ScD, a molecular epidemiologist and an associate professor of surgery and of medicine at WashU Medicine. "This brings us closer to identifying risk earlier and developing prevention strategies that are tailored to an individual's biology."

Looking Beyond Individual Cancer Risk Factors

Cao's team has previously studied numerous factors that can shape cancer risk over a person's lifetime, including obesity, metabolic dysregulation, alcohol consumption, sedentary behavior, poor diet quality and cesarean delivery.

Each of these factors can provide clues about why cancer develops at younger ages. However, no single factor appears to explain very much of the overall trend on its own.

That led Cao, who is also a research member of Siteman, and her colleagues to look for a broader way of measuring how many different influences may work together over time to increase cancer susceptibility.

Support from Cancer Grand Challenges has allowed Cao, as co-lead of Team PROSPECT, to investigate this question on a much larger scale.

For the new study, the researchers examined data from more than 154,000 young adults enrolled in the UK Biobank, which contains extensive biological, health, and lifestyle information.

They also analyzed more than 10,000 participants in the United States who are part of the National Institutes of Health's (NIH) All of Us Research Program, an initiative designed to create a comprehensive health database involving more than 1 million people living in the U.S.

Measuring How Fast the Body Is Aging

To determine biological aging, the researchers, including first author Ruiyi Tian, a doctoral student in the Cao lab, looked at two different scales.

One was systemic aging, which measures aging across the body as a whole. The other was organ-specific aging, which estimates how rapidly individual organs or biological systems are aging.

For systemic aging, the researchers relied on established approaches that use clinical biomarkers, including PhenoAge and the Klemera-Doubal Method. They also used a metabolomic age score designed to capture age-related patterns in a person's metabolism.

PhenoAge, for example, uses nine blood biochemistry markers to estimate biological aging. These include albumin, made by the liver, and creatinine, a waste product removed by the kidneys.

For organ-specific aging, the researchers analyzed blood proteomic data, which measure levels of numerous proteins associated with specific organ systems. Those protein patterns were then used to estimate the biological age of individual organs.

The team calculated the average difference between biological and chronological age within each birth cohort. They then used standard deviation to measure how far each group differed from the overall study average. Standard deviation is a measure of how spread out data points are around the average.

Younger Generations Show Older Biological Profiles

The generational differences were apparent in both the UK and U.S. populations.

Among UK participants, people born between 1965 and 1974 had systemic aging that was 23% of one standard deviation higher than people born between 1950 and 1954, even after chronological age was taken into account.

Put more simply, members of the younger generation tended to have slightly older biological profiles than members of the older generation when researchers compared them at the same chronological age.

An even larger difference appeared in the U.S. data.

Participants born between 1990 and 1999 had systemic aging that was 92% of one standard deviation higher than those born between 1965 and 1969.

The researchers then examined whether these biological aging differences were connected to cancer.

Faster Aging Linked to Early-Onset Cancer

Greater systemic aging in the younger group was associated with an 8% increased risk of early-onset solid cancers. The strongest associations involved lung, gastrointestinal, and uterine cancers.

When the participants were separated into three groups according to their level of systemic aging, another pattern emerged.

People with the most advanced systemic aging had a 15% increased risk of early-onset solid cancer compared with participants showing the least advanced aging.

The association remained even after researchers accounted for inherited genetic cancer risks and genetic susceptibility to accelerated aging.

Looking at individual biological systems revealed more specific connections.

Advanced immune system aging was associated with a higher risk of early-onset lung cancer. Advanced adipose (fat) tissue aging was linked to a higher risk of early-onset colorectal cancer.

"If we can identify younger people with the highest cancer risk when they are still healthy, we can focus on prevention and early-detection strategies for the individuals who will benefit most from early interventions," Cao said.

Searching for the Causes of Cancer in Younger Adults

The research is part of Team PROSPECT, a Cancer Grand Challenges team co-led by Cao.

Cancer Grand Challenges is an international research funding initiative co-founded by Cancer Research UK and the National Cancer Institute (NCI). It brings together scientists from different specialties and countries to investigate some of the most difficult problems in cancer research.

One of those problems is explaining why early-onset cancers are becoming more common.

"Right now, we don't have a definitive answer to what's driving the rise of early-onset cancers around the world, but studies like this are helping us piece together the bigger picture, showing that cancer may be influenced not just by changes inside individual cells, but by wider changes happening across the body as a whole," said David Scott, PhD, director of Cancer Grand Challenges. "Research on this scale is possible through Cancer Grand Challenges, which brings together scientists from different fields around the world to tackle these complex questions together."

Cao and her colleagues are now working to better understand why cancer is increasingly affecting younger generations.

A major focus is determining how changes in the environment, lifestyle and society may leave long-lasting biological marks on the body. Those effects could include accelerated aging as well as other signs that make some people more vulnerable to disease.

By tracing how these risks accumulate throughout life, researchers hope to uncover more of the biological origins of early-onset cancers.

The ultimate goal is not simply to understand why cancer develops earlier, but to identify people at elevated risk while they are still healthy. That could make it possible to move prevention and screening earlier and tailor interventions to an individual's biology, shifting cancer care toward stopping disease before it begins.

This work was part of the PROSPECT team supported by the Cancer Grand Challenges initiative funded by Cancer Research UK, grant numbers CGCATF-2023/100043 and CGCATF-2023/100037; the National Cancer Institute of the NIH, grant numbers OT2CA297577 and OT2CA297576; the French National Cancer Institute; and the Bowelbabe Fund for Cancer Research UK. The project was also supported by grants from NIH/National Cancer Institute, grant number R37CA246175; the NIH/National Institute of Diabetes and Digestive and Kidney Diseases, grant number P30DK052574; the Alvin J. Siteman Cancer Center through the Foundation for Barnes-Jewish Hospital. Further support was provided by a pre-doctoral fellowship in the Cancer Biology pathway supported by NIH Molecular Oncology Training Grant T32CA113275 to Washington University School of Medicine in St. Louis; the Pediatric Gastroenterology Research Training Program grant T32DK077653 to Washington University School of Medicine in St. Louis; the Washington University School of Medicine in St. Louis Institute of Clinical and Translational Sciences, grant number UL1TR002345; and the Foundation for Barnes-Jewish Hospital. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Journal Reference:

1. Ruiyi Tian, Xiaoyu Zong, Duo Ren, Stefani Tica, Daniel Hong, Oluseye Oduyale, Jason D. Buenrostro, Ramaswamy Govindan, Yin Cao. Biological aging and generational shifts in early-onset cancer risk. Nature Medicine, 2026; 32 (8): 2983 DOI: 10.1038/s41591-026-04448-w

Courtesy:

WashU Medicine. "Cancer is rising in younger adults. Faster biological aging may help explain why." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260913082200.htm>.

 

 

Scientists find a hidden cause of high blood pressure that routine tests can miss

A hidden nighttime hormone pattern may reveal one of the most commonly missed causes of high blood pressure. Credit: Shutterstock

A common and frequently missed cause of high blood pressure may be easier to detect with help from a wearable device that tracks hormone changes throughout the day and night.

New research published in Science Translational Medicine focuses on primary aldosteronism, a hormone disorder that may affect up to one in five people with high blood pressure. The condition is associated with an increased risk of heart disease, stroke, diabetes, and other serious health problems.

Researchers from the University of Bristol and the University of Manchester in the UK, the University of Bergen in Norway, and collaborators in Stockholm and Athens found that people with primary aldosteronism can experience bursts of hormone production both during the day and while asleep at night. Those nighttime surges are especially important because routine blood tests are rarely performed during sleep.

A Wearable Device Tracks Hormones Around the Clock

To capture these hidden changes, the research team used a portable device developed at the University of Bristol that allowed patients to have their hormone levels monitored continuously while living normally at home rather than staying in a hospital or research facility.

This type of continuous monitoring could reveal abnormalities that may be missed by conventional testing, potentially helping doctors identify hormone-related conditions earlier.

Study co-lead author Dr. Thomas Upton, Clinical Research Fellow in Automated Sampling Clinical Fellow at the University of Bristol, and Senior Clinical Fellow at Bristol Hospitals NHS Foundation Trust said: "Primary aldosteronism is an important cause of high blood pressure and the most common cause of secondary hypertension we see in our blood pressure clinic. It could be affecting millions of people in the UK. However, due to the way hormones change during the day and the current complexity of the diagnostic process, diagnosis is often delayed or never made at all.

"In our study, patients were monitored at home during normal activity, and this allowed us to see how hormones changed over time in realistic settings. This approach could potentially revolutionize how we diagnose hypertension and ultimately reduce cardiovascular disease - particularly heart disease and strokes - that could have been prevented."

Measuring Hormones Every 20 Minutes

The proof-of-concept study followed 60 patients in Bristol, Bergen, Stockholm, and Athens over a 24-hour period. Hormone levels were measured every 20 minutes using a lightweight wearable device about the size of a mobile phone that attaches at the waist.

Because the device samples hormones from the skin, participants were able to continue with their usual activities, including sleeping at night, while researchers collected detailed hormone data.

The technology, known as U-RHYTHM, was adopted and further developed by the spinout company Dynamic Therapeutics in 2023.

Study senior author Dr. Eder Zavala, UKRI Future Leader Fellow at the University of Manchester, said: "By continuously monitoring hormones over 24 hours, we were able to reveal a previously hidden pattern of nocturnal hormone bursts. This gives us a much clearer understanding of the disease and could ultimately help doctors detect it earlier and treat patients more effectively.

"A more detailed mathematical and computational analysis of daily hormonal profiles could eventually also help uncover earlier and more subtle forms of the disease, opening new opportunities to improve outcomes for patients living with high blood pressure."

Why Standard Blood Tests May Miss the Disorder

Researchers used computational analysis to study changes in aldosterone, a hormone that helps control salt and water balance in the body. They also tracked two closely related hormones, 18-hydroxycortisol and 18-oxocortisol.

The results suggest that current diagnostic approaches may miss some patients because aldosterone does not remain consistently elevated.

Even in some of the most severe cases, hormone levels sometimes dropped below the minimum thresholds typically used to diagnose primary aldosteronism. A single blood test taken at one moment could therefore capture a period when hormone levels appear relatively normal.

Instead of remaining constantly high, aldosterone showed repeated bursts of secretion at night while the overall day-night rhythm of hormone activity remained intact.

Nighttime Hormone Bursts Offer a New Clue

The hormone spikes came from the adrenal glands and were especially pronounced in patients whose primary aldosteronism was caused by a problem affecting only one adrenal gland rather than both.

Importantly, the unusual hormone patterns disappeared after the affected adrenal gland was surgically removed. That finding provided additional evidence that the bursts were directly associated with the disease.

Study co-author Prof Stafford Lightman, Professor of Medicine at the University of Bristol and inventor of the U-RHYTHM technology, added: "The findings suggest that clinicians may need to rethink how they look for the disorder, which the Endocrine Society clinical practice guidelines now recommend should be considered for all people with hypertension, also known as high blood pressure.

"Future diagnosis could move away from single time point blood tests and towards tracking the body's hormone rhythms over time, particularly the overnight patterns that appear to hold crucial clues to disease. Further research is needed to define the best clinical pathways, using dynamic hormone measurement, to ensure early diagnosis of this common and potentially curable cause of high blood pressure."

Toward Earlier Detection of High Blood Pressure Causes

The findings raise the possibility that future testing for primary aldosteronism could rely less on a single blood sample and more on monitoring how hormones change over time.

Because the disorder can be treated and, in some cases, potentially cured, detecting it earlier could help reduce the risk of preventable cardiovascular complications.

The research was funded by EU Horizon 2020, the Trond Mohn Foundation, the UKRI Biotechnology and Biological Sciences Research Council (BBSRC), Medical Research Council, University Hospitals Bristol and Weston NHS Foundation, the Swedish Medical Research Council and Knut and Alice Wallenberg Foundation.

The findings support the University of Bristol's research 'Grand Challenge' focus on Understanding and Preventing Cardiovascular Disease and builds on NIHR-funded initiatives aimed at earlier identification of people with hypertension and other cardiovascular risk factors.

 

Journal Reference:

1. Marianne A. Grytaas, Thomas Upton, Isabella Marinelli, Paal Methlie, Marianne Øksnes, Dimitra A. Vassiliadi, Sophie Bensing, Georgina Russell, Kristian Løvås, Dimitris Margaritopoulos, Ileana R. Botusan, Katerina Simunkova, Maria Balomenaki, Katarina Berinder, Belinda Lombard, Thea Sjøgren, Ida Løvik, Bergithe E. Oftedal, Anette Heie, Grethe Å. Ueland, Olle Kämpe, Stylianos Tsagarakis, Stafford L. Lightman, Eder Zavala, Eystein S. Husebye. Tissue corticosteroid rhythms are dysregulated predominantly during sleep in primary aldosteronism. Science Translational Medicine, 2026; 18 (864) DOI: 10.1126/scitranslmed.aeb7517

Courtesy:

University of Bristol. "Scientists find a hidden cause of high blood pressure that routine tests can miss." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260913081916.htm>. 

 

Scientists finally see DNA “zip” itself together for the first time

 

DNA strands zipping together. Credit: Professor Agnes Noy, University of York

DNA carries a negative electrical charge. Because objects with the same charge normally push away from each other, DNA molecules might be expected to repel one another. Yet inside living cells, DNA must sometimes come into close contact and recognize matching sequences. These interactions are essential for processes including genetic recombination and gene silencing, and they can also play a role in cancer.

Scientists have now captured a remarkably detailed view of how this happens. Using powerful atomic force microscopy, researchers watched short pieces of DNA align with extraordinary precision, matching one another groove for groove. Computer simulations then revealed what appears to make this close contact possible: positively charged metal ions can settle into the grooves of DNA and serve as tiny molecular bridges between the two molecules.

Tiny Ions Help DNA Overcome Repulsion

Professor Agnes Noy, from the School of Physics, Engineering and Technology at the University of York, co-led the research. She said: "This discovery could help researchers identify regions of the genome specially involved in DNA pairing. These regions may become particularly important when mutations disrupt normal cellular processes and contribute to cancer."

The results provide experimental support for an idea proposed about twenty years ago called the "DNA zipper" model. Professor Alexey Kornyshev from Imperial College London and his collaborators originally suggested that salt ions surrounding DNA could produce alternating patterns of electrical charge. Those patterns, according to the model, would help neighboring DNA molecules align with one another much like two interlocking spiral staircases.

Until now, directly observing this proposed mechanism had proved difficult.

Scientists Put the "DNA Zipper" to the Test

To investigate the process, the researchers scanned DNA samples with atomic force microscopy, a technique capable of mapping surfaces at extremely small scales. These scans allowed the team to construct detailed topographical maps showing how the DNA molecules were positioned.

At the same time, sophisticated computer simulations followed individual atoms and ions as they moved around the DNA. Combining the two approaches gave researchers both a direct view of DNA pairing and a way to understand the molecular forces responsible for it.

The simulations showed that double-charged metal ions can effectively behave like two charged arms. Each ion can interact with both DNA molecules at once, forming a bridge across the space separating them and helping hold the two strands in alignment.

Dr. Thomas Catley, co-lead author from the School of Chemical Materials and Biological Engineering at the University of Sheffield, said: "It was incredible to be able to directly visualize the long-hypothesized mechanism for the first time. The advanced imaging techniques at our disposal are allowing us to uncover these key DNA interactions which have implications in many key cellular processes."

Dr. Victor Velasco-Berrelleza from the University of Sheffield, who performed the simulations, added: "Microscopy shows us what happens, but the simulations allow us to uncover the molecular mechanism behind it."

Some DNA Sequences Pair More Strongly

The researchers also found that DNA does not pair equally well along every sequence. Some stretches of DNA created much stronger contacts than others, producing distinct hotspots where two helices were especially likely to line up.

That finding could help researchers pinpoint parts of the genome that are particularly involved in DNA recognition and pairing. Such regions may become especially significant when mutations interfere with normal cellular activity and contribute to cancer.

The discovery could also have uses beyond medicine. Because some DNA sequences can be programmed to interact more strongly than others, scientists may eventually be able to take advantage of these properties to build customized DNA structures for biotechnology.

The study, "Imaging and mechanism of DNA-DNA recognition mediated by divalent ions," was published in the journal Nucleic Acids Research.

 

Journal Reference:

1. Thomas E Catley, Victor Velasco-Berrelleza, Daniel E Rollins, Alice L B Pyne, Agnes Noy. Imaging and mechanism of DNA–DNA recognition mediated by divalent ions. Nucleic Acids Research, 2026; 54 (16) DOI: 10.1093/nar/gkag817

Courtesy:

University of York. "Scientists finally see DNA “zip” itself together for the first time." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260909231717.htm>. 

 

Your sleep may be hiding an early clue to Alzheimer’s

 Could subtle changes during sleep reveal vulnerability to Alzheimer's disease years before memory problems become noticeable? Researchers at ULiège, supported by the Stop Alzheimer's Foundation, are investigating whether the sleeping brain may contain early clues.

Scientists from the University of Liège (GIGA Neurosciences) examined sleep patterns in more than 500 healthy people. Among participants in middle age, more frequent nighttime micro awakenings were associated with a higher genetic risk of developing Alzheimer's disease. That relationship was not detected among younger adults.

The findings, published in the journal Sleep, raise the possibility that sleep measurements could eventually help researchers identify people who may be more vulnerable to Alzheimer's before symptoms develop.

Looking for Alzheimer's Clues Before Symptoms

Researchers have spent years investigating connections between disturbed sleep and neurodegenerative diseases. The University of Liège study adds another piece to that research by suggesting that the relationship between sleep and Alzheimer's risk may begin well before recognizable symptoms emerge.

Because genetics play a partial role in Alzheimer's disease (Alzheimer's disease is neither purely hereditary nor entirely independent of genes), the researchers calculated a polygenic risk (i.e., summarizing the combined influence of your genes on your probability of developing a given disease in a single figure) for more than 500 healthy participants.

Most were young adults (aged 18 to 31), while the study also included an older group (aged 50 to 69). Importantly, the polygenic risk measured in the study remained low and cannot determine whether any particular person will eventually develop Alzheimer's disease.

The researchers then compared these genetic risk estimates with different characteristics of each participant's sleep.

Tiny Awakenings During the Night

The analysis revealed an association between genetic risk for Alzheimer's disease and the frequency of nighttime micro awakenings. These are very brief bursts of brain activity that can interrupt the normal sleep cycle without causing someone to become fully awake.

Among the younger participants, researchers found no connection between these micro awakenings and Alzheimer's genetic risk. A different pattern appeared in the older group. Participants who experienced more frequent micro awakenings also tended to have higher genetic risk, despite being healthy, relatively young and free of Alzheimer's symptoms.

"These micro-awakenings are therefore not insignificant," emphasizes Puneet Talwar, a researcher at the GIGA ULiège laboratory, "certain profiles could promote the accumulation of proteins involved in Alzheimer's disease and be associated with increased vulnerability."

A Tiny Brain Region Draws Attention

The researchers also examined the locus coeruleus, a tiny area deep within the brainstem that is roughly the size of a grain of rice. It plays an important role in regulating wakefulness, attention, and sleep.

"This region is difficult to observe, but it appears to play a role in the early mechanisms linked to the disease," explains Gilles Vandewalle, co-director of the GIGA CRC In Vivo Imaging technology platform and Fund for Scientific Research - FNRS Research Director at ULiège.

In 2025, a preliminary study carried out with the 7-Tesla MRI scanner at the ULiège platform allowed the team to examine the locus coeruleus in greater detail. The researchers found that characteristics of sleep quality (speed of falling asleep, depth) were associated with the condition of the brainstem beginning at a young age.

They also found that healthy functioning of the locus coeruleus was related to the quality of REM sleep, a stage of sleep that plays an important role in memory.

The locus coeruleus is especially interesting to Alzheimer's researchers because it is among the earliest brain regions where abnormal protein deposits can appear. Such deposits may begin accumulating as early as adolescence, although scientists still do not fully understand what these early changes mean.

Could Sleep Become an Early Alzheimer's Marker?

Taken together, the findings point toward possible new approaches for Alzheimer's screening and prevention. In the future, analyzing sleep could potentially complement other methods for identifying people who may be vulnerable to the disease before symptoms become apparent.

"Sleep could become an accessible marker for the early identification of vulnerable individuals," adds Gilles Vandewalle.

Researchers are also interested in whether improving sleep could eventually help prevent or slow disease progression among people with a genetic predisposition to Alzheimer's.

"This research shows that sleep is not only an indicator of health, but also a potential lever for intervention," adds Lucie Leroux, head of French-speaking activities at the Stop Alzheimer's Foundation.

More than 220,000 people in Belgium are affected by Alzheimer's disease. For now, however, the new findings show statistical associations rather than proof that particular sleep patterns cause or predict the disease. Additional research will be needed to confirm the results, and the findings cannot currently be used to determine whether an individual will develop Alzheimer's.

Even so, the research provides another glimpse into changes that may occur long before Alzheimer's becomes clinically visible and underscores the value of basic research aimed at understanding and, eventually, anticipating the disease.

Journal Reference:

1. Nasrin Mortazavi, Puneet Talwar, Ekaterina Koshmanova, Roya Sharifpour, Elise Beckers, Alexandre Berger, Islay Campbell, Ilenia Paparella, Fermin Balda, Ismael Dardour Hamzaoui, Christian Berthomier, Christine Bastin, Christophe Phillips, Pierre Maquet, Fabienne Collette, Mikhail Zubkov, Laurent Lamalle, Gilles Vandewalle. REM sleep quality is associated with balanced tonic activity of the locus coeruleus during wakefulness. Journal of Biomedical Science, 2025; 32 (1) DOI: 10.1186/s12929-025-01127-9

Courtesy:

University of Liège. "Your sleep may be hiding an early clue to Alzheimer’s." ScienceDaily. ScienceDaily, 28 August 2026. <www.sciencedaily.com/releases/2026/08/260828005218.htm>. 

 

 

 

 

 

 

A cancer therapy put severe rheumatoid arthritis into remission

 Immunotherapies such as CAR T-cell therapy were originally developed mainly to fight cancer. But scientists are now investigating whether these personalized treatments, made from a patient's own immune cells, could also help treat or even potentially cure autoimmune diseases.

Researchers at Charité - Universitätsmedizin Berlin have now tested CAR T-cell therapy in six people with particularly severe rheumatoid arthritis. The world's first clinical trial of its kind, reported in Nature Medicine, produced encouraging early results. Disease activity fell substantially in every participant, and by the end of the observation period, three patients no longer needed rheumatoid arthritis medication.

Why Rheumatoid Arthritis Can Be So Difficult To Treat

Rheumatoid arthritis is a chronic autoimmune disease in which the immune system mistakenly attacks the joints. Repeated inflammation causes swelling and can eventually damage the joints.

Existing medications are often effective at controlling inflammation, but they generally do not cure the disease. As a result, many patients need lifelong treatment with anti-inflammatory drugs and medications that suppress the immune system, which can also cause side effects.

For some people, even newer therapies do not work well enough. Doctors describe these cases as treatment-refractory rheumatoid arthritis. Patients can continue to experience pain, limited mobility, and major reductions in quality of life despite trying multiple treatments.

"One reason could be disease-driving B cells - memory cells of the adaptive immune system that may survive in the lymph nodes, bone marrow or joint tissue after an infection, where they produce harmful antibodies directed against the body's own tissues and repeatedly reignite the inflammation," explains Prof. David Simon, who designed the trial for this patient group together with Prof. Gerhard Krönke at Charité's Department of Rheumatology and Clinical Immunology.

The researchers are testing whether CAR T cells can seek out these disease-driving B cells even when they are buried deep within body tissues. Their goal is to eliminate as much of the abnormal B-cell memory as possible and effectively give the B-cell system a new start.

Using Cancer Immunotherapy To Reset the Immune System

CAR T cells were first developed as a cancer treatment, but their potential uses are expanding. In cancer therapy, a patient's immune cells are modified so they can recognize and destroy tumor cells. For autoimmune diseases, scientists instead want to direct those engineered cells toward immune cells that help sustain the disease.

"The identifying marker on many B cells, both abnormal B cells in cancers of the blood or lymphatic system and disease-driving B cells in rheumatoid arthritis, is the surface molecule CD19. You could think of it as a kind of 'name tag'," explains David Simon. "To enable CAR T cells to detect and eliminate the disease-causing cells, we equip patients' own immune cells with a receptor that acts like a search sensor for CD19."

To produce this form of CD19 CAR T-cell therapy, doctors first collect T cells from the patient's blood. T cells are immune cells that normally help recognize and destroy infected or abnormal cells.

Scientists then genetically modify those T cells in the laboratory. The cells receive a chimeric, or artificial, antigen receptor known as a CAR, which is designed to bind specifically to CD19.

Before receiving the modified cells, patients undergo a short course of preparatory chemotherapy. This temporarily lowers the number of certain immune cells, creating room for the CAR T cells to multiply and function effectively.

The engineered cells are then returned to the patient in a single infusion. Once inside the body, they search for cells carrying CD19 and attack them. This temporarily removes all CD19-positive B cells, including long-lived disease-driving cells in the joints that can otherwise be difficult to reach. By clearing out those cells, the treatment may allow the immune system to reset.

First Trial in Severe Rheumatoid Arthritis

For the first clinical trial evaluating both the safety and effectiveness of CD19 CAR T-cell therapy in rheumatoid arthritis, the Charité team initially enrolled six patients with especially severe disease.

The group included three women and three men between the ages of 31 and 69. During the previous decade, they had received as many as eight targeted or biologic therapies, but none had controlled their disease adequately.

Researchers wanted to learn whether CAR T cells could reach the disease-driving B cells inside the joints and whether the approach could do so safely.

The first phase of the COMPARE trial produced results the team considers highly encouraging.

"Disease activity decreased markedly in all six patients. During follow-up of up to one year, three patients were in sustained remission without any medication for rheumatoid arthritis," reports Gerhard Krönke, who leads the joint Clinical Rheumatology research group at Charité and the German Rheumatology Research Center (DRFZ), a Leibniz Institute. "This is particularly remarkable given that none of the established treatments had previously been able to relieve their symptoms adequately."

CAR T Cells Reached Hidden Disease Reservoirs

The treatment appeared to do more than temporarily reduce inflammation in the joints. Researchers found that the modified immune cells also reached and eliminated disease-promoting B cells in deeper locations, including the bone marrow, lymph nodes, and joint tissue.

During regular follow-up visits over the following 12 months, levels of the autoantibodies associated with rheumatoid arthritis dropped sharply.

David Simon adds: "When the B-cell system later recovered, predominantly naïve B cells that had not yet been shaped by the disease returned. In contrast, the B cells directed against the body's own tissues that had been present before treatment were no longer detectable in almost all patients, an indication that the treatment may indeed be able to reset the pathological immune memory."

Importantly, antibodies generated by earlier vaccinations, including those against chickenpox and tetanus, could still be detected. That suggests protective antibody memory was largely preserved even though the therapy caused a profound temporary depletion of B cells.

Researchers still need to determine whether the therapy has any longer-term effects on the immune system.

Promising Results, but the Therapy Remains Experimental

The trial suggests that a single CAR T-cell treatment can, in some patients, produce a sustained period without symptoms or rheumatoid arthritis medication. This state of disease inactivity is known as remission.

For carefully selected patients whose rheumatoid arthritis does not respond adequately to available treatments, researchers hope it may eventually be possible to directly reset pathological immune memory and stop the ongoing inflammation rather than continuously suppressing it with medication.

However, CAR T-cell therapy for autoimmune diseases, including rheumatoid arthritis, is still experimental. Researchers do not yet have long-term experience with the treatment.

Responses also differed among the six participants. Some did not achieve a complete response, and one patient's disease returned after an initial period of medication-free remission.

So far, however, the researchers consider the safety findings encouraging.

"After the participants received the CD19 CAR T cells, we observed only a temporary, mild-to-moderate cytokine release syndrome (CRS) in all participants, which was readily manageable. There were no severe neurological complications or other serious adverse events, and infections were rare," explains Dr. Marie Luise Hütter-Krönke, Medical Director of the Hematology Early Clinical Trial Unit at Charité's Department of Hematology, Oncology and Cancer Immunology.

A Larger Comparison Is Next

The second phase of the trial will include ten additional patients. Researchers plan to compare CAR T-cell therapy with an already approved rheumatoid arthritis drug that also targets B cells.

The comparison should help determine whether CAR T cells produce stronger or longer-lasting effects and whether they truly reset immune memory.

If these results are confirmed in this phase and in future larger studies, CAR T-cell therapy could eventually offer another option for people with severe rheumatoid arthritis whose lives are significantly affected by the disease and who currently have no adequate treatment.

About the Study

The first of the two phases of the COMPARE study was designed to assess the safety and effectiveness of CD19 CAR T-cell therapy in treatment-refractory rheumatoid arthritis.

Major contributors included researchers from Charité's Department of Rheumatology and Clinical Immunology and the Department of Hematology, Oncology and Cancer Immunology at Campus Benjamin Franklin, along with scientists from the Cluster of Excellence ImmunoPreCept, the German Rheumatology Research Center (DRFZ), a Leibniz Institute, and the Fraunhofer Institute for Translational Medicine and Pharmacology ITMP.

The study was initiated and designed at Charité and also received support from Kyverna Therapeutics. The immunotherapy company had no role in designing the study, collecting or analyzing the data, or presenting the results.

Journal Reference:

1. Fredrik N. Albach, Marie C. Rehm, Marie Luise Hütter-Krönke, Thanh Hang Le, Julia M. Giezen, Murat Torgutalp, Arne Sattler, Ioanna Minopoulou, Robert Biesen, Edgar Wiebe, Vincent Casteleyn, Thorben Witte, Christian Furth, Jan Zernicke, Melanie Nuesch Germano, Johan Verhagen, Artur Wilhelm, Maria Dzamukova, Klaus Engel, Simon Schallenberg, Aimo Kannt, Nicole Ziegler, Michaela Fehringer, Udo Schneider, Nadine Unterwalder, Mark Beling, Alexander Pfeil, Elpida Phithak, Martin Krusche, Olaf Penack, Tobias Alexander, Werner Stenzel, Manfred Wuhrer, Kamran Movassaghi, Thomas Dörner, Eicke Latz, Thomas Vogl, Antonia Busse, Georg Schett, Hans Ulrich Scherer, Rene E. M. Toes, Arnd Kleyer, Ulrich Keller, Lars Bullinger, David Simon, Gerhard Krönke. CD19 CAR T cell therapy for treatment-refractory seropositive rheumatoid arthritis: a phase 1 trial. Nature Medicine, 2026; DOI: 10.1038/s41591-026-04603-3

Courtesy:

Charité - Universitätsmedizin Berlin. "A cancer therapy put severe rheumatoid arthritis into remission." ScienceDaily. ScienceDaily, 29 August 2026. <www.sciencedaily.com/releases/2026/08/260828082330.htm>. 

 

 

 

 

 

Researchers unveil sustainable spirulina solution to vitamin B12 deficiency

Scientists have found a way to grow Spirulina that produces biologically active vitamin B12 at levels comparable to beef, potentially overcoming one of the biggest nutritional limitations of this widely promoted algae.

The research, published in the scientific journal Discover Food, was led by Dr. Asaf Tzachor, Founder and Academic Director of the Aviram Sustainability and Climate Program at Reichman University, together with researchers from Iceland, Denmark and Austria. Using advanced biotechnology and carefully controlled light conditions, the team produced carbon-neutral, nutrient-rich Spirulina biomass containing active vitamin B12. According to the researchers, this is the first time biologically active vitamin B12 has been reported in Spirulina.

A Global Vitamin B12 Problem

Vitamin B12 is an essential micronutrient involved in several critical processes in the body, including red blood cell formation and normal nervous system function. More than a billion people worldwide are estimated to have low levels of the vitamin.

For many people, meat and dairy products are important dietary sources of B12. The recommended intake cited by the researchers is 2.4 µg/day. However, producing animal-based foods at the scale required to meet global demand also carries environmental costs, which has driven interest in more sustainable alternatives.

Spirulina blue green algae (Arthrospira platensis) has often been promoted as one such option because it is nutrient dense and can be cultivated with a relatively small environmental footprint. But there has been a major obstacle.

Traditional Spirulina contains much of its B12 in the form of pseudo-vitamin B12. Although chemically similar to the vitamin humans need, this form is not bioavailable to people, meaning the body cannot effectively use it. That limitation has prevented conventional Spirulina from serving as a reliable replacement for animal-sourced vitamin B12.

Using Light to Change Spirulina's Nutrition

To address that problem, researchers from Reichman University, University of Natural Resources and Life Sciences, Vienna, Ruppin Academic Center, Danish Technological Institute, and MATIS, Iceland, carried out an exploratory study of a biotechnology platform developed by VAXA Technologies in Iceland.

The team examined the system's engineering design, its inputs (such as energy), and the nutritional composition of the biomass it produced.

A central feature of the technology is photonic management (modified light conditions). By changing the light environment in which Spirulina grows, the researchers were able to encourage production of biologically active vitamin B12.

The cultivated Spirulina also contained other bioactive compounds associated with antioxidant, anti-inflammatory, and immune-boosting properties.

Most notably, the resulting carbon-neutral biomass contained 1.64 µg of active vitamin B12 per 100 grams, compared with 0.7-1.5 μg per 100 grams in beef.

Dr. Asaf Tzachor explains, "the findings demonstrate that photosynthetically controlled Spirulina can produce desirable levels of active vitamin B12, offering a sustainable alternative to traditional animal-source foods."

Could Spirulina Supply Vitamin B12 at Scale?

The researchers also explored what could happen if the system were expanded far beyond its current scale.

In one scenario, reallocating electricity currently used by heavy industry in Iceland could support production of 277,950 tonnes of Spirulina biomass each year. The researchers estimate that this amount would contain about 4555 grams of active vitamin B12 annually.

According to their calculations, that quantity could provide the recommended dietary allowance (RDA) for more than 13.8 million children aged 1-3.

More ambitious production scenarios could potentially supply enough vitamin B12 to meet the RDA for more than 26.5 million children aged 1-3 and more than 50 million children aged 0-6 months.

These figures are projections based on possible scale-up scenarios rather than existing production levels, but they illustrate the nutritional potential the researchers see in the technology.

A More Sustainable Source of an Essential Vitamin

If the approach can be successfully expanded, photosynthetically controlled Spirulina could provide another route for addressing vitamin B12 deficiency while reducing some dependence on meat and dairy production.

The work also highlights how biotechnology can alter the nutritional properties of microorganisms and other rapidly growing food sources. Rather than simply cultivating conventional Spirulina, researchers are changing the conditions under which it grows to encourage production of specific compounds that are useful to humans.

The findings represent a step toward developing more sustainable sources of essential nutrients, although further research and larger-scale production will be needed to determine how the technology could fit into real-world food systems.

Reichman University and the Aviram Foundation established the Aviram Sustainability and Climate Program in response to growing environmental and public health challenges around the world. The program trains students from a range of disciplines to develop strategies for addressing resource scarcity, climate change, and extreme weather events, as well as food, water, and energy crises.

 

Journal Reference:

1. A. Tzachor, S. P. van den Oever, H. K. Mayer, M. Asfur, A. Smidt-Jensen, M. Geirsdóttir, S. Jensen, B. O. Smárason. Photonic management of Spirulina (Arthrospira platensis) in scalable photobioreactors to achieve biologically active unopposed vitamin B12. Discover Food, 2024; 4 (1) DOI: 10.1007/s44187-024-00152-1

Courtesy:

Reichman University. "Researchers unveil sustainable spirulina solution to vitamin B12 deficiency." ScienceDaily. ScienceDaily, 30 August 2026. <www.sciencedaily.com/releases/2026/08/260829035227.htm>. 

 

 

 

Widely prescribed blood pressure drugs linked to 33% higher kidney risk in type 2 diabetes

 

New findings presented at the 63rd ERA Congress suggest that a commonly prescribed group of blood pressure drugs may be linked to worse kidney outcomes in people with type 2 diabetes (T2D), including patients already taking newer medications designed to protect kidney function.

The medications, known as dihydropyridine calcium-channel blockers (DCCBs), lower blood pressure by relaxing blood vessels. They are often prescribed as second-line treatments for people with diabetic kidney disease (DKD). In the new study, patients who took DCCBs in addition to standard therapies experienced a significantly greater risk of major adverse kidney events than patients treated with other blood pressure medications.

Protecting the Kidneys in Type 2 Diabetes

DKD is among the most common causes of kidney failure worldwide. The condition develops as prolonged high blood sugar damages tiny blood vessels within the kidneys, gradually interfering with their ability to remove waste from the bloodstream. Keeping blood pressure under control is a key part of managing the disease because elevated blood pressure can speed up this damage.

Treatment for DKD has changed considerably in recent years with the introduction of two important classes of medication. Renin-angiotensin system (RAS) inhibitors lower blood pressure while also reducing pressure inside the kidney's filtering structures. Sodium-glucose cotransporter-2 (SGLT2) inhibitors were initially developed to treat diabetes, but they are now also recognized for their ability to protect kidney function and lower the risk of kidney failure. The two drug classes are now part of standard treatment for many people with DKD.

Study Tracks More Than 31,000 Patients

Researchers examined health data from 31,031 adults with T2D between 2016 and 2021. Every participant was receiving both RAS and SGLT2 inhibitors. Of the total group, 12,172 (39.2%) were also taking DCCBs, while 18,859 (60%) were being treated with other antihypertensive medications. The median follow-up period was approximately 3.5 years.

After accounting for differences in patients' initial clinical and demographic characteristics, the researchers found that DCCB use was associated with a 33% greater risk of a major adverse kidney event (R 1.33, 95%, CI 1.03-1.73).

Researchers classified these events as either a major loss of kidney filtration capacity, involving a decline of 40% or more in estimated glomerular filtration rate (eGFR), the standard measure of kidney function, or progression to end-stage kidney disease that required dialysis or transplantation.

"DCCBs are widely used as second-line blood pressure treatments in patients with DKD," said Dr. Timna Agur, lead author of the study. "Our findings raise important questions about whether these medications are always the best option for patients already receiving modern kidney-protective therapies."

Why DCCBs Could Affect Kidney Function

The researchers suggest that the association may be related to how DCCBs alter blood flow through the kidneys. In DKD, the kidneys are already dealing with elevated pressure and hyperfiltration, a condition in which their filtering structures are placed under excessive strain.

DCCBs may relax the blood vessels that carry blood into these filtering units more strongly than they affect the vessels carrying blood away. According to the researchers, this imbalance could increase pressure inside the filtering structures and potentially contribute to continued kidney damage.

"We initially thought the kidney-protective effects of SGLT2 inhibitors might counterbalance the potential harms associated with DCCBs," said Dr. Agur. "However, the increased risk of kidney disease progression appeared to persist even in this group."

More Research Is Needed

Because the study was observational, the researchers emphasize that it cannot show that DCCBs directly caused the poorer kidney outcomes. Still, they say the association deserves attention because these medications are so frequently prescribed to people with DKD.

"Further prospective studies and randomized controlled trials are needed to confirm these observations and better define the safest blood pressure treatment strategies for patients with DKD," concluded Dr. Agur. "However, given how commonly these medications are prescribed, any increase in kidney risk could have important implications for large numbers of patients with DKD."

Story Source:

Materials provided by European Renal Association (ERA). Note: Content may be edited for style and length.

 

Courtesy:

European Renal Association (ERA). "Widely prescribed blood pressure drugs linked to 33% higher kidney risk in type 2 diabetes." ScienceDaily. ScienceDaily, 18 August 2026. <www.sciencedaily.com/releases/2026/08/260816044844.htm>. 

 

 

 

 

Scientists turn probiotic bacteria into tiny drug factories for pancreatic cancer

Cancer immunotherapy has dramatically changed how doctors treat many forms of cancer, yet pancreatic cancer has remained particularly resistant to these advances. A major obstacle is the environment that develops around pancreatic tumors. These tumors often create a "cold" tumor microenvironment that blocks immune cells from launching an effective attack.

Researchers at the University of Chicago have now developed a new approach that could help overcome this problem. In a study published in Science Advances, the team used BifidoSumIL-2, an engineered strain of Bifidobacterium longum, a probiotic bacterium naturally found in the gut, to carry an immune-stimulating treatment directly into tumors.

In animal models, the therapy slowed the growth of pancreatic tumors by selectively activating T cells that fight cancer. Its effects became even stronger when researchers combined it with chemotherapy, radiotherapy or immunotherapy. The findings suggest that BifidoSumIL-2 could eventually provide a new way to improve how pancreatic tumors respond to treatment.

Using Bacteria to Deliver Cancer Therapy

"A big unmet medical need has been pancreatic cancer, and so that was going to be our mountain to climb," said Ralph Weichselbaum, MD, the Daniel K. Ludwig Distinguished Service Professor and Chair of Radiation and Cellular Oncology at the University of Chicago.

BifidoSumIL-2 was created to release a modified version of interleukin-2 (IL-2) once it reaches a tumor. IL-2 is a potent immune signaling molecule that activates T cells involved in attacking cancer. Conventional IL-2 treatment, however, can produce serious side effects and can also stimulate immune cells that actually weaken the antitumor response.

The researchers sought to avoid these problems by using SumIL-2, a modified form of IL-2 engineered to more precisely activate cancer-fighting T cells while reducing stimulation of regulatory T cells. They then placed SumIL-2 inside Bifidobacterium longum so that the therapeutic molecule could be concentrated within tumors instead of throughout the body.

Developing the treatment required scientists from several disciplines to work together, including specialists in microbiology, synthetic biology, oncology, and immunology.

"This was a highly interdisciplinary effort," said Mark Mimee, PhD, Assistant Professor of Microbiology at the University of Chicago. "We had to bring together people who understand bacteria, people who understand tumors, and people who understand the immune system to make something like this possible."

Why Bifidobacterium Can Target Tumors

Bifidobacterium offered the researchers an unusual advantage as a delivery system. The bacterium grows in anaerobic environments, meaning places with very little oxygen. Low oxygen levels are common inside many solid tumors, including pancreatic tumors, while healthy tissues generally contain more oxygen and are therefore less suitable for the bacteria.

"Bifidobacterium is an obligate anaerobe, so it doesn't grow in the presence of oxygen," Mimee said. When the bacteria are injected systemically, they are cleared from healthy tissues with abundant oxygen. Inside the low-oxygen regions of tumors, however, they can become active.

That preference allows the engineered bacteria to function as microscopic drug factories inside tumors. Once there, they produce SumIL-2 where the treatment is needed rather than broadly throughout the body. Researchers also noted that Bifidobacterium has shown a favorable safety profile in preclinical models and is already well known as a probiotic organism. It is commonly present in yogurt and is generally recognized as a safe, off-the-shelf probiotic.

Engineering the organism was not simple.

"Bifidobacterium is not the easiest organism to work with," Mimee said. "It's anaerobic, it grows slowly, and the genetic tools for manipulating it are much more limited compared to model bacteria like E. coli. A lot of the work was just figuring out how to reliably engineer it."

Stronger Results With Combination Treatments

Tests in animal models showed that BifidoSumIL-2 preferentially gathered inside tumors, stimulated immune activity, and slowed the growth of pancreatic cancer. It also changed the tumor microenvironment in a potentially beneficial way by increasing the activity of cancer-fighting CD8+ T cells.

The results improved further when BifidoSumIL-2 was paired with established cancer treatments. Combining the bacterial therapy with chemotherapy, radiation therapy, or anti-PD-L1 immunotherapy led to better tumor control and longer survival than the individual treatments achieved on their own.

"This combination potential is one of the study's most important findings; BifidoSumIL-2 not only works by itself -- it works with radiotherapy, chemotherapy, and immunotherapy," Weichselbaum said.

Despite the encouraging findings, BifidoSumIL-2 has not been tested in humans. Future research will need to examine its long-term safety, the possibility of effects outside the intended tumor, how long the immune response lasts, and whether the bacteria might eventually be given orally instead of through injection. The researchers also want to investigate whether the strategy can be combined with newer pancreatic cancer treatments, including KRAS inhibitors.

The Growing "Bugs as Drugs" Approach

The research adds to growing interest in a strategy known as "bugs as drugs." By engineering probiotic bacteria to seek out tumors and produce therapies directly inside them, scientists may be able to concentrate powerful immune treatments where they are most useful while reducing unwanted effects elsewhere in the body.

The study, "Engineered probiotic Bifidobacterium for tumor-targeted pancreatic cancer therapy" was supported by funds from the Ludwig Foundation and the National Institutes of Health.

Additional authors include Jaehyun Lee, Kaiting Yang, Christina Nowicki, Wei Liu, Emile Naccasha, and Hua Liang from the University of Chicago; Zhichen Sun from the University of Texas Southwestern, Dallas; and Yang-Xin Fu from Tsinghua University, Beijing, China.

UChicago Medicine and the Biological Sciences Division continue to be at the forefront of cancer care and research. In April 2027, UChicago Medicine will open the AbbVie Foundation Cancer Pavilion, Chicago's first freestanding cancer pavilion, to bring advanced diagnostics, innovative treatments, translational discoveries, and comprehensive support to patients and the community.

Journal Reference:

1. Jaehyun Lee, Kaiting Yang, Christina A. Nowicki, Wei Liu, Kangdi Li, Emile Naccasha, Zhichen Sun, Yang-Xin Fu, Hua Liang, Ralph R. Weichselbaum, Mark Mimee. Engineered probiotic Bifidobacterium for tumor-targeted pancreatic cancer therapy. Science Advances, 2026; 12 (30) DOI: 10.1126/sciadv.adz1388

Courtesy:

University of Chicago Medical Center. "Scientists turn probiotic bacteria into tiny drug factories for pancreatic cancer." ScienceDaily. ScienceDaily, 19 August 2026. <www.sciencedaily.com/releases/2026/08/260816044830.htm>.

 

 

 

 

 

 

Coffee drinkers have less fat, more muscle, and surprising hormone differences

Coffee is consumed around the world every day, and earlier research has associated coffee drinking with a reduced risk of conditions including type 2 diabetes and cardiovascular disease. Scientists still do not fully understand the biological processes that might explain those connections. Now, new research from Finland suggests that regular coffee consumption is associated with healthier body composition, favorable metabolic markers, and distinct patterns involving sex hormones in men and women.

Researchers at the University of Oulu analyzed information from 2,264 people who were 46 years old and taking part in the Northern Finland Birth Cohort 1966. The team investigated how participants' usual coffee intake related to circulating metabolites, indicators of cardiometabolic risk, and sex hormone levels.

Coffee Drinkers Had Less Fat and More Muscle

People who consumed more coffee tended to have lower levels of both total body fat and visceral fat, along with greater skeletal muscle mass. These differences appeared even though participants with higher and lower coffee intake had a similar body mass index (BMI).

Higher coffee consumption was also associated with lower circulating concentrations of branched-chain amino acids in both men and women. When chronically elevated, these biomarkers have previously been associated with insulin resistance and a greater risk of developing type 2 diabetes.

Coffee Intake Was Linked to Different Hormone Patterns

Some of the clearest differences appeared among men. Greater coffee consumption was associated with a more favorable glucose-insulin profile, higher levels of total and bioavailable testosterone, and greater concentrations of sex hormone-binding globulin (SHBG). However, free testosterone and the free androgen index were modestly lower.

The hormonal associations were less extensive in women. Higher coffee consumption was mainly associated with increased SHBG and lower measures of free androgens.

"Coffee is consumed by millions of people every day, yet we still know surprisingly little about how it relates to our metabolism and hormones. What stood out in our findings was a distinct hormonal signature that didn't disappear even after we took into account BMI and lifestyle factors, with several of these associations differing between men and women," says Luca Verroest, lead author of the study and Doctoral Researcher at the University of Oulu.

Hormones Could Offer a Clue to Coffee's Health Links

The findings raise the possibility that hormonal pathways could help explain some of the previously observed relationship between coffee consumption and metabolic health. Because the research was observational, however, it cannot establish that drinking coffee directly caused any of the biological differences identified in the study.

The setting also makes the research especially relevant. Finland ranks among the world's highest coffee-consuming countries, with average annual consumption of approximately 11.8 kilograms (26 pounds) per person.

Researchers say the results offer a starting point for studies designed to determine whether coffee itself produces these biological changes and, if so, which compounds may be responsible. Scientists are currently investigating these questions using animal models, with the longer-term aim of moving toward human intervention studies.

Additional research will be necessary before the findings can be used to shape dietary recommendations.

The study, "Associations of habitual coffee intake with testosterone and cardiometabolic markers: the Northern Finland Birth Cohort 1966 study," was published in the European Journal of Nutrition.

 

Journal Reference:

1. Luca Verroest, Jari Jokelainen, Shalini Choudhary, Jaroslaw Walkowiak, Toni Karhu, Saranya Palaniswamy, Juha Auvinen, Marjo-Riitta Jarvelin, Karl-Heinz Herzig, Ghulam Shere Raza. Associations of habitual coffee intake with testosterone and cardiometabolic markers: the Northern Finland birth cohort 1966 study. European Journal of Nutrition, 2026; 65 (5) DOI: 10.1007/s00394-026-04038-z

Courtesy:

University of Oulu, Finland. "Coffee drinkers have less fat, more muscle, and surprising hormone differences." ScienceDaily. ScienceDaily, 19 August 2026. <www.sciencedaily.com/releases/2026/08/260819041228.htm>. 

 

 

 

This ultrasound treatment may help stop arthritis before it starts

Researchers at The University of Alabama in Huntsville (UAH), part of The University of Alabama System, have identified a promising new use for continuous low-intensity ultrasound that could one day help treat joint injuries and reduce the risk of post-traumatic osteoarthritis. Their findings suggest the non-invasive approach may shift the body's immune response away from long-lasting inflammation and toward tissue repair, offering a potential drug-free strategy for improving healing.

The study, published in the Nature journal Scientific Reports, was led by Dr. Anuradha Subramanian, professor of chemical and materials engineering. It combined biological research conducted by Dr. Shahid Khan during his doctoral studies with computational and statistical analysis developed by Dr. Satyaki Roy, professor of mathematical sciences, along with contributions from graduate student Owen Trippany. The research was funded by the National Institutes of Health through an R01 grant awarded to Subramanian.

How Ultrasound Influences Immune Cells

The team focused on macrophages, specialized immune cells that play a key role in both inflammation and tissue repair, to understand how they respond to continuous low-intensity ultrasound.

"Following injury, the body recruits inflammatory 'defender' macrophages (M1) to clear damaged tissue and healer macrophages (M2) to support repair and recovery," Subramanian explains. "Persistent dominance of defender macrophages can create a prolonged inflammatory environment that contributes to post-traumatic osteoarthritis."

The researchers wanted to determine whether ultrasound could encourage these immune cells to transition from an inflammatory state to one that promotes healing.

"In an 'M1' state, microphages promote inflammation to fight damage or infection, but prolonged M1 activity can also harm healthy tissue," Subramanian notes. "In contrast, 'M2-like' macrophages support tissue repair and recovery. Shifting macrophages toward an M2-like state is important, because it may help reduce chronic inflammation while encouraging healing in damaged joints. Our findings suggest that continuous low-intensity ultrasound may help restore this balance by promoting a more reparative macrophage response."

Roy says chronic inflammation is a major factor in the development of post-traumatic osteoarthritis.

"Post-traumatic osteoarthritis is driven in part by persistent inflammation that limits tissue repair and accelerates joint degeneration," Roy adds. "Our team is interested in continuous low-intensity ultrasound because it offers a non-pharmacological, non-invasive approach that may help regulate immune cell behavior and promote a more reparative healing environment in injured joints."

A More Realistic Model of Joint Injury

To better recreate the conditions inside an injured joint, the researchers relied on fibronectin fragments, molecules generated as damaged tissue breaks down, instead of using only conventional laboratory methods to trigger inflammation. This approach produced a model that more closely reflects the biological environment that develops after a joint injury.

The team also combined transcriptomics, the large-scale study of gene activity, with an advanced computational method known as differential clustering. Rather than analyzing genes one by one, this technique identifies groups of genes whose behavior changes together, providing a broader picture of how immune cells respond to ultrasound treatment.

"This allowed us to study not only which genes changed, but also how groups of genes changed their coordinated behavior in response to ultrasound stimulation," Roy says.

Early Results Show Reduced Inflammation

The researchers found that continuous low-intensity ultrasound lowered biological markers linked to inflammation while increasing markers associated with a more reparative, M2-like macrophage state.

Although the research is still limited to laboratory experiments, the findings suggest that non-drug, non-invasive technologies could eventually be used to influence immune cell behavior and improve healing after joint injuries. The researchers believe the technique could become part of future treatments designed to slow the progression of osteoarthritis and improve recovery after joint trauma.

"The next steps will involve validating these findings in animal models of early post-traumatic osteoarthritis and studying how ultrasound-based modulation affects long-term tissue repair in joint injury settings," Subramanian says.

Journal Reference:

1. Shahid Khan, Owen Trippany, Anuradha Subramanian, Satyaki Roy. Continuous low-intensity ultrasound influences the transcriptomic profile in M1 macrophages by downregulating inflammation and promoting M2-like markers. Scientific Reports, 2026; DOI: 10.1038/s41598-026-53228-6

Courtesy:

The University of Alabama in Hunstville. "This ultrasound treatment may help stop arthritis before it starts." ScienceDaily. ScienceDaily, 12 July 2026. <www.sciencedaily.com/releases/2026/07/260710003521.htm>. 

 

 

Scientists finally crack nature's secret for building better cancer drugs

Scientists have uncovered how bacteria naturally manufacture multiple versions of powerful cancer drugs, solving a mystery that has puzzled researchers for decades. The discovery could help speed the development of new treatments for cancers that are still difficult to treat.

For years, scientists have hoped to harness bacterial enzymes to create new drug variants through a process known as combinatorial biosynthesis. However, progress has been limited because researchers did not fully understand how the enzymes coordinate their work.

Published in Nature Communications, the new study reveals how bacterial enzymes communicate with one another to assemble a family of closely related anti-cancer compounds. That family includes Romidepsin (Istodax), an FDA-approved treatment for certain blood cancers. By uncovering this natural "mix and match" system and reproducing its underlying principles in the laboratory, the researchers have established a new strategy for designing future cancer therapies.

"For decades, we've known that bacteria can naturally produce multiple versions of powerful anti-cancer drugs, yet we had no idea how they achieved this," said first author Dr. Munro Passmore, Research Fellow, Department of Chemistry, University of Warwick. "This work finally cracks that code. We've identified how the different enzymes communicate and cooperate to produce these drug variants, something that has eluded researchers because the system is so elegantly economical. It's the breakthrough we needed to actually engineer these drugs ourselves."

Tiny Molecular Connectors Reveal Nature's Drug-Making Strategy

The researchers discovered that small molecular regions known as 'docking domains' serve as connectors between the core drug-building machinery and the enzymes responsible for adding different components. These docking domains share a conserved connection point that allows them to interact with multiple enzyme partners.

This flexible design explains how bacteria can create a variety of related drug molecules while still maintaining the precision needed for the compounds to remain effective.

The study also sheds light on how these natural drug-producing systems evolved. According to the researchers, the newly identified compound most likely developed from a related drug-producing pathway through gene duplication and recombination over time.

Prof. Greg Challis, Monash Warwick Alliance Professor of Sustainable Chemistry, University of Warwick and Monash University concludes: "This research gives us a blueprint to do what nature does, but better and faster. By reverse-engineering nature's evolutionary logic, we can now design synthetic pathways that generate new anti-cancer drug candidates with properties optimized for clinical use, such as superior potency, improved selectivity, fewer side effects. Our immediate goal is to build an expanded library of candidates for various cancers where new treatments are urgently needed. This discovery is moving us from understanding how the systems work to building new ones."

How the Discovery Could Improve Cancer Drug Development

The work focuses on a class of anti-cancer medicines known as HDAC inhibitors. These drugs block histone deacetylases, enzymes that help regulate which genes are switched on or off inside cells. Romidepsin (Istodax) is an FDA-approved HDAC inhibitor used to treat T-cell lymphomas.

A chemically related compound called FR-901375 has been known for decades, but scientists had never identified the biological pathway bacteria use to produce it. This study finally fills in that missing piece.

Like other HDAC inhibitors in its family, FR-901375 belongs to a group of complex cyclic molecules called depsipeptides. These compounds are assembled from amino acid building blocks along with a conserved hydroxy acid pharmacophore, all connected through a combination of peptide and ester bonds.

Inside bacteria, these molecules are built by massive protein complexes called PKS-NRPS hybrids, which combine the activities of polyketide synthase (PKS) and nonribosomal peptide synthetase (NRPS). The new research shows that the key to this assembly process is the docking domains, which act like molecular connectors that allow one part of the production line to recognize and pass its product to the next. This mechanism is what enables combinatorial biosynthesis and allows bacteria to naturally generate multiple drug variants.

How the Researchers Solved the Mystery

To uncover how this system works, the team combined structural biology, biochemistry, genetics, and computational modeling.

Their work included:

• Bioinformatic searches of public databases that identified the FR-901375 biosynthetic gene cluster in Pseudomonas chlororaphis subsp. piscium, with the findings confirmed by mass spectrometry analysis of extracted metabolites.
• In vitro reconstitution experiments using purified protein domains that demonstrated productive enzyme-enzyme interactions, verified with intact protein mass spectrometry.
• AlphaFold computational modeling to predict protein complex structures, followed by carbene footprinting mass spectrometry to experimentally map the interaction sites.
• Site-directed mutagenesis experiments that confirmed the importance of the predicted binding residues.
• Gene deletion studies in bacterial strains showing that the docking domains are essential for the system to function in vivo.
• Comparative analysis of biosynthetic gene clusters from multiple HDAC inhibitor-producing bacteria, revealing evolutionarily conserved features shared across these natural drug-making systems.

Journal Reference:

1. Munro Passmore, Xinyun Jian, Xinyi Zhao, Emmanuel L. C. de los Santos, Douglas M. Roberts, Józef R. Lewandowski, Matthew Jenner, Lona M. Alkhalaf, Gregory L. Challis. Molecular basis for depsipeptide HDAC inhibitor combinatorial biosynthesis. Nature Communications, 2026; 17 (1) DOI: 10.1038/s41467-026-74383-4

Courtesy:

University of Warwick. "Scientists finally crack nature's secret for building better cancer drugs." ScienceDaily. ScienceDaily, 8 July 2026. <www.sciencedaily.com/releases/2026/07/260701205001.htm>.

 

 

 

Alzheimer's tau protein has a surprising secret role in memory

New research has revealed that tau, a protein best known for its connection to Alzheimer's disease, is also essential for creating long lasting memories. The discovery provides new insight into how healthy memory works and could help guide future efforts to develop treatments for dementia.

The study, led by Flinders University in partnership with researchers from the University of New South Wales and Macquarie University, was published in Nature Communications. It found that tau helps organize and stabilize memories so they can be retained over time.

The researchers studied "remote memory" in mice, which refers to memories recalled days or weeks after an experience. They discovered that tau is not necessary for learning something new or remembering it shortly afterward. Instead, it plays a crucial role in making those memories durable over the long term.

Because the research was conducted in mice, the findings cannot be directly applied to human memory or Alzheimer's disease. Even so, the results offer valuable clues that could shape future dementia research and treatment strategies.

Tau's Role in Long Lasting Memory

Senior author Associate Professor Arne Ittner, a neuroscientist from Flinders' College of Medicine and Public Health, says the findings help explain why people with dementia may still be able to learn new information initially, yet struggle to retain it.

"Why some memories last while others fade has long puzzled scientists and our study shows that tau plays a key role in how the brain forms long-lasting memories. Without it, memories can still form in the moment, but they are weaker," says Associate Professor Ittner.

The team focused on specialized brain cells called "engram cells," which create the physical record of a memory. When a new experience occurs, only a small number of these cells are selected to store it.

According to the study, tau is active during this critical stage of memory formation, helping determine exactly which engram cells are recruited to preserve the experience.

One of the study's lead authors, Renée Kosonen, says tau acts like an organizer that helps the brain build accurate and lasting memories.

"Our findings show that tau helps determine which cells are selected to store a memory, shaping how an experience forms a lasting memory trace," says Ms Kosonen, a researcher at Flinders' Neuroscience and Dementia Research.

How Tau Organizes Memory

The researchers also found that tau reduces unnecessary or "noise" activity in the brain during memory formation. By limiting this background activity, tau allows only a specific group of cells to become part of a memory, producing clearer and more stable memory traces.

The team identified an important molecular process behind this effect. As learning takes place, tau undergoes a subtle chemical change called phosphorylation, which helps coordinate the activity of engram cells.

Although abnormal tau phosphorylation is a well known feature of Alzheimer's disease, the study shows that controlled, low level phosphorylation is a normal and essential part of healthy brain function.

New Clues About Alzheimer's Disease

The researchers made another surprising discovery. Even in the absence of tau, memory traces still existed and could be recovered by directly stimulating engram cells. This suggests that tau is not required to store memories themselves. Instead, it appears to be needed to connect natural cues, such as sights and sounds, with the ability to recall those memories.

The findings also provide new insight into how Alzheimer's related tau may interfere with memory. When disease associated forms of tau were present in engram cells during learning, they disrupted the creation of new memories. When those abnormal forms appeared after memories had already formed, they interfered with the brain's ability to retrieve them.

These effects were associated with abnormal patterns of brain activity, suggesting that memory problems in dementia may result not only from memories being lost, but also from disruptions in how memories are organized and accessed.

"Knowing how tau supports the formation and recall of memory could help us better understand what goes wrong in memory loss," says Associate Professor Ittner.

"Future research will hopefully be able to confirm concepts developed in our study in human memory and show their implication in dementia."

The researchers conclude that tau should be viewed not only as a protein involved in Alzheimer's disease, but also as a fundamental regulator of how the brain organizes, stores, and retrieves lasting memories. That new perspective could deepen scientists' understanding of both healthy memory and the biological changes that contribute to Alzheimer's disease.

Journal Reference:

1. Renée Kosonen, Kristie Stefanoska, Yijun Lin, Samantha Edwards, Emmanuel Prikas, Josefine Bertz, Anne Poljak, Lars M. Ittner, Arne Ittner. Tau T205 phosphorylation modulates engram cell recruitment and remote memory in mice. Nature Communications, 2026; DOI: 10.1038/s41467-026-73207-9

Courtesy:

Flinders University. "Alzheimer's tau protein has a surprising secret role in memory." ScienceDaily. ScienceDaily, 12 July 2026. <www.sciencedaily.com/releases/2026/07/260710003535.htm>.