Life-saving stem cell centre welcomes first donors

7 minutes agoShareSaveRob Sissons, East Midlands health correspondentShareSaveBBCThe UK’s first stem cell collection centre strictly dedicated to transplants has started welcoming donors.The Anthony Nolan Cell Collection Centre, based at Nottingham’s Queen’s Medical Centre (QMC), will help more people across the UK donate potentially life-saving cells to patients with blood cancers and disorders.The Anthony Nolan charity said the centre would create 1,300 new donation slots a year, helping to tackle a “longstanding global shortage of cell collection facilities”.Jordan, from London, said he was “proud” to be one of the first to donate. “I am really happy because today I could save someone’s life,” he added.The centre will be run by the Anthony Nolan charity, in partnership with the National Institute for Health and Care Research (NIHR) Nottingham Clinical Research Facility.Jordan was called by the charity to donate stem cells after analysis of a saliva sample he gave nine years ago, when he signed up to the stem cell register at a freshers’ fair at the University of Exeter, proved to be a good match to a stranger.”It is such an easy thing to do to help someone else,” he said. “I’m not the biggest fan of needles, but I’m happy to do anything if it helps another person.”‘Special’ feelingAnthony Nolan has more than 900,000 people on its own register of potential donors.It said a “longstanding global shortage of cell collection facilities” meant some patients did not receive a transplant at the best time.Growing demand for cell-based treatments has put donation facilities at some NHS and private hospitals under more pressure than ever, it added.According to its own data, in 2022-23, only a fifth of donors on the UK registry were able to donate on the date requested by the patient’s medical team due to capacity issues.Not having a transplant at the right time can have an irreversible impact on a patient’s mental and physical health, said Anthony Nolan, and sometimes leave them in a life-threatening condition. The charity said the chance of being matched from its UK-wide register was one in 800, in the first five years of being on the register.Jordan said it felt “special” to help a stranger, for whom a stem cell transplant might be their only hope of staying alive.”I like to think if something were to happen to me, then someone would be willing to do the same,” he added.What is a stem cell transplant? A stem cell or bone marrow transplant is a life-saving treatment for thousands of patients with blood cancers and disorders. It replaces damaged blood cells with healthy ones. Stem cells are special cells produced by bone marrow, a spongy tissue found in the centre of some bones, that can turn into different types of blood cells.Donation is simple, Nicola Alderson – chief operating officer at Anthony Nolan – said.”You are put on to a machine that has a needle in both arms,” she said. “The blood goes through the machine which takes out the stem cells and puts the rest of the blood back through.” The process usually takes about five hours. Once the cells are collected from the bloodstream, they are typically transplanted into the recipient within 72 hours.Anthony Nolan said any contact between a donor and patient depended on privacy regulations of the patient’s country, and was led by the patient.UK rules allow direct contact from two years since the last transplant, although some overseas registries may not allow contact until five years post-donation.Anthony Nolan co-ordinates transplants for the NHS, collecting and delivering cells to hospitals across the UK and sending cells abroad. It is involved in more than 1,000 UK transplants between donors and unrelated recipients each year and sends cells abroad to another 300 patients. Ms Alderson said prior to the new centre, the charity had struggled to get stem cells collected “at the time the clinical community need us to”.”It is only one in five times where we have been able to get collections to donors on the day doctors have asked for them,” she added.She said when recipients saw a bag of stem cells, “it is an incredible moment”.”Ultimately, that small bag can save someone’s life. It is a bag of magic,” she added.”We will make sure [donors] have the best experience at our new centre.”The centre has been part-funded by Omaze, which partnered with Anthony Nolan and raised £3.7m through a house prize draw in June.It is estimated the money will help fund the centre’s work for 18 months.Kathryn Fairbrother, director of clinical operations for research and innovation at Nottingham University Hospitals (NUH) NHS Trust – which runs the QMC – added: “There are opportunities for Anthony Nolan and for ourselves to do research that we wouldn’t have done before.”One of the research projects planned involves using stem cells to treat liver disease.Stem cell transplant recipients, like Raj, will benefit from the new centre.The 32-year-old, a University of Liverpool student, received a stem cell transplant in Leicester in 2020 after being diagnosed with a rare blood cancer called myelofibrosis. His cells came from an anonymous donor in Germany.”I sent him an anonymous thank you letter but I haven’t tried to get in direct contact yet. I’d like to,” Raj said.”It took me about a year and a half to two years to recover. It took quite a long time, and I was off sick from work for about a year.”Raj added: “The Nottingham development is a brilliant set-up. “Being able to be more efficient collecting and delivering stem cells to patients who don’t have time to wait is fantastic.”Raj would like to see more people sign up to become potential donors at Anthony Nolan.They need to be aged 16 to 30 years old to register, and can stay on as a potential donor until the age of 61. Potential donors send off a cheek swab sample and wait to see if they are a match for anyone. “We need more. It is the ultimate act of kindness,” Raj added.SuppliedMore on this story Related internet links

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Samaritans facing volunteer exodus over proposed branch closures

9 minutes agoShareSaveMichael BuchananSocial affairs correspondentShareSaveSamaritansHundreds of Samaritans volunteers say they will leave the suicide prevention charity if plans to close more than 100 branches are supported at a meeting this weekend.Some opponents of the changes fear an exodus of staff could put the charity’s ability to answer calls in doubt.The controversial plans, unveiled in July, would see at least half the Samaritans branches in the UK and Ireland close.Volunteers would instead work out of larger offices or answer calls from home as the charity moves to embrace a remote working model.In a statement, the Samaritans said its proposals would mean “we can answer more calls, cut wait times and make it easier for people to volunteer with us”.Growing oppositionIf passed, the first branches would begin to close in April in the UK and 2027 in Ireland, with a gradual reduction over the coming decade.Critics of the plans say the changes will decimate the Samaritans’ work in local communities and have accused the charity’s leadership of repeatedly ignoring requests to provide the rationale for the plans.Some branches have called for a vote of no confidence in the chairman at a meeting next month.More than 50 branches, over a quarter of the total, immediately raised concerns when the plans were unveiled and it seems that opposition has only grown.The list of branches that would close has not been released, but James Watkins fears his one in Rhyl, Denbighshire, would go.It’s situated in the heart of the town, in one of the most deprived neighbourhoods in Britain, with high levels of mental health problems.Mr Watkins, 58, says that volunteers are drawn to helping their own community as much as staffing the charity’s nationwide phone line.The branch’s volunteers, he said, had recently been out at a local college and at the train station raising awareness of their presence.”All of those things emanate from the fact we have a local branch and would likely go if we closed. Our branch has been going for over 50 years and our connections with our community has grown and grown,” said Mr Watkins.He’s one of between 40 and 50 volunteers in Rhyl, but after speaking to colleagues said he was not aware that any of them would remain if the branch closed.Last month, Mr Watkins organised a survey of volunteers across Wales. He says he received a response from 210 people, about one third of all Welsh volunteers.Three quarters of people who responded said they would not move if their own branch was closed. The same proportion said they would not be interested in remote volunteering.”With less people, [the Samaritans] are not going to be able to answer as many calls. This is the point we keep making and it seems to be falling on deaf ears. This could be the beginning of the end for the Samaritans.”‘Airy fairy’ recruitment plansThe charity’s leadership have called its proposals “future-proofing” and said that having more than 200 branches “is not sustainable and hinders us” from providing the best service.The Samaritans considers itself the fourth emergency service and estimates that it answers a call every 10 seconds. Despite the controversy, the charity insists it will continue to be there “for those struggling to cope across the UK and Ireland, day and night, 365 days a year”.The proposals, say the charity, are intended to increase the number of volunteers, including by introducing remote working.”That’s a red herring,” said Mark Watkins, a volunteer on the Isle of Wight for the past 17 years.He points out that remote working has not been properly piloted, and describes as “airy fairy” plans to source more volunteers. He doesn’t believe that any of his branch’s 65 volunteers would remain if the Isle of Wight branch were to close.”If you’re alone in your house at 03:00 and you are taking a call that we would characterise as suicide in progress, you have no shift buddy there to support you – that has never happened in the 70 years of the Samaritans. Callers have a right to be concerned,” said Mark Watkins.The Samaritans say that remote volunteering is currently being piloted and if it is approved, it would only be an option alongside working in a branch.Colm MartinWhile the plans have been open to consultation, branch directors and volunteers from the north of Scotland to the south of England have told the BBC that they’ve not been listened to.”There is a lot of despair and disillusionment,” said Colm Martin, who has been volunteering at London’s Kingston branch for five years.”There has been no listening which is ironic for a charity that’s all about listening.”Mr Martin has been a vocal critic of the proposals and says there is distrust of initiatives from Samaritans’ management after an app had to be closed down and a new internal email system had proven hugely problematic.”They have provided no evidence for these changes [to branches]. They have a ready-made focus group [thousands of volunteers] – they could have asked us what we think.”Such is the anger that a letter signed by seven branch directors has been sent to the trustees of the Samaritans calling for the chairman Keith Leslie to be removed at a meeting in late October.”We do not feel these concerns are being fully heard, and we fear that implementation of the current in-principle decisions could seriously harm and diminish the organisation,” they write.Almost 150 branches are independent organisations, responsible for all their fundraising locally and receiving little, if any, financial support from the charity’s headquarters.Some have been gifted offices free of charge by local organisations, but if those branches were to close, the charity’s headquarters would benefit from any sale of the premises, adding another layer of unhappiness for many volunteers.”We have been listening to feedback from our 23,000 volunteers throughout this process and this will be considered carefully in the final decision making,” said the charity’s chief executive in a statement. “Samaritans’ life-saving work is needed now more than ever but I’m confident that by everyone pulling together for our beneficiaries and callers, our service will be stronger and better prepared than ever before to meet the challenges of the future.”If you are suffering distress or despair, details of help and support in the UK are available at BBC’s Action Line.

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This high-sugar fruit may actually lower diabetes risk

If presented with two snacks, one containing seven grams of sugar and another with over 30 grams of sugar, choosing the healthier option should be a no-brainer, correct? Well, maybe not. Less sugar is not automatically healthier.
For the nearly 100 million adults in the United States who are currently living with prediabetes, a tropical fruit that can reduce the risk of diabetes sounds too good to be true. Tropical fruits contain anywhere between ten to 50 grams of sugar, with mangos on the high end of the spectrum, making them seem a poor snack choice based on that alone. But research by clinical nutrition researcher Raedeh Basiri indicates that mangos, despite having more sugar than many low-sugar snacks, may offer protective factors for adults with prediabetes.
“It is not just the sugar content that matters, but the overall food context that matters,” said Basiri, assistant professor in George Mason’s Department of Nutrition and Food Studies. This study is the first long-term clinical trial to demonstrate both metabolic and body composition benefits of mangoes in prediabetes.
Simply put, it’s more than the sugar in the food; it’s about the whole food. The sugars naturally found in mangos, and other fruits, are complemented by fiber and other vitamins and nutrients that offer additional health benefits. Food with added sugar, such as breakfast cereals, and even low-sugar snack options, may not have the same nutritional value and can even increase diabetes risk.
“The goal is to encourage people to include whole fruits, like mango, as part of healthy eating behaviors and practical dietary strategies for diabetes prevention,” said Basiri. “Individuals at high risk of diabetes should not only focus on the sugar content of foods, but on how sugars are delivered.”
Basiri and her team split study participants into two groups; one group received a fresh mango daily, while the other group was given a low-sugar granola bar each day. Over six months, researchers measured participants’ blood glucose levels, bodily responses to insulin, and body fat.
At the conclusion of the study, findings revealed that the high-sugar mango (32 grams of sugar) proved more beneficial than a low-sugar granola bar (11 grams of sugar). The group that consumed the daily mango showed improved blood glucose control, enhanced insulin sensitivity, and reduced body fat.

“Daily Mango Intake Improves Glycemic and Body Composition Outcomes in Adults with Prediabetes: A Randomized Controlled Study” was published in Foods in August 2025.
This study was funded by the National Mango Board. The authors declare no other potential conflicts of interest. The funders had no role in the design of the study, in the collection, analysis, interpretation of data, or the decision to publish results.
About the researcher
Raedeh Basiri is a registered dietitian and an assistant professor in the Department of Nutrition and Food Studies at George Mason’s College of Public Health. Basiri is a clinical nutrition researcher specializing in personalized nutrition therapy and the use of emerging technologies, such as continuous glucose monitoring, to improve outcomes in individuals with prediabetes, diabetes, and metabolic syndrome. Her work combines randomized controlled trials and large-scale data analysis to investigate how whole foods and dietary patterns impact insulin resistance, glycemic control, sleep, and both mental and gut health. Basiri takes a rigorous, interdisciplinary approach and is deeply committed to chronic disease prevention, collaborative research, and mentoring future professionals.

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Hidden bacterial molecules in the brain reveal new secrets of sleep

What causes us to sleep? The answer may lie not only in our brains, but in their complex interplay with the micro-organisms spawned in our intestines.
New research from Washington State University suggests a new paradigm in understanding sleep, demonstrating that a substance in the mesh-like walls of bacteria, known as peptidoglycan, is naturally present in the brains of mice and closely aligned with the sleep cycle.
Those findings serve to update a broader hypothesis that has been in development at WSU for years — proposing that sleep arises from communication between the body’s sleep regulatory systems and the multitude of microbes living inside us.
“This added a new dimension to what we already know,” said Erika English, a PhD candidate at WSU and lead author on two recently published scientific papers introducing the findings.
This view of sleep as arising from that “holobiont condition” joins a growing body of evidence suggesting that our gut microbiomes play an important role in cognition, appetite, sex drive and other activity — a view that turns traditional brain-centric models of cognition upside-down and has implications for our understanding of evolution and free will, as well as the development of future treatments for sleep disorders.
The recent findings regarding peptidoglycan, or PG, lend weight to that hypothesis and point to a possible regulatory role for bacterial cell wall products in sleep. PG is known to promote sleep when injected in animals, but until recently, the conventional view held that it did not naturally migrate to the brain.
English found that PG, along with its receptor molecules involved in PG signaling and communication, was present in different locations within the brain, at levels that changed with the time of day and sleep deprivation.

The findings were reported in July in Frontiers in Neuroscience; longtime WSU sleep researcher and Regents Professor James Krueger co-authored the paper. English is also lead author of a recent paper with Krueger in the journal Sleep Medicine Reviews that proposes the “holobiont condition” hypothesis of sleep.
That paper combines two prevailing views. One posits that sleep is regulated by the brain and neurological systems. Another focuses on “local sleep,” which frames slumber as the result of an accumulation of sleep-like states among small cellular networks throughout the body. Such sleep-like states have been observed among cells in vitro, known as the “sleep in a dish” model.
As these smaller pockets of sleep accumulate, like lights going off in a house, the body tips from wakefulness toward sleep.
The new hypothesis merges those theories, proposing that sleep results from the interplay between the body and its resident micro-organisms — two autonomous systems that interact and overlap.
“It’s not one or the other, it’s both. They have to work together,” English said. “Sleep really is a process. It happens at many different speeds for different levels of cellular and tissue organization and it comes about because of extensive coordination.”
Links between the microbiome and behavior are emerging on several fronts, indicating that micro-organisms formed in the gut play an important role in cognition and fundamental human behaviors. This work upends the traditional view of human neurology, suggesting that it is not completely top-down — i.e., the result of decision-making in the brain — but bottom-up — i.e., driven by the tiny organisms whose evolution shaped animals to serve as their hosts and whose needs influence the activities and cognition of their hosts.

“We have a whole community of microbes living within us. Those microbes have a much longer evolutionary history than any mammal, bird or insect – much longer, billions of years longer,” said Krueger, who was named a “Living Legend in Sleep Research” by the Sleep Research Society in 2023. “We think sleep evolution began eons ago with the activity/inactivity cycle of bacteria, and the molecules that were driving that are related to the ones driving cognition today.”
English’s work expands upon known links between bacteria and sleep, including the fact that sleep patterns affect the function of the gut microbiome and that bacterial infections cause people to sleep more.
The new findings begin to delve into questions that English looks forward to exploring further.
“Now that the world has come to appreciate how important microbes are, not just for disease but also for health, it’s a very exciting time to start to expand on our understanding of how we are communicating with our microbes and how our microbes are communicating with us,” she said.

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Brain fat, not just plaques, may be the hidden driver of Alzheimer’s

It was long thought that fat in the brain played no role in neurodegenerative diseases, but Purdue University researchers are challenging that assumption.
The research findings, published in Immunity, show that excess fat in the brain’s resident immune cells, called microglia, impairs their ability to combat disease. This insight opens a path to lipid biology-based neuroimmune therapies that could treat diseases like Alzheimer’s by enhancing microglial function and neuronal health. This work was led by Gaurav Chopra, the James Tarpo Jr. and Margaret Tarpo Professor of Chemistry and (by courtesy) of Computer Science at Purdue.
While most Alzheimer’s drug development targets the primary pathologies of the disease — plaques of a misfolded protein called amyloid beta and tangles of the protein tau — Chopra is focused on the abnormally fat-rich cells surrounding diseased regions of the brain. In earlier work published in Nature, Chopra and collaborators showed that, in the presence of disease, astrocytes — another type of cells that support neurons — release a fatty acid that is toxic to brain cells. Another collaborative work with the University of Pennsylvania, published last year in Nature, also linked mitochondrial dysfunction in neurons with fat deposits in glial cells during aging — a major risk factor for neurodegeneration.
“In our view, directly targeting plaques or tangles will not solve the problem; we need to restore function of immune cells in the brain,” Chopra said. “We’re finding that reducing accumulation of fat in the diseased brain is the key, as accumulated fat makes it harder for the immune system to do its job and maintain balance. By targeting these pathways, we can restore the ability of immune cells like microglia to fight disease and keep the brain in balance, which is what they’re meant to do.”
Chopra’s team worked in collaboration with researchers at Cleveland Clinic led by Dimitrios Davalos, assistant professor of molecular medicine. Chopra is also the director of Merck-Purdue Center and a member of the Purdue Institute for Integrative Neuroscience; the Purdue Institute for Drug Discovery; the Purdue Institute of Inflammation, Immunology and Infectious Disease; and the Regenstrief Center for Healthcare Engineering.
Chopra’s work is part of Purdue’s presidential One Health initiative, which brings together research on human, animal and plant health. His research supports the initiative’s focus on advanced chemistry, where Purdue faculty study complex chemical systems and develop new techniques and applications.
More than 100 years ago, Alois Alzheimer identified abnormalities in the brain of a woman with the disease that now bears his name, including plaques, tangles and cells filled with droplets of fatty compounds called lipids. Until recently, these lipid droplets were dismissed as by-products of disease.

But the links that Chopra and his team have found between neurodegenerative disease and fats in microglia and astrocytes — both types of glial cells that support neurons in the brain — strongly suggest otherwise. Chopra says this research lays the foundation for a “new lipid model of neurodegeneration.” He likes to call these fat accumulations “lipid plaques,” as they don’t resemble spherical droplets.
“It is not the lipid droplets that are pathogenic, but the accumulation of these droplets is bad. We think the composition of lipid molecules that accumulate within brain cells is one of the major drivers of neuroinflammation, leading to different pathologies, such as aging, Alzheimer’s disease and other conditions related to inflammatory insults in the brain. The specific composition of these lipid plaques may define particular brain diseases,” Chopra said.
The Immunity paper focuses on microglia, the “bona fide immune cells of the brain,” which clear out debris, such as misfolded proteins like amyloid beta and tau, by absorbing and breaking them down through a process called phagocytosis. Chopra’s team examined microglia in the presence of amyloid beta and asked a simple question: What happens to microglia when they come into contact with amyloid beta?
Images of brain tissue from people with Alzheimer’s disease showed amyloid beta plaques surrounded by microglia. Microglia located within 10 micrometers of these plaques contained twice as many lipid droplets as those farther away. These lipid droplet-laden microglia closest to the plaques cleared 40% less amyloid beta than ordinary microglia from brains without disease.
In their investigation into why microglia were impaired in Alzheimer’s brains, the team used specialized techniques and found that microglia in contact with plaques and disease-related inflammation produced an excess of free fatty acids. While microglia normally use free fatty acids as an energy source — and some production of these fatty acids is even beneficial — Chopra and his team discovered the microglia closest to amyloid beta plaques convert these free fatty acids to triacylglycerol, a stored form of fat, in such large quantities that they become overloaded and immobilized by their own accumulation. The formation of these lipid droplets depends on age and disease progression, becoming more prominent as Alzheimer’s disease advances.
By tracing the complex series of steps microglia use to convert free fatty acids to triacylglycerol, the research team zeroed in on the final step of this pathway. They found abnormally high levels of an enzyme called DGAT2 catalyzes the final step of converting free fatty acids to triacylglycerol. They expected to see equally high levels of the DGAT2 gene — since the gene must be copied to produce the protein — but that was not the case. The enzyme accumulates because it is not degrading as quickly as it normally would, rather than being overproduced. This accumulation of DGAT2 causes microglia to divert fatty acids into long-term storage and fat accumulation instead of using them for energy or repair.

“We showed that amyloid beta is directly responsible for the fat that forms inside microglia,” Chopra said. “Because of these fatty deposits, microglial cells become dysfunctional — they stop clearing amyloid beta and stop doing their job.”
Chopra said the researchers don’t yet know what causes the DGAT2 enzyme to persist. However, in their search for a remedy, the team tested two molecules: one that inhibits DGAT2’s function and another that promotes its degradation. The degradation of the DGAT2 enzyme was ultimately beneficial to reduce fat in the brains, improve function of microglia and their ability to eat amyloid-beta plaques, and improve markers of neuronal health in Alzheimer’s disease animal models.
“What we’ve seen is that when we target the fat-making enzyme and either remove or degrade it, we restore the microglia’s ability to fight disease and maintain balance in the brain — which is what they’re meant to do,” Chopra said.
“This is an exciting finding that reveals how a toxic protein plaque directly influences how lipids are formed and metabolized by microglial cells in Alzheimer’s brains,” said Priya Prakash, a first co-author of the study. “While most recent work in this area has focused on the genetic basis of the disease, our research paves the way for understanding how lipids and their pathways within the brain’s immune cells can be targeted to restore their function and combat the disease.”
“It’s incredibly exciting to connect fat metabolism to immune dysfunction in Alzheimer’s,” said Palak Manchanda, the other first co-author. “By pinpointing this lipid burden and the DGAT2 switch that drives it, we reveal a completely new therapeutic angle: Restore microglial metabolism and you may restore the brain’s own defense against disease.”
At Purdue, Chopra was joined in the research by Prakash, Manchanda, Kanchan Bisht, Kaushik Sharma, Prageeth R. Wijewardhane, Caitlin Randolph, Matthew Clark, Jonathan Fine, Elizabeth Thayer and Chi Zhang. Their research was produced with support from the U.S. Department of Defense and the National Institutes of Health.

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Scientists reveal pill that helps shed 20% of body weight

New research presented at the Annual Meeting of the European Association for the Study of Diabetes in Vienna, Austria (Sept 15-19) and simultaneously published in NEJM shows that daily treatment with the new once-daily GLP-1 agonist orforglipron results in substantial weight loss in people living with obesity that do not have type 2 diabetes. The study is by Dr Sean Wharton, McMaster University, Hamilton, ON, Canada and Wharton Weight Management Clinic, Burlington, ON, Canada, and colleagues. The study is sponsored by Eli Lilly, the manufacturer of orforglipron. 
Orforglipron is a small-molecule, oral glucagon-like peptide-1 (GLP-1) receptor agonist. In this phase 3, multinational, randomised, double-blind trial, the authors examined the safety and efficacy of once-daily orforglipron at doses of 6 mg, 12 mg, or 36 mg, as compared with placebo (assigned in a 3:3:3:4 ratio) as an adjunct to healthy diet and physical activity for 72 weeks. All the patients had obesity but not diabetes. The primary end point was the percent change in body weight from baseline to week 72.
A total of 3127 patients in 9 countries / jurisdictions (USA, China, Brazil, India, Japan, South Korea, Spain, Slovakia and Taiwan) underwent randomisation. The mean relative change in body weight from baseline to week 72 was −7.5% with 6 mg of orforglipron, −8.4% with 12 mg of orforglipron, and −11.2% with 36 mg of orforglipron, as compared with −2.1% with placebo.
Among the patients in the orforglipron 36 mg group, 54.6% had reduction of 10% or more of body weight, 36.0% had a reduction of 15% or more, and 18.4% had a reduction of 20% or more, as compared with 12.9%, 5.9%, and 2.8% of the patients, respectively, in the placebo group.
Other outcomes such as waist circumference, systolic blood pressure, triglyceride levels, and non-HDL cholesterol levels significantly improved with orforglipron treatment (see table 3 full paper). Adverse events (see table 4) resulted in treatment discontinuation in 5.3% to 10.3% of the patients in the orforglipron groups and in 2.7% of those in the placebo group. The most common adverse events with orforglipron were gastrointestinal effects, which were mostly mild to moderate, consistent with the GLP-1 class of medications.
The authors note that the use of medications such as GLP-1 receptor agonists (such as semaglutide) are reported to result in mean weight reductions of approximately 15% to above 20% and have shown additional health benefits, including decreased cardiovascular risk. However, most available GLP-1 based medications are administered as a subcutaneous injection, which may limit treatment initiation and adherence.
The authors say: “After 72 weeks of treatment, all the patients in the three orforglipron groups had a significant and clinically meaningful dose-dependent reduction in body weight. The patients who received the highest dose of orforglipron had an average 11.2% weight reduction; more than one third had a reduction of at least 15%, and nearly one fifth had a reduction of at least 20%. All measured cardiometabolic levels improved with orforglipron treatment as compared with placebo… A weight reduction of 10% or more is a recognised therapeutic threshold, one that has been linked to meaningful cardiometabolic benefits. In our current trial, patients who received orforglipron had a mean weight reduction of as much as 11.2%, and such reductions were associated with improvements in levels of systolic and diastolic blood pressure, as well as blood fats, blood sugar profiles, and high-sensitivity C-reactive protein – a marker of systemic inflammation.”
The authors note the trial’s limitations include the lack of comparison with currently approved obesity-management medications, the use of cutoffs for BMI inclusion criteria that have been developed in White populations and that exclude patients with lower BMI values who may also have adiposity-related risks, and the increasing availability of obesity-management medications, which could have an effect on treatment adherence and efficacy results. The strengths of the trial include a highly diverse, large population from nine countries and jurisdictions on four continents – including more than 35% enrolment of men.

They conclude: “In patients with obesity, the use of orforglipron resulted in statistically and clinically significant weight reductions and an adverse-event profile that was consistent with findings regarding other GLP-1 receptor agonists.”
Dr Wharton adds: “This could mean an expansion of obesity interventions to groups who are currently excluded due to the cost of and lack of access to injectable medications.”
Orforglipron is not yet approved by the US Food and Drug Administration (FDA) or other similar agencies worldwide. 

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Flagship NHS pledge hanging in the balance – experts

The government’s flagship NHS pledge to get back to hitting the 18-week waiting time target in England by the end of the parliament is hanging in the balance, experts say.An analysis by the Health Foundation shows, on current trends, waiting times will still be over 20 weeks by July 2029.The think-tank is warning the huge efforts being put into reducing waiting times also risks distracting from other priorities in the NHS, including improving access to GPs.But the government said it was pleased with the progress being made – and expected the pace of improvement to increase.The 18-week target requires 92% of patients to wait less than that amount of time. It has not been hit for a decade.Waiting times ballooned during the pandemic as hospitals scaled back on the amount of routine care they were doing.When Labour came to power, there were 7.6 million patients on waiting lists for treatments such as knee and hip replacements with 58.8% waiting less than 18 weeks.Over the past year that has improved to 61.3%.But even if the current rate of improvement continues, it will not be quite enough to hit the target, the Health Foundation said.Just over a third of trusts are making the necessary progress set out under the government’s waiting time plan published at the start of this year, the analysis said.And the think-tank warned progress could suffer if the rate of referrals rises more quickly than expected – something that is quite possible given the ageing population.The prospect of more industrial action – resident doctor members of the British Medical Association are still in dispute with the government – could further complicate matters, it added.Dr Francesca Cavallaro, from the Health Foundation, said: “The government has clearly made progress in reducing waiting times, but on current trends our analysis shows that the NHS would just fall short of meeting the 18-week standard by the end of the parliament. “The scale of the challenge remains significant and even getting close to meeting the target would be a considerable achievement. “But placing so much emphasis on the 18-week target risks slower progress on other key issues, such as improving access to GPs, which we know is the public’s top priority for the NHS.”A Department of Health and Social Care spokesman said a lot of progress was being made and productivity in the health service was improving. He said the extra money being invested in the NHS, which was introducing modern technology and leading to more evening and weekend working, would help accelerate progress.But he acknowledged strikes had caused problems. “We urge the BMA to work with us, not against us, as we drive down the longest waits and get the NHS back on track.”Tim Mitchell, president of the Royal College of Surgeons of England, said: “This analysis otherwise confirms what surgeons see every day – the NHS is still struggling to meet demand, and unless surgical capacity expands, the government will almost certainly fall short of its target.”

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‘She doesn’t get another childhood’: The lives on hold waiting for wheelchairs

16 minutes agoShareSaveMunaza RafiqDisability producerShareSaveFamily handoutMore than a thousand disabled children across the UK are waiting for wheelchairs and mobility equipment that could transform their lives, Whizz Kidz say.The charity, which helps wheelchair users up to 25 years old, has been forced to close its specialist wheelchairs waitlist for the first time in its 35-year history. They say escalating costs and squeezed NHS budgets are creating a “huge demand” for their service, leading to long delays.NHS England says it’s working with local healthcare providers to deliver better services and NHS Scotland says it’s committed to ensuring vital services were protected. The Department for Health Northern Ireland says by the end of August, the regional service had delivered 87% of all wheelchair categories within 13 weeks.Whizz Kidz recorded a thousand children waiting for equipment when it decided to close the waitlist, but say many more are missing out. BBC News has spoken to two families about the impact the long waits are having on them. ‘She doesn’t get another childhood’Family handoutWren has cerebral palsy, affecting her speech, all four of her limbs and her posture, meaning she needs help with everyday activities.At home the 11-year-old uses an NHS manual self propelled chair. It took more than a year to get this chair, well over the NHS’s official target of 18 weeks.While Wren’s mum, Anna, says the arrival of her NHS chair was greatly received – Wren will soon grow out of it.Anna also told the BBC it’s heavy and cumbersome, meaning Wren can only self propel it a few metres before she needs help.The family turned to Whizz Kidz when they were told Wren is not eligible for a powered wheelchair through the NHS.Whizz Kidz provided her with a chair to use at school, but her family is worried that Wren will soon outgrow that chair too.Using her powered wheelchair at school is “one way for her to assert her independence,” Anna says. “She has great fun whizzing around.”But the family is unsure when they’ll get a new one when she grows, given the back-log at the charity.”I don’t want Wren’s world to get smaller as she gets bigger,” Anna says.”She doesn’t get another childhood and we want to keep the options open for her for whatever she wants to do.”Whizz Kidz pointed to a number of factors for the increase in demand for their services. The charity says NHS wheelchair services were implementing a stricter criteria whilst facing squeezed budgets. It also said costs were escalating across the industry. The average specialist wheelchair costs £4,800, according to the charity, with inflation continuing to push up the cost of equipment. Sarah Pugh, CEO of Whizz Kidz called the situation” a national crisis”.”Behind every statistic is a child missing school trips, missing playtime with friends, or living in pain,” she says.”This cannot be acceptable in the UK in 2025. We urgently need the public’s support to reopen the list – because childhood can’t wait.”Whizz Kidz has launched the Childhood Can’t Wait appeal, to raise £750,000 to reopen the waitlist and cut waiting times.’I don’t have any independence’Family handoutLike most teenagers her age, Ivy loves spending days in the park with her friends, shopping and gaming.But unlike most teenagers, she relies on her friends and family to help her out. Ivy has single ventricle circulation, a life-limiting heart condition, which means only one side of her heart is working. Ivy, is able to walk, but only very short distances. It means she’s not eligible for a powered chair, but does have a manual wheelchair from the NHS. However the exhaustion caused by her condition means she’s unable to propel herself and relies on others to push her. “I have to rely on my mum to drive me to school—and it’s only a 15-minute walk,” Ivy says. “I have to have my friends push my manual wheelchair around from lesson to lesson…It’s not fair.””I get left out when I’m in the wheelchair because obviously I can’t take myself around.”Ivy had hoped starting secondary school in 2024 would provide her with more freedom, which is why her mum Emma applied to Whizz Kidz for an electrical attachment for Ivy’s wheelchair to make life easier. They applied in January that year and are still waiting. Emma acknowledges that they are not in high need, but says the attachment “would just enhance her [Ivy’s] life massively, to not have to rely on somebody else all the time”.There’s also a mental and physical toll on the family.”It gets quite heavy pushing a wheelchair around for 12 hours at a time – your shoulders and your back ache,” Emma says.Emma’s ultimate goal for Ivy is to live life like any normal teenager and enjoy her life without constraints. “It would hugely enhance our lives and give Ivy that independence… we would have to make some real big sacrifices to be able to afford the electrical attachment on our own,” Emma says.The BBC asked the NHS in each part of the UK for their response. The Department for Health Northern Ireland says by the end of August, the regional service had delivered 87% of all wheelchair categories within 13 weeks.NHS England told us they offer personal wheelchair budgets for people to pick a wheelchair that meets their individual needs, adding it was working to deliver” better services that improve access and experiences for wheelchair users”.In Scotland a spokesperson said the government was committed to ensuring vital services were protected and eligibility criteria for the provision of children’s wheelchairs has remained unchanged since 2014.The Welsh government has not yet responded.

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UK drug price rises ‘necessary’, says Patrick Vallance

The price the NHS pays for medicines will need to rise to stop a wave of pharmaceutical investment leaving the UK, science minister Patrick Vallance has said.His comments follow several recent announcements from some of the world’s largest drug companies either pausing or scrapping UK projects.Critics in the sector say low prices for new drugs, a lack of government investment, and tariff pressure from US President Donald Trump have been pushing firms away from the UK.Lord Vallance told the BBC “price increases are going to be a necessary part” of solving that problem.”Where the additional money would come from to pay higher prices is a matter for the department of health and the Treasury to figure out,” he added.Lord Vallance was speaking at the opening of US vaccine giant Moderna’s new centre in Oxfordshire where millions of flu and Covid jabs will be made.Health Secretary Wes Streeting, who cut the ribbon at the development project on Wednesday, told the BBC there was “a live conversation between government departments and the pharma industry” on drug pricing.Lord Vallance added: “We must end up with a deal of some sort… because it’s in the interest of the economy, it’s in the interest of patients.”According to the government, Moderna is investing more than a £1bn in UK research and development as part of a 10-year partnership to create new treatments jobs and boost pandemic resilience.Its commitment, made three years ago, stands in contrast to Merck’s decision this month to scrap a £1bn project in Liverpool and AstraZeneca’s pausing of a £200m investment in Cambridge, also this month.Meanwhile, Novartis said in August that NHS patients will lose access to new cutting-edge treatments because of skyrocketing costs.It said it was not considering the UK for major new investments in manufacturing, research, or advanced technology because of “systemic barriers”.Another pharmaceutical firm Eli Lily told the Financial Times on Wednesday the UK was “probably the worst country in Europe” for drug prices.Over the last 10 years, UK spending on medicines has fallen from 15% of the NHS budget to 9%, while the rest of the developed world spends between 14% and 20%.Elsewhere, Trump has put pressure on pharmaceutical companies to lower prices and invest more in the US.Last month, talks broke down between Streeting and pharma firms over the cost of medicines for the UK.The UK government said at the time it had put forward a “generous and unprecedented offer to accelerate growth” in the pharmaceutical sector.Streeting previously insisted that he would not allow pharma companies to “rip off” taxpayers and described drug companies’ approach as “short-sighted”.However, he struck a more conciliatory tone on Wednesday saying “it’s a live conversation – not just domestically with the industry but internationally with the US as well”. “There’s an intersection between the growth ambitions of the government, the health ambitions of the government, the trade ambitions of the government and bilateral relations with the US,” he added.

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Head nurse describes ‘chaotic’ night baby died

11 hours agoShareSaveJoshua AskewSouth EastShareSaveFamily handoutThe night a baby died with an undiagnosed heart condition in a Kent hospital was “quite chaotic”, a court has been told.Head nurse Ronald Carrido was giving evidence at an inquest into the death of seven month-old Tommy Kneebone on 21 January, 2023, at Tunbridge Wells Hospital in Pembury, Kent.Mr Carrido told the inquest he called for consultant help “when there was no improvement in Tommy, when he was deteriorating”.The boy’s mother, Shanice Kneebone, previously told Kent and Medway Coroner’s Court in Maidstone that “no-one took her concerns seriously” at the hospital. At the hearing on Wednesday, his parents also heard from the consultant on duty that night.Breaking down in tears, Doctor Chhaya Patankar told the inquest when she went into his room at 19:00 GMT, Tommy looked at her with “such bright, beautiful eyes”.Family handoutThe paediatric consultant said she examined Tommy, listened to his heartbeat and checked his liver. He “responded like any baby would do,” she said.Dr Patankar said the baby had mild respiratory distress, which “fitted with” what she had been told. “But there was a lack of the broader picture,” she said.Tommy’s parents first noticed he had a cough when they returned from a holiday abroad in October 2022.The court previously heard Ms Kneebone had taken him to a GP and A&E several times before his death without his underlying cardiomyopathy being identified.Tommy died at 04:20 on 21 January. The inquest continues.More on this storyRelated internet links

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