The recreational drugs cannabis, cocaine and amphetamines significantly increase the risk of stroke – including among younger users – Cambridge researchers have concluded after analysing data from more than 100 million people. Our analysis suggests that it is these drugs themselves that increase the risk of stroke, not just other lifestyle factors among users Eric Harshfield Stroke is a major global health challenge – the third leading cause of death and disability combined. But it also a condition that, for the most part, results from modifiable risk factors, such as poor diet, lack of exercise and other lifestyle factors. In 2024, 8.8% of adults aged 16 to 59 years in England and Wales – around 2.9 million individuals - reported having used a legal or illegal recreational drug in the past year. Recent data from the USA reports that over half of all those aged over 12 have used drugs such as cocaine, cannabis and opiates at least once. There is increasing evidence that these drugs may increase the risk of stroke, but the evidence is often of differing quality and is observational only, meaning it is impossible to say whether the use of these drugs itself increases the risk of stroke, or whether this is purely a correlation. To investigate this further, a team from the Department of Clinical Neurosciences at the University of Cambridge first carried out a meta-analysis of studies encompassing more than 100 million people. A meta-analysis is a method for pooling and analysing cohort data from all of the published evidence. This approach allows researchers to bring together studies which, on their own may not provide sufficient evidence and sometimes disagree with each other, to provide more robust conclusions. In findings published today in the International Journal of Stroke, the team found that the use of cocaine and amphetamines was associated with around double the risk of stroke (cocaine increased the risk by 96%, amphetamines by 122%), while cannabis use increased the risk by around 37%. The team found no statistically significant link between opioid use and stroke risk. When the researchers restricted their analysis to individuals under 55 years, they found that amphetamine use almost tripled the risk of stroke (an increase of 174%); cannabis use increase stroke risk but by a smaller amount (14%), while cocaine use increased the risk by 97%. To analyse these links further, the researchers used a statistical technique known as Mendelian randomisation, which looks at naturally occurring genetic variants related to risk factors and stroke and uses these to evaluate whether there is evidence to support a causal association with a particular risk factor. This analysis showed that cocaine use disorders were particularly associated with brain haemorrhage and cardioembolic stroke (where a blood clot forms in the heart and travels to the brain, blocking blood flow and leading to damage of brain tissue). Cannabis use disorders were associated with stroke overall, particularly large artery stroke. This genetic evidence suggests a causal link, rather than just correlation. Problematic alcohol use was linked to an increased risk of cardioembolic stroke and large artery stroke, while alcohol addiction increased the risk of stroke overall. The researchers were unable to use Mendelian randomisation to look at associations with amphetamine as there are currently no large genetic datasets available with information on their usage. The researchers suggest that possible reasons why these drugs are linked to an increased risk of stroke include sudden spikes in blood pressure, blood vessel spasm and constriction, heart rhythm problems, increased blood clotting (especially cannabis), and inflammation or vasculitis (especially amphetamines). These are all well-established pathways known to cause both ischaemic strokes, which result from blood clots, and haemorrhagic strokes. Dr Megan Ritson from the Stroke Research Group at the University of Cambridge said: “This is the most comprehensive analysis ever conducted on recreational drug use and stroke risk and provides compelling evidence that drugs like cocaine, amphetamines, and cannabis are causal risk factors for stroke. These findings give us stronger evidence to guide future research and public health strategies.” Dr Eric Harshfield, Alzheimer's Society Research Fellow at the Department of Clinical Neurosciences, said: “Our analysis suggests that it is these drugs themselves that increase the risk of stroke, not just other lifestyle factors among users. Taken together, our findings emphasise the importance of public health measures to reduce substance abuse as a way of helping also reduce stroke risk.” The research was funded by the British Heart Foundation, with additional support from the National Institute for Health and Care Research Cambridge Biomedical Research Centre. Reference Ritson, M, et al. Does Illicit Drug Use Increase Stroke Risk? A Systematic review, Meta-Analyses and Mendelian Randomization analysis. International Journal of Stroke; 9 March 2026; DOI: 10.1177/17474930261418926 The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Experts are warning that far from being over-diagnosed, people with ADHD are waiting too long for assessment, support and treatment. Overdiagnosis is not a problem, but misdiagnosis may be as people are driven into the private sector by long waits, and sadly, missed diagnoses remain common Tamsin Ford In a paper, published today in the British Journal of Psychiatry, a group of experts say there is no robust evidence that ADHD is over-diagnosed in the UK. They refute the view that ‘nowadays everyone has ADHD’, which is gaining traction in public discourse and has been amplified by some leading politicians, as demand rises for NHS assessments and services. Bringing together academics, clinicians, people with lived experience and carers, the group say this narrative risks misleading the public and policymakers and overshadows a more pressing concern - unmet need. Professor Tamsin Ford, Head of the Department of Psychiatry at the University of Cambridge, senior co-author on the paper, said: “While many more people with ADHD are being recognised and treated, we are failing to support many more. Overdiagnosis is not a problem, but misdiagnosis may be as people are driven into the private sector by long waits; and sadly, missed diagnoses remain common.” Professor Samuele Cortese from the University of Southampton, the study’s first author, said: “Rather than focusing on increases or decreases in diagnostic rates, attention should be directed toward the extent to which those with ADHD are being adequately diagnosed and treated. “While misdiagnosis and inappropriate diagnosis do occur, the available evidence indicates that under-diagnosis and under-treatment remain the predominant challenges.” When standardised diagnostic criteria are applied, the prevalence of ADHD internationally is around 5 per cent in children and 3 per cent in adults. While prevalence has increased over time, NHS administrative data in England remains substantially below these expected levels, suggesting that many people with ADHD are living without a diagnosis and adequate support. The group acknowledge that misdiagnosis can occur in some cases, particularly where assessments rely heavily on self-reporting or where alternative conditions are not fully considered. The researchers stress that the absence of biological diagnostic markers means that thorough, multidisciplinary clinical assessment is essential. Field trials show that when clinicians are properly trained, an ADHD diagnosis is amongst the most reliable for a mental health condition. Professor Chris Hollis from the University of Nottingham, a co-author, said: “Similar to physiological traits, such as blood pressure or weight, ADHD symptoms are distributed along a continuum. But as with hypertension or obesity, there are diagnostic severity thresholds that determine health risks and what interventions should be used. Similarly, in ADHD a risk-stratified stepped-care approach may be useful.” The team highlight significant pressure on UK services, with long waiting times and growing demand, especially among adults who were not diagnosed in childhood. They point to figures showing around 27 per cent children and young people diagnosed with ADHD reported waiting one to two years, while 14 per cent waited two to three years. Evidence shows that untreated ADHD is associated with serious long-term risks, while effective treatments are available, backed by strong evidence, and generally well tolerated. “The costs of untreated ADHD are often overlooked,” said Professor Cortese. “They include increased risk of academic failure, suicidal behaviour, substance abuse, criminality, injury and death. The failure to provide treatments which have been shown to reduce these risks represents a major ethical issue that needs to be urgently addressed.” The authors call for improved funding, workforce training and a more balanced, evidence-based conversation to ensure accurate diagnosis while expanding access to care for those who need it. Cambridge Children's Hospital The editorial highlights that a group of children where ADHD may tend to be missed or under diagnosed are those that have co-occurring conditions. One such group is children with long term physical health problems, who have elevated rates of ADHD. This is often under-detected and under-treated. Cambridge Children's Hospital aims to fully integrate physical and mental healthcare, including detecting and treating neurodevelopmental conditions such as ADHD in children who also have physical health needs. Early detection and intervention have a positive impact on emotions, behaviour, educational attainment and peer relationships, as well as helping children cope with the health care they may need to receive, such as staying in hospital, procedures or operations. Studies have shown that children with epilepsy have up to six times the population rate of ADHD, yet often have difficulty obtaining treatment but when they are successfully treated there is a significant improvement in functioning and quality of life. Reference Cortese, S et al. ADHD (over) diagnosis: fiction, fashion, and failure. British Journal of Psychiatry; 6 March 2026; DOI: 10.1192/bjp.2026.10546 Adapted from a press release from the University of Southampton The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Differences in cellular pathway activity flip the switch from nocturnality to diurnality and explain a major evolutionary change humans have undergone. Early mammals were nocturnal, sleeping during the day while large predators were active. However, after the extinction of dinosaurs, several different lineages of mammals independently transitioned to become active during the day. Exactly how this dramatic change occurred has proved elusive. A new study, published in the journal Science, has revealed a cellular switch which holds the answer. Led by researchers from the MRC Laboratory for Molecular Biology, the study looked at how cells from a range of nocturnal (active at night) and diurnal (active in the day) mammals, like humans, respond to environmental signals. Changes in temperature or osmolarity, as happens to the body throughout the day, caused the cells to respond in opposite ways, including in fundamental cellular functions. This divergence flips the timing of cellular activity, essentially acting as a day/night ‘switch’ at a molecular level. The researchers pinpointed these differing responses to the mechanistic Target of Rapamycin (mTOR) and With-no-lysine (WNK) kinase pathways, central signalling networks in cells responsible for regulating several key functions, including protein synthesis. This suggested that modification of their activity could enable nocturnal mammals to switch to more diurnal activity. To explore this hypothesis, the researchers administered diet-based treatments to mice to target the mTOR pathway, as mTOR activity is highly sensitive to nutrient levels. Once mTOR function was reduced, the mice began behaving more like diurnal animals, shifting their active hours into the daytime. This underlined that mTOR signalling goes beyond influencing metabolism; it also helps dictate when an animal is active. The researchers then looked to contextualise this finding against the backdrop of mammalian evolution. After analysing genetic data across several species, co-author Matthew Christmas from Uppsala University found that genes regulating mTOR and WNK have evolved faster in diurnal mammals. This points to the importance these pathways have played in the shift from nighttime to daytime over millennia. This discovery helps explain one of the most important evolutionary events in mammalian history and provides a piece of the puzzle for understanding human health. To date, most explorations of pre-clinical biomedical research have depended on the mouse model, yet this study highlights that nocturnal rodents differ from humans in key cellular pathways linked to timing and metabolism. This study also carries clear implications for circadian medicine, a growing field that examines how the timing of treatments influences their effectiveness. “That this radically different response of cellular ‘clocks’ to the same temperature shift seemed to be broadly true across mammalian species, when comparing those that are more active at night versus those that are more active during the day,” said co-author Dr Nina Rzechorzek, from Cambridge’s Department of Engineering. “We need more research to understand exactly how and why this happens, but it could teach us a lot about how biological clocks work and how they impact health and disease.” Several of the key external factors harnessed in this study to influence animals’ circadian rhythms are vulnerable to environmental changes. As climate change disrupts temperature levels and food production capabilities, this work suggests mammals may change the time of day they are active in response. This will disrupt the fragile balance of relationships in our ecosystems and is an impact of climate change, which has perhaps been overlooked thus far. This work was funded by UKRI MRC, UKRI Future Leaders Fellowship, Wellcome and the Royal Society. The project was further supported by Blue Sky collaboration between AstraZeneca UK Limited and the Medical Research Council (BSF38). Reference: Andrew D. Beale et al. ‘A cellular basis for the mammalian nocturnal-diurnal switch.’ Science (2026). DOI: 10.1126/science.ady2822 Adapted from an LMB media release. The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Robots are becoming increasingly capable in vision and movement, yet touch remains one of their major weaknesses. Now, researchers have developed a miniature tactile sensor that could give robots something much closer to a human sense of touch. The technology, developed by researchers at the University of Cambridge, is based on liquid metal composites and graphene – a two-dimensional form of carbon. The ‘skin’ allows robots to detect not just how hard they are pressing on an object, but also the direction of applied forces, whether an object is slipping, and even how rough a surface is, at a scale small enough to rival the spatial resolution of human fingertips. Their results are reported in the journal Nature Materials. Human fingers rely on multiple types of mechanoreceptors to sense pressure, force, vibration, and texture simultaneously. Reproducing this level of multidimensional tactile perception in artificial systems is a significant challenge, especially in devices that are both small and durable enough for practical use. “Most existing tactile sensors are either too bulky, too fragile, too complex to manufacture or unable to accurately distinguish between normal and tangential forces,” said Professor Tawfique Hasan from the Cambridge Graphene Centre, who led the research. “This has been a major barrier to achieving truly dexterous robotic manipulation.” To overcome this, the research team developed a soft, flexible composite material, combining graphene sheets, deformable metal microdroplets, and nickel particles, embedded in a silicone matrix. Inspired by the microstructures found in human skin, the researchers shaped the material into tiny pyramids, some as small as 200 micrometres across. These pyramid structures concentrate stress at their tips, enabling the sensor to detect extremely small forces while maintaining a wide measurement range. The result is a tactile sensor sensitive enough to detect a grain of sand. Compared with existing flexible tactile sensors, the new device improves size and detection limits by roughly an order of magnitude. The sensor can also distinguish shear forces from normal pressure, a capability that allows it to detect when an object begins to slip. By measuring signals from four electrodes beneath each pyramid, the sensor can mathematically reconstruct the full three-dimensional force vector in real time. In demonstrations, the team integrated the sensors into robotic grippers. The robots were able to grasp fragile objects, such as thin paper tubes, without crushing them. Unlike conventional force sensors, which rely on prior information about an object’s properties, the new system adapts in real time through slip detection. At even smaller scales, microsensor arrays could identify the mass, geometry, and material density of tiny metal spheres by analysing force magnitude and direction. This opens the door to applications in minimally invasive surgery or microrobotics, where conventional force sensors are far too large. Beyond robotics, the technology could have significant implications for prosthetics. Advanced artificial limbs increasingly rely on tactile feedback to provide users with a sense of touch. Highly sensitive, miniaturised 3D force sensors could enable more natural interactions with objects, improving control, safety, and user confidence. “Our approach shows that bulky mechanical structures or complex optics are not required to achieve high-resolution 3D tactile sensing,” said lead author Dr Guolin Yun, a former Royal Society Newton International Fellow at Cambridge, and now Professor at the University of Science and Technology of China. “By combining smart materials with skin-inspired structures, we achieve performance that comes remarkably close to human touch.” Looking ahead, the researchers believe the sensors could be miniaturised even further, potentially below 50 micrometres, approaching the density of mechanoreceptors in human skin. Future versions may also integrate temperature and humidity sensing, moving closer to a fully multimodal artificial skin. As robots increasingly move out of controlled factory environments and into homes, hospitals, and unpredictable real-world settings, such advances in touch could be transformative — allowing machines not just to see and act, but to truly feel. A patent application has been filed through Cambridge Enterprise, the University’s innovation arm. The research was supported by the Royal Society, the Henry Royce Institute, and the Advanced Research and Invention Agency (ARIA). Tawfique Hasan is a Fellow of Churchill College, Cambridge. Reference: Guolin Yun et al. ‘Multiscale-structured miniaturized 3D force sensors.’ Nature Materials (2026). DOI: 10.1038/s41563-026-02508-7 Adapted from a story originally published on the Electrical Engineering website. The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Cambridge scientists have shown that when tumours first emerge, interactions with healthy cells in the underlying supportive tissue determine their ability to survive, grow, and progress to advanced stages of disease. The way healthy tissue responds to the emergence of early tumours also plays a crucial role in whether disease develops Greta Skrupskelyte The study, carried out in mice and further validated using human tissue, may explain why some tiny, newly-formed tumours disappear, while others manage to survive and eventually grow into cancer. Tumours arise when our DNA accumulates errors, or mutations, causing the cells to grow faster and ignore signals that would otherwise instruct damaged cells to die before they can cause harm. However, these same mutations can also accumulate in the tissues of healthy people during ageing without developing into cancer. To examine why this should be the case, scientists at the University of Cambridge have been studying what additional factors influence tumour formation at the very early stages and what determines whether they persist and develop into cancer. Previous collaborative work by the team had shown that when a newly-formed microscopic tumour first emerges in a tissue, it can be removed by other mutant cells surrounding it, which compete for space within the tissue. But this does not always happen. Scientists have puzzled for some time over why some of these so-called ‘incipient tumours’ manage to outwit the body’s defences and flourish, creating the conditions for advanced disease to develop. To answer this question, a team led by scientists at the Cambridge Stem Cell Institute and the Department of Physiology, Development and Neuroscience, University of Cambridge, modelled early stages of cancer in the upper part of the mouse digestive tract. The researchers replicated key features of human disease by exposing mice to a chemical found in tobacco smoke, a known cancer risk factor. This causes mutations in the cells lining the oesophagus (gullet), leading to the development of microscopic tumours, most of which disappear naturally as described above – but some persist. The team then tracked these nascent tumours over time, from the point when they were made up of just over a handful of altered cells (around 10 cells) through to later stages of disease. They analysed the tumours and surrounding cells using high‑resolution confocal microscopy and a range of tools, including single‑cell RNA sequencing and genetic cell tracking, to understand what each cell was doing. In addition, the team grew three-dimensional tissue in the lab, allowing them to model the interactions between the tumour cells and surrounding tissue. In findings published today in Nature, the researchers found that at these early stages, the tumour sends a ‘distress signal’ to nearby fibroblasts – supportive ‘first-aid’ cells in the underlying tissue. This communication triggers a response that closely resembles wound healing. The fibroblasts behave as though the tissue has been damaged, producing a fibrotic scaffold around the tumour cells. This creates a supportive micro‑environment – a ‘pre-cancerous niche’ – that shelters the tumour from being cleared and helps it persist and grow. Remarkably, the researchers found that this fibrotic scaffold alone was enough to give healthy, non-mutant cells tumour-like properties, even in the absence of cancer-causing mutations. This suggests that beyond genetic alterations, early tumours are shaped by how healthy cells in the underlying tissue respond, with lasting consequences for disease progression. When the researchers examined tissue from early-stage oesophageal cancers in humans, they found similar clusters of tumour cells sending stress signals, as well as the same fibrotic scaffolding seen in the mouse models, demonstrating that this mechanism is also relevant in people. Dr Greta Skrupskelyte from the Cambridge Stem Cell Institute, one of the lead authors, said: “A decade ago it was assumed that it is the mutated cells themselves that determine whether or not a cancer arises. Our findings show that the way healthy tissue responds to the emergence of early tumours also plays a crucial role in whether disease develops.” When the team blocked the communication between the tumour cells and the underlying tissue, they found that the pre-cancerous niche did not form efficiently, and far fewer early tumours survived. Dr Maria Alcolea, also from the Cambridge Stem Cell Institute, said: “Understanding the mechanisms that allow these newly-formed microscopic tumours to persist and develop into cancer opens up new possibilities for preventing the disease before it takes hold. “If we can find a way to block tumour cells from communicating with surrounding tissue, we may have a new way to stop cancer in its tracks.” The researchers say the findings could also, in future, help improve early diagnosis of oesophageal cancer, a disease that is often caught at a late stage, when treatment options are more limited. Dr Skrupskelyte added: “Although the clinical aspects of our work are at a very early stage, it has given us some biomarkers – red flags – that could help identify cancer much earlier. If validated, it could help us catch oesophageal cancer at a much earlier stage, when it is far easier to treat.” The research was mainly funded by Worldwide Cancer Research, the Wellcome Trust, The Royal Society, the Medical Research Council and the Isaac Newton Trust. The University of Cambridge and Addenbrooke's Charitable Trust (ACT) are fundraising for Cambridge Cancer Research Hospital, a new hospital that will transform how we diagnose and treat cancer, with early detection at the heart of its mission. Set to be built on the Cambridge Biomedical Campus, the hospital will bring together clinical excellence from Addenbrooke’s Hospital and world-leading researchers at the University of Cambridge. The research carried out there aims to change the lives of cancer patients across the UK and beyond. Find out more here. Reference Skrupskelyte, G et al. Precancerous niche remodelling dictates nascent tumour persistence. Nature; 4 March 2026; DOI: 10.1038/s41586-026-10157-8 Image The survival of emerging tumours (labelled in red) is dictated by reciprocal interactions with the fibroblast-derived niche (labelled in greyscale) - presented in side view and top down view as 3D rendered confocal images (nuclei, blue). The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

A year after stopping taking weight loss drugs such as Ozempic and Wegovy, people regain on average 60% of their lost weight – but beyond this, their weight regain plateaus, with individuals managing to keep off 25% of the weight lost to treatment, say researchers at the University of Cambridge. Drugs such as Ozempic and Wegovy act like brakes on our appetite. When people stop taking them, they are essentially taking their foot off the brake Brajan Budini It isn’t clear, however, whether the weight regain constitutes both fat and muscle, or mainly fat. Previous studies have suggested that lean body mass – including muscle – can constitute up to 40% of total weight lost during treatment. More than a billion people worldwide are living with obesity, which increases the risk of diseases such as 2 diabetes, cardiovascular disease and cancer. Weight loss can help mitigate these complications, but losing weight through diet and exercise alone can prove challenging. In the past few years, a new generation of weight loss drugs has emerged that target a protein known as the glucagon-like peptide 1 receptor (GLP-1R). These drugs help control blood sugar and reduce appetite, and clinical trials have shown they can lead to weight losses of 15 to 20%. Approximately half of all patients who begin taking these drugs discontinue their use within the first year, however, and three-quarters have stopped after two years. This is likely to be due to their potential side effects and to limited access under insurance coverage policies and national prescribing guidelines. A team of students at Trinity College, University of Cambridge, has investigated the impact of stopping the medication, modelling the trajectory of weight regain over 12 months and beyond. Their findings are published today in eClinicalMedicine. The team first carried out a systematic review of existing scientific and medical literature, identifying and summarising all the relevant evidence. They followed this with a meta‑analysis, which pools the results of multiple studies to estimate an overall effect. This approach allowed them to draw more robust conclusions from studies which, on their own, may provide insufficient evidence and sometimes disagree with each other. In total, the team examined 48 relevant studies, comprising 36 randomised controlled trials (RCTs) and 12 non-randomised studies. As most of these studies only followed patients for a few weeks after stopping the drugs, the team selected the six RCTs (comprising more than 3,200 individuals in total) that followed patients for up to 52 weeks after discontinuation of the weight loss drugs. They used these to model the trajectory of weight regain, including to extrapolate beyond 52 weeks. The model estimated that when individuals stopped taking the medication, they underwent rapid initial weight regain, which slowed progressively. By 52 weeks, individuals had regained 60% of their original weight loss. At 60 weeks, weight regain begins to plateau and is projected to taper off at 75% of the original weight loss. This means that 25% of the initial weight loss may be sustained in the long term. For an individual who had lost a fifth of their weight while on the drugs, this would correspond to a sustained weight reduction of around 5%. Weight regain trajectories appeared broadly similar for the different types of weight loss drugs targeting GLP-1R. Brajan Budini, a medical student at the School of Clinical Medicine and Trinity College, University of Cambridge, said: “Drugs such as Ozempic and Wegovy act like brakes on our appetite, making us feel full sooner, which means we eat less and therefore lose weight. When people stop taking them, they are essentially taking their foot off the brake, and this can lead to rapid weight regain.” The researchers say there are several reasons why people may not return to their original weight even a year after stopping the medications. One reason is that by reducing appetite, these drugs may help individuals develop healthier eating habits, such as reduced portion sizes or more nutritionally-balanced meals, and these habits may persist even after treatment is discontinued. The drugs may also affect the body long-term, altering hormone levels and ‘resetting’ the brain’s appetite control mechanisms. Steven Luo, also a medical student at the School of Clinical Medicine and Trinity College, said: “When stopping weight loss drugs, doctors and patients should be aware of the potential for weight regain and consider ways to mitigate this risk. “It’s important that people are given advice on improving their diet and exercise, rather than relying solely on the drugs, as this may help them maintain good habits when they stop taking them.” There are significant concerns about the long-term consequences of GLP-1R drugs on body composition, with studies indicating that 40 to 60% of the weight lost during treatment is muscle. It was not clear whether individuals regain both fat and muscle. Budini added: “Our projections show that even though people regain most of the weight they have lost, they still maintain some of the weight loss, but what we currently don’t know is if the same proportion of lean mass is recovered. If the regained weight is disproportionately fat, individuals may ultimately be worse off than before in their fat-to-lean mass ratio, which may have adverse consequences for their health.” The researchers say there are several limitations to their study. Most importantly, the trial data used to fit their model only extended to 52 weeks after cessation. They also restricted their analysis to studies reporting at least 3kg on-treatment average weight loss. Reference Budini, B & Luo, S et al. Trajectory of weight regain after cessation of GLP-1 receptor agonists: a systematic review and nonlinear meta-regression. eClinicalMedicine; 4 Mar 2026; DOI: 10.1016/j.eclinm.2026.103796 The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.