For GPs, solutions for treating osteoarthritis are frustratingly limited – it’s like the weather, everyone talks about it but nobody does anything about it. While standard care can relieve symptoms, there is currently no way to regenerate the actual lost cartilage in the joints. Some experimental treatments have proven successful in animal models and in petri dishes, but those are still many years away from being approved and available on the market.
But what if there was a currently available drug that could be repurposed? Since overweight and obesity worsen osteoarthritis symptoms by placing excess strain on weight-bearing joints, GLP-1 agonists such as semaglutide have proven that they can help by promoting rapid weight loss, as demonstrated by the STEP-9 trial.
Research into GLP-1s has now revealed that they may offer a whole constellation of other benefits, such as a potential reduction in stroke risk. Now, it appears that GLP-1 agonists may have a direct effect on osteoarthritis independent of weight loss. In our podcast, we look at a recently published article in Cell Metabolism that suggests that GLP-1 agonists might go beyond just the weight loss – promote actual cartilage regrowth by jumpstarting the joint cells’ energy processing pathways. We also explore some of the caveats of potentially using GLP-1 agonists in this way, such as a lack of understanding of the long term effects, as well as the well-documented occurrence of muscle loss.
Researchers at WashU Medicine have identified a potent pathway that begins in the brain and leads to loss of all body fat without reducing food intake. The study is reported in Nature Metabolism.
The team – led by senior author Erica L. Scheller, DDS, PhD, an associate professor in the Division of Bone and Mineral Diseases in the Department of Medicine; Xiao Zhang, PhD, a former graduate student in Scheller’s lab who is now a postdoctoral fellow at the University of Pennsylvania School of Medicine; and Sree Panicker, a graduate student in Scheller’s lab – was inspired by a unique population of fat cells located deep within the skeleton.
“About 70% of our bone marrow is filled with fat that doesn’t respond to diet or exercise,” said senior author Scheller. “We wanted to figure out why.”
The team found that these special cells, called constitutive bone marrow adipocytes, expressed high levels of proteins that inhibit fat breakdown. This causes resistance to fat loss in day-to-day settings. “We call these cells stable adipocytes,” said Zhang, the study’s first author. In mice, sustained injection of leptin, a hormone, into the brain was able to unlock the stable adipocytes by putting the body into a state of low glucose and insulin. This reduced the inhibitors of fat breakdown, causing complete loss of body fat within days, even though the mice were still eating normally.
This pathway is so powerful that the scientists caution against using it in humans until it is better understood. Stable adipocytes occur in places like the bone marrow, in the hands and feet, and around important glands. In severe wasting disorders, loss of fat within these cells is associated with bone fractures and reduced quality of life. Scheller’s team hopes to prevent this loss and preserve health in patients with severe wasting disorders by defining the mechanisms of stable fat loss. Conversely, methods to activate fat loss from stubborn adipocytes may support future treatments for obesity. This work was funded by the National Institutes of Health (NIH).
The low oxygen levels at high altitude have long been known to be associated with lower diabetes rates. Photo by Mike Markov on Unsplash
Scientists have long known that people living at high altitudes, where oxygen levels are low, have lower rates of diabetes than people living closer to sea level. But the mechanism of this protection has remained a mystery.
Now, researchers at Gladstone Institutes have explained the roots of the phenomenon, discovering that red blood cells act as glucose sponges in low-oxygen conditions like those found on the world’s highest mountaintops.
In a new study in the journal Cell Metabolism, the team showed how red blood cells can shift their metabolism to soak up sugar from the bloodstream. At high altitude, this adaptation fuels the cells’ ability to more efficiently deliver oxygen to tissues throughout the body, but it also has the beneficial side effect of lowering blood sugar levels.
The findings solve a longstanding puzzle in physiology, says Gladstone Investigator Isha Jain, PhD, the senior author of the study.
“Red blood cells represent a hidden compartment of glucose metabolism that has not been appreciated until now,” says Jain, who is also a core investigator at Arc Institute and a professor of biochemistry at UC San Francisco. “This discovery could open up entirely new ways to think about controlling blood sugar.”
The Hidden Glucose Sink
Jain has spent years probing how low blood-oxygen levels, called hypoxia, affect health and metabolism. During a previous study, her team noticed that mice breathing low-oxygen air had dramatically lower blood glucose levels than normal. That meant the animals were quickly using up glucose after they ate—a hallmark of lower diabetes risk. But when the researchers used imaging to track where the glucose was going, major organs couldn’t account for it.
“When we gave sugar to the mice in hypoxia, it disappeared from their bloodstream almost instantly,” says Yolanda Martí-Mateos, PhD, a postdoctoral scholar in Jain’s lab and first author of the new study. “We looked at muscle, brain, liver—all the usual suspects—but nothing in these organs could explain what was happening.”
Using another imaging technique, the team revealed that red blood cells were the missing “glucose sink”—a term used to describe anything that pulls in and uses a lot of glucose from the bloodstream. The cells, having long been considered metabolically simple, seemed like unlikely candidates.
But further mouse experiments confirmed that red blood cells were indeed absorbing the glucose. In low-oxygen conditions, mice not only produced significantly more red blood cells, but each cell took up more glucose than red blood cells produced under normal oxygen.
To understand the molecular mechanisms of this observation, Jain’s team collaborated with Angelo D’Alessandro, PhD, of the University of Colorado Anschutz Medical Campus, and Allan Doctor, MD, from University of Maryland, who has long studied the function of red blood cells.
The researchers showed how, in low-oxygen conditions, glucose is used by red blood cells to produce a molecule that helps cells release oxygen to tissues—something that’s needed in excess when oxygen is scarce.
“What surprised me most was the magnitude of the effect,” D’Alessandro says. “Red blood cells are usually thought of as passive oxygen carriers. Yet, we found that they can account for a substantial fraction of whole-body glucose consumption, especially under hypoxia.”
A New Path to Diabetes Treatment
The scientists went on to show that the benefits of chronic hypoxia persisted for weeks to months after mice returned to normal oxygen levels.
They also tested HypoxyStat, a drug recently developed in Jain’s lab to mimic the effects of low-oxygen air. HypoxyStat is a pill that works by making hemoglobin in red blood cells grab onto oxygen more tightly, keeping it from reaching tissues. The drug completely reversed high blood sugar in mouse models of diabetes, working even better than existing medications.
“This is one of the first use of HypoxyStat beyond mitochondrial disease,” Jain says. “It opens the door to thinking about diabetes treatment in a fundamentally different way—by recruiting red blood cells as glucose sinks.”
The findings could extend beyond diabetes to exercise physiology or pathological hypoxia after traumatic injury, D’Alessandro notes, where trauma remains a leading cause of mortality in younger populations and shifts in red blood cell levels and metabolism may influence glucose availability and muscle performance.
“This is just the beginning,” Jain says. “There’s still so much to learn about how the whole body adapts to changes in oxygen, and how we could leverage these mechanisms to treat a range of conditions.”
A low-fat vegan diet that doesn’t limit calories or carbohydrates could help people with type 1 diabetes reduce insulin use and insulin costs, according to new research by the Physicians Committee for Responsible Medicine published in BMC Nutrition.
The new research, which is a secondary analysis of a 2024 Physicians Committee study, compared the effect of a low-fat vegan diet to a portion-controlled diet on insulin use and insulin costs in people with type 1 diabetes. The analysis found that the total dose of insulin decreased by 28%, or 12.1 units, per day in the vegan group, compared to no significant change in the portion-controlled group. The reductions in insulin use in the vegan group likely reflect improved insulin sensitivity, or how well the body responds to insulin. Total insulin costs decreased by 27%, or $1.08 per day, in the vegan group, compared to no significant change in the portion-controlled group.
The 2024 study found that a vegan diet also led to an average weight loss of 11 pounds, improved insulin sensitivity and glycaemic control, and improved cholesterol levels and kidney function in people with type 1 diabetes.
The new research comes as insulin prices in the United States continue to rise. Spending on insulin in the United States tripled in the past 10 years, reaching $22.3 billion in 2022, due to the increased usage and higher price of insulin, according to the American Diabetes Association. The inflation-adjusted cost of insulin increased by 24% from 2017 to 2022.
“As insulin prices continue to rise, people with type 1 diabetes should consider a low-fat vegan diet, which can help improve their insulin sensitivity and reduce the amount of insulin they need, potentially saving them hundreds of dollars a year,” says Hana Kahleova, MD, PhD, the lead author of the study and director of clinical research at the Physicians Committee for Responsible Medicine.
The results of a phase 3 clinical trial for enlicitide, a novel oral medication designed to lower cholesterol have been reported in a recent New England Journal of Medicine article. The study, involving nearly 3000 adults with existing or at high risk of cardiovascular disease, compared a daily 20mg dose against a placebo over one year.
Researchers found that the drug significantly reduced LDL cholesterol by approximately 57% within 24 weeks, alongside notable decreases in other harmful lipids. These improvements remained consistent and durable throughout the 52-week treatment period. Crucially, the safety profile of the oral inhibitor appeared comparable to the placebo, with no meaningful difference in side effects. The authors conclude that this convenient pill could offer a highly effective alternative to existing injectable therapies for managing heart disease risk.
By Dr Kashmal Kalan, Medical Director, Alvi Armani
In 2023, global prescriptions for GLP-1 weight loss medications rose by more than 40%, with drugs like Ozempic and Wegovy moving from specialist clinics into everyday conversation. Alongside this surge, a new concern is appearing more frequently in consultation rooms: unexpected hair loss.
For many patients, the timing is deeply unsettling. After months of discipline and visible progress, they start to notice more hair in the shower, on their pillow, or in their brush. The immediate fear is that something has gone wrong – that the medication is damaging their body, that the weight loss has come at a hidden cost, or something more serious.
In most cases, the reality is more nuanced. At Alvi Armani, we are seeing a consistent pattern: hair loss following rapid weight loss is real, but it is rarely caused by GLP-1 medications alone, despite how often this link is assumed. Instead, it reflects how the body responds to sudden physiological stress.
Hair loss often arrives late
The most common diagnosis in these cases is telogen effluvium, a form of temporary shedding that occurs when a large number of hair follicles shift prematurely into a resting phase. The critical detail is timing – the hair does not fall out immediately but rather sheds months after the original trigger.
This delay is what makes the experience so confusing. By the time hair begins to thin, weight loss may already feel stable, lifestyle changes established, and the initial stress long past. But biologically, the body is only now expressing the shock it absorbed earlier.
In some individuals, this shedding also unmasks an underlying genetic tendency toward pattern hair loss, known as androgenetic alopecia. While rapid weight loss does not create this condition, it can reveal it sooner than expected. What begins as temporary shedding may gradually shift into more persistent thinning – a progression that is emotionally difficult precisely because it feels so unexpected.
Why the body sacrifices hair first
Hair is not essential to survival. When the body experiences stress – whether through rapid fat loss, hormonal shifts, illness, or nutritional restriction – it reallocates resources to protect vital systems. Hair growth is one of the first processes to be downregulated.
Importantly, stress-related shedding does not create a new condition. It accelerates what was already encoded in the body. The hair is not “breaking down”; it is responding to a shift in internal priorities.
The speed of change is critical. Gradual, steady weight loss allows the body time to adapt hormonally and metabolically. Rapid loss, particularly when paired with appetite suppression, elevated stress hormones, or inadequate protein intake, creates a perfect storm for hair disruption.
From a biological perspective, shedding is not a malfunction, but rather an adaptive response. But from a patient’s perspective, it feels personal, visible, and deeply unsettling.
Who tends to notice it most
Women often become aware of thinning first, partly because longer hair makes shedding more obvious, and partly because changes in density carry greater emotional weight. Individuals with a family history of hair loss are also more vulnerable, as are those who lose a significant percentage of body weight in a short period of time.
Nutrition matters more than most realise
Hair is metabolically demanding tissue. It requires consistent access to protein, iron, zinc, and a range of micronutrients to maintain its growth cycle. When intake drops sharply because of appetite suppression, restrictive dieting, or poorly supervised medication use, hair becomes collateral damage.
This is why medically guided weight loss is so important. GLP-1 medications can be powerful tools, but they must be paired with nutritional planning. The body can tolerate change; what it struggles with is deprivation disguised as progress.
Temporary or permanent?
For many patients, telogen effluvium resolves within six to nine months once the body stabilises. Hair regrowth is slow, but it does occur.
However, in those with genetic susceptibility, the episode may mark the beginning of more sustained thinning. This does not mean damage has been done, but it does mean the window for early intervention matters. The earlier changes are recognised, the more options exist to slow or stabilise progression.
When hair loss deserves attention
Shedding should not be ignored if it persists beyond three to six months, if overall density continues to decline, or if there is a strong family history of pattern hair loss. Hair changes are often the first visible signal that the body is struggling to adapt to internal stress.
Early assessment allows for accurate diagnosis, realistic expectations, and far better long-term outcomes.
A final thought on balance
GLP-1 medications have transformed the weight loss landscape, and for many people, they offer genuine health benefits. But transformation should never come at the cost of physiological stability.
Hair is not separate from health. It is one of its most sensitive mirrors. Protecting the body protects the hair. Sustainable change, guided by medical support, remains the most reliable way to achieve results that last – without unexpected consequences.
The development of a self-regulating, implantable living technology that could offer hope for millions with diabetes and other chronic diseases
The crystal capsules developed by the researchers. They made the cover of Science Translational Medicine.
A pioneering study marks a major step toward eliminating the need for daily insulin injections for people with diabetes. The research introduces a living, cell-based implant that can function as an autonomous artificial pancreas, essentially a living drug that is long-term, thanks to a novel crystalline shield technology.
Once implanted, the system operates entirely on its own: it continuously senses blood-glucose levels, produces insulin within the implant itself, and releases the exact amount needed – precisely when it is needed. In effect, the implant becomes a self-regulating, drug-manufacturing organ inside the body, requiring no external pumps, injections, or patient intervention.
One of the study’s most significant breakthroughs addresses the longstanding challenge of immune rejection, which has limited the success of cell-based therapies for decades. The researchers developed engineered therapeutic crystals that shield the implant from the immune system, preventing it from being recognised as a foreign object. This protective strategy enables the implant to function reliably and continuously for several years.
The technology has already been successfully tested in a mouse model for effective and long-term regulation of glucose levels and in non-human primates for cell viability and functionality. These results represent a critical milestone and strongly support the potential for future translation to human patients.
From Postdoctoral Insight to Global Collaboration
The study was led by Assistant Professor Shady Farah of the Faculty of Chemical Engineering at the Technion – Israel Institute of Technology, in co-correspondence with MIT, and in collaboration with Harvard University, Johns Hopkins University, and the University of Massachusetts. Asst Prof Farah began developing the concept with colleagues in 2018 during his postdoctoral fellowship at MIT and Boston Children’s Hospital/Harvard Medical School, under the supervision of Prof Daniel Anderson and Prof Robert (Bob) Langer, a world leader in tissue engineering and co-founder of Moderna.
Today, the research continues in Asst Prof Farah’s laboratory at the Technion, in close collaboration with leading US institutions, including MIT, Harvard, the University of Massachusetts, Boston Children’s Hospital, and the Johns Hopkins University School of Medicine.
A Platform with Far-Reaching Potential
While the immediate focus is diabetes, the researchers emphasise that this implantable, closed-loop platform could be adapted to treat a wide range of chronic conditions requiring continuous delivery of biological therapeutics – including haemophilia and other metabolic or genetic diseases.
If successfully translated to the clinic, this technology could redefine how chronic diseases are treated, shifting from repeated drug administration to living, self-regulating therapies that work seamlessly from within.
A University of Exeter-led study has quantified the role of obesity in common long-term conditions, showing for the first time the effect of losing weight in preventing multiple diseases.
Conditions that often occur together may share an underlying cause, which can be key to prevention or treatment. The picture of which conditions co-occur is complex, so researchers paired them together, to allow them to identify shared causes more simply. The study found that obesity is the main shared cause between ten pairs of commonly occurring conditions.
The research specifically measured how much weight reduction would reduce the risk of the next diagnosis. In the largest study of its kind, published in Communications Medicine – Nature, the team studied 71 conditions which often occur together, such as type 2 diabetes and osteoarthritis, or kidney disease and chronic obstructive pulmonary disease (COPD).
The GEMINI study, funded by the UKRI Medical Research Council and supported by the National Institute for Health and Care Research (NIHR), used genetics and healthcare data drawn from a number of large datasets internationally. They found that obesity was part of the cause for 61 of the 71 conditions. They also found that obesity explained all of the genetic overlap in ten pairs of conditions, suggesting it is the main driver for why they frequently occur together.
Body mass index, or BMI, is a scaled measure of weight – a number over 30 units indicates obesity, while less than 25 indicates “normal” weight. The study quantified how much a reduction in BMI would reduce the risk of both conditions at a population level for people overweight or living with obesity. For example, for every thousand people who have both chronic kidney disease and osteoarthritis, a BMI reduction of 4.5 units would have prevented 17 of them developing both conditions or nine people per thousand with type 2 diabetes and osteoarthritis.
The team also established the pairs of conditions where obesity is not the main cause and are now investigating other mechanisms.
Study lead Professor Jack Bowden, at the University of Exeter Medical School: “We’ve long known that certain diseases often occur together, and also that obesity increases the risk of many diseases. This largescale study is the first to use genetics to quantify the role of obesity in causing diseases to occur in the same individuals. We found that for some disease pairings, obesity is the major driving force. Our research provides much more detail about the links between obesity and disease, which will help clinicians target specific advice to patients going forward.”
Study author Professor Jane Masoli, of the University of Exeter Medical School, who is a Consultant Geriatrician and regional NIHR Ageing lead, said: “Currently nine million people in the UK live with two or more long-term conditions. Understanding how to prevent diseases accumulating is a key national research and healthcare priority. This study further strengthens the case to tackle obesity through public health programmes, reinforcing the importance of lifelong obesity management in the NHS strategy on prevention. Our work shows that this could reduce the risk of accumulating multiple health conditions, supporting people to live longer, healthier lives.”
This research represents another important publication from the GEMINI (Genetic Evaluation of Multimorbidity towards INdividualisation of Interventions) collaborative. Led by the University of Exeter, GEMINI includes people with multimorbidity, health care professionals including those in primary care and experts in statistics and genetics, and was one of six programmes funded by the UKRI strategic priorities fund, an £830 million investment in multimorbidity research.
The GEMINI team are working to further understand why some conditions more frequently co-occur in the same patients. The team are quantifying the role of other, known modifiable risk factors beyond obesity, and are finding novel genes and pathways that could point to new ways to intervene and improve health. GEMINI data, results, and code are free to download (https://github.com/GEMINI-multimorbidity), and the pairwise genetic and observational correlations can be viewed interactively (https://gemini-multimorbidity.shinyapps.io/atlas/).
The longer a person has type 2 diabetes, the greater the risk of cardiovascular disease. A new study from Karolinska Institutet, published in the journal Diabetes, shows that changes in red blood cells may be an important explanation, and identifies a specific molecule as a possible biomarker.
People with type 2 diabetes are at increased risk of heart attack and stroke, and the risk increases the longer they have lived with the disease. Previous research has shown that red blood cells can affect blood vessel function in diabetes. Now, a new study shows that the duration of the disease plays a decisive role in when and how these changes occur – and that long-term type 2 diabetes can make red blood cells directly harmful to blood vessels.
The researchers studied both animals and patients with type 2 diabetes. Red blood cells from mice with long-term diabetes and patients who had had the disease for over seven years had a harmful effect on blood vessel function. No such effect was seen in newly diagnosed individuals, but after seven years of follow-up, their blood cells had developed the same harmful properties. When the researchers restored the levels of microRNA-210 in the red blood cells, vascular function improved.
“What really stands out in our study is that it is not only the presence of type 2 diabetes that matters, but how long you have had the disease. It is only after several years that red blood cells develop a harmful effect on blood vessels,” says Zhichao Zhou, associate professor at the Department of Medicine, Solna, Karolinska Institutet, and lead author of the study.
The study points to microRNA-210 in red blood cells as a possible biomarker for early detection of the risk of cardiovascular complications. Researchers are now working to investigate whether this can be used in larger population studies.
“If we can identify which patients are at greatest risk before vascular damage has already occurred, we can also become better at preventing complications,” says Eftychia Kontidou, doctoral student from the same group and the first author of the study.
Thousands of families have taken part in a landmark UK study led by researchers at the University of Birmingham which shows that childhood screening for type 1 diabetes is effective, laying the groundwork for a UK-wide childhood screening programme.
Results from the first phase of the ELSA (Early Surveillance for Autoimmune diabetes) study, co-funded by charities Diabetes UK and Breakthrough T1D, have been published in a research letter in The Lancet Diabetes & Endocrinology today.
The findings mark a major step towards a future in which type 1 diabetes can be detected in children before symptoms appear. Currently, over a quarter of children aren’t diagnosed with type 1 diabetes until they are in diabetic ketoacidosis (DKA), a potentially fatal condition that requires urgent hospital treatment. Early detection can dramatically reduce emergency diagnoses and could give children access to new immunotherapy treatments that can delay the need for insulin for years.
We are working towards a future where type 1 diabetes can be detected in a timely manner
Professor Parth Narendran, lead researcher
Launched in 2022, ELSA is the first UK study of its kind, tested blood samples from 17,931 children aged 3-13 for autoantibodies, markers of type 1 diabetes that can appear years before symptoms.
Children without autoantibodies are unlikely to develop type 1 diabetes, while those with one autoantibody have a 15% chance of developing the condition within 10 years. Having two or more autoantibodies indicates the immune system has already started attacking the insulin-producing cells in the pancreas and it is almost certain these children will eventually need insulin therapy. This is known as early-stage type 1 diabetes.
Among the 17,283 children aged 3-13 years who were screened for type 1 diabetes risk at the time of analysis:
75 had one autoantibody, signaling increased future risk.
160 had two or more autoantibodies but did not yet require insulin therapy, indicating early-stage type 1 diabetes.
7 were found to have undiagnosed type 1 diabetes with all needing to start insulin immediately.
Lead researcher, Parth Narendran, Professor of Diabetes Medicine at the University of Birmingham, said: “We are extremely grateful to all the families who have participated in the study and generously given their time to help understand how a UK-wide screening programme could be developed. Together with Diabetes UK, Breakthrough T1D and the National Institute for Health and Care Research, we are working towards a future where type 1 diabetes can be detected in a timely manner, and families appropriately supported and treated with medicines to delay the need for insulin.
“We are also grateful to partners across the Birmingham Health and Life Sciences District and beyond as well as the NIHR for the support they have provided in getting us to where we are.”
Interventions before diagnosis
Families of children found to have early-stage type 1 diabetes received tailored education and ongoing support to prepare for the eventual onset of type 1 diabetes symptoms and to ensure insulin therapy can begin promptly when needed, reducing the chances of needing emergency treatment. Those with one autoantibody also received ongoing support and monitoring.
Some families were also offered teplizumab, the first ever immunotherapy for type 1 diabetes, which can delay the need for insulin by around three years in people with early-stage type 1 diabetes. The first patient was treated at Birmingham Children’s Hospital. Teplizumab was licensed by the Medicines and Healthcare products Regulatory Agency (MHRA) in the UK in August 2025, and is currently being assessed by the National Institute for Health and Care Excellence (NICE) to determine whether it should be available through the NHS.
As of November 2025, more than 37,000 families have signed up to the ELSA programme. Building on this strong foundation, the second phase of the research, ELSA 2, launches today. ELSA 2 will expand screening to all children in the UK aged 2-17 years, with a focus on younger children (2-3 years) and older teenagers (14-17 years). The research team aims to recruit 30,000 additional children across these new age groups.
ELSA 2 will also establish new NHS Early-Stage Type 1 Diabetes Clinics, providing families taking part with clinical and psychological support and creating a clear pathway from screening to diagnosis, monitoring and treatment.
Case study: Knowing what’s coming … has made an enormous difference
Amy Norman, 44, from the West Midlands, was diagnosed with type 1 diabetes at the age of 13. She recently discovered via the ELSA study that her 11-year-old daughter, Imogen, is in the early stages of type 1 diabetes but has been able to slow its progression as the second child in the UK to access a breakthrough immunotherapy drug – teplizumab. She said: “Being part of the ELSA study has helped us as a family to prepare for the future in a way we never expected. Knowing what’s coming – rather than being taken by surprise – has made an enormous difference to our confidence and peace of mind.
“When I was diagnosed, I had no warning and ended up quite poorly in hospital with diabetic ketoacidosis (DKA). When Imogen’s diagnosis arrives, we hope that having this awareness will reduce her chances of experiencing DKA and the added trauma that comes from a sudden illness.
“Imogen took part in the study to further research and help others, but it has helped her too – being forewarned is being forearmed. She was always going to develop type 1 diabetes, but through ELSA we’ve been able to slow down the process and prepare – we know what is coming, but we’re not scared.”
A game-changer: showing what we can achieve in Birmingham
Professor Neil Hanley, Pro-Vice-Chancellor and Head of the College of Medicine and Health at the University of Birmingham, said, “This is a game-changer. This trial shows we can spare countless children the trauma of an emergency diagnosis, ensure they get early support, and potentially give them access to revolutionary new treatments that could delay or even prevent type 1 diabetes.
“Dr Parth Narendran and his team deserve huge credit; and this breakthrough shows what we can achieve in Birmingham. We have world-class clinicians and scientists working side-by-side, backed by great innovation infrastructure and a vibrant, diverse and affordable city – and, as a result, we are changing lives with next generation diagnostics, therapeutics, and clinical care.”
Rewriting the story of type 1 diabetes
Dr Elizabeth Robertson, Director of Research and Clinical at Diabetes UK, said: “For too many families, a child’s type 1 diabetes diagnosis still comes as a frightening emergency. But that doesn’t have to be the case. Thanks to scientific breakthroughs, we now have the tools to identify children in the very earliest stages of type 1 diabetes – giving families precious time to prepare, avoid emergency hospital admissions, and access treatments that can delay the need for insulin for years.
“The ELSA study, co-funded by Diabetes UK, is generating the evidence needed to make type 1 diabetes screening a reality for every family in the UK. We’re incredibly grateful to the 37,000 families who’ve already signed up and urge others to get involved. Together, we can transform type 1 diabetes care for future generations.”
Rachel Connor, Director of Research Partnerships at Breakthrough T1D, said: “This is about rewriting the story of type 1 diabetes for thousands of families. Instead of a devastating emergency, we can offer time, choices, and hope. By finding children in the earliest stages, we’re not just preparing families, we’re opening the door to treatments that can delay the need for insulin by years. That extra time means childhoods with fewer injections, fewer hospital visits and more normality. Thanks to research like ELSA, what once struck as an unexpected crisis can become an actively managed healthcare process, changing the course of T1D for the better.”
The findings from ELSA’s first phase signal a major step towards a future in which type 1 diabetes can be detected early, managed proactively, and potentially delayed through immunotherapy. ELSA demonstrates that childhood screening in the UK is feasible, acceptable to families, and capable of preventing emergency diagnoses. Continued research through ELSA 2 will assess how screening can be scaled across the NHS and evaluate its cost-effectiveness.
