Publisher Health

Experts from around the world are raising alarms about the rapid global rise of ultra-processed foods, warning that UPFs are reshaping diets and driving a surge in chronic health problems. A major three paper Series in The Lancet finds that ultra-processed foods (UPFs) are rapidly replacing fresh and minimally processed meals around the world. The evidence links rising UPF intake to poorer diet quality and higher risks of multiple chronic diseases. The authors explain that although more research on UPFs will continue to be valuable, the current science is already strong enough to justify immediate public health action. Waiting for further studies would allow UPFs to gain an even stronger hold in global diets. The Series stresses that improving diets cannot fall solely on individual behavior. Real progress requires coordinated policies that limit UPF production, marketing, and availability, while also addressing high levels of fat, sugar and salt in the food supply and expanding access to healthy food. The authors describe UPFs as products of an industrial food system built around corporate profit rather than nutrition or sustainability. They warn that only a united international response can counter the political influence of UPF companies, which remains the biggest obstacle to effective dietary policy reform.Rising UPF Consumption Sparks Global Health Concerns
A new three paper Series in The Lancet, written by 43 international experts, warns that the rapid spread of ultra-processed foods (UPFs) across global diets is creating a serious public health challenge. The authors detail how UPF companies use a range of strategies to increase sales and block policies designed to protect consumers. The Series offers a plan for stronger government action, greater community involvement, and broader access to affordable, nutritious foods.
Professor Carlos Monteiro, University of Sao Paulo, Brazil, explains, “The growing consumption of ultra-processed foods is reshaping diets worldwide, displacing fresh and minimally processed foods and meals. This change in what people eat is fueled by powerful global corporations who generate huge profits by prioritizing ultra-processed products, supported by extensive marketing and political lobbying to stop effective public health policies to support healthy eating.”
Calls for Strong, Coordinated Policy Action
Professor Camila Corvalan, University of Chile, Chile, adds, “Addressing this challenge requires governments to step up and introduce bold, coordinated policy action — from including markers of UPFs in front-of-package labels to restricting marketing and implementing taxes on these products to fund greater access to affordable, nutritious foods.”
Dr. Phillip Baker, University of Sydney, Australia, continues, “We need a strong global public health response — like the coordinated efforts to challenge the tobacco industry. Including safeguarding policy spaces from political lobbying and building powerful coalitions to advocate for healthy, fair and sustainable food systems and stand-up to corporate power.”
UPFs, based on the Nova classification, are industrially produced branded foods created from low cost ingredients such as hydrogenated oils, protein isolates or glucose/fructose syrup, along with cosmetic additives (e.g. dyes, artificial sweeteners, emulsifiers). These products are intentionally formulated and promoted to replace fresh foods and traditional meals, while maximizing profits for manufacturers (for a detailed definition see paper 1, panel 1).

Research Shows Clear Links Between UPFs and Chronic Disease
The first paper in The Lancet Series reviews scientific evidence gathered since the Nova classification was developed by Prof Carlos Monteiro and colleagues in 2009. The findings consistently show that UPFs are crowding out traditional dietary patterns, lowering overall diet quality, and contributing to higher risks of many chronic diseases.
National surveys also reveal substantial increases in UPF consumption (paper 1, figure 1). The proportion of dietary energy from UPFs tripled in Spain (11% to 32%) and China (4% to 10%) over the past three decades, and rose from 10% to 23% in Mexico and Brazil during the previous forty years. In the USA and UK, levels have remained above 50% for the past two decades, with slight increases over time.
Growing Body of Evidence Underscores Health Risks
The Series reports that diets high in UPFs are associated with overeating, poor nutrient balance (too much sugar and unhealthy fats, too little fibre and protein), and greater exposure to potentially harmful additives. A systematic review of 104 long-term studies found that 92 showed higher risks for at least one chronic disease, with meta-analyses identifying significant associations with 12 health conditions including obesity, type 2 diabetes, cardiovascular disease, depression, and premature death (paper 1, figure 4, appendix p23-24).
While the authors acknowledge scientific debates about Nova and UPF definitions — including the need for more long-term trials, clearer mechanisms, and recognition of product subgroups with differing nutritional qualities — they emphasize that further research should not delay immediate public health action.

Professor Mathilde Touvier, French National Institute for Health and Medical Research (Inserm), France, states, “While healthy debate about UPFs within the scientific community is welcomed, this should be distinguished from attempts by vested interests to undermine the current evidence. The growing body of research suggests diets high in ultra-processed foods are harming health globally and justifies the need for policy action.”
Policy Solutions to Reduce UPFs and Improve Diet Quality
The second paper in the Series outlines policy options to curb UPF production, marketing, and consumption, holding major companies accountable for promoting unhealthy diets (paper 2, table 1). These recommendations are intended to strengthen existing legislation targeting high fat, salt and sugar (HFSS) foods.
Professor Barry Popkin, University of North Carolina, US, says “We call for including ingredients that are markers of UPFs (eg, colors, flavors, and sweeteners) in front-of-package labels, alongside excessive saturated fat, sugar, and salt, to prevent unhealthy ingredient substitutions, and enable more effective regulation.”
Marketing Restrictions, School Policies, and Fresh Food Access
The authors recommend stronger marketing limits, particularly for promotions aimed at children, digital advertising, and brand-level marketing. They also suggest banning UPFs in public settings such as schools and hospitals, and capping shelf space for UPFs in supermarkets. One example of successful reform is Brazil’s national school feeding program, which has removed most UPFs and will require 90% of school food to be fresh or minimally processed by 2026 (paper 2, panel 4).
Alongside regulation, the authors highlight the need to expand access to fresh foods. Taxing selected UPFs could help support subsidies for healthier options, particularly for low-income households.
Professor Marion Nestle, New York University, US, notes, “Improving diets worldwide requires policies tailored to each country’s unique situation and how entrenched UPFs have become in people’s daily eating habits. While priorities may differ, urgent action is needed everywhere to regulate ultra-processed foods alongside existing efforts to reduce high fat, salt, and sugar content.”
Associate Professor Gyorgy Scrinis, University of Melbourne, Australia, adds, “Importantly, policies must ensure that fresh and minimally processed foods are accessible and affordable — not just for those with time to cook, but for busy families and individuals who rely on convenient options. Only by combining stricter regulation on poor quality food products with realistic support for more nutritious choices can we truly promote better diets for all.”
How Corporate Power Drives the Global UPF Boom
The third paper shows that the sharp rise in UPF consumption is being driven primarily by global food corporations rather than individual behavior. These companies use low cost ingredients, large-scale production methods, and highly persuasive marketing to encourage widespread consumption.
With global annual sales reaching $1.9 trillion, UPFs represent the most profitable segment of the food industry. Manufacturers of these products have delivered more than half of the $2.9 trillion in shareholder payouts made by publicly listed food companies since 1962. The profits help fuel expansion, marketing power, and political influence, reinforcing corporate dominance over modern food systems.
The Series explains that UPF companies rely on sophisticated political strategies to protect their interests — blocking regulations, influencing scientific debates, shaping public opinion, supporting hundreds of interest groups, lobbying, donating to political campaigns, and engaging in litigation to delay policy action (paper 3, table 1 and figure 2).
Professor Simon Barquera, the National Institute of Public Health of Mexico, Mexico, states, “Powerful corporations — not individuals’ choices — are behind the global rise of ultra-processed foods. Through interest groups, these corporations often position themselves as part of the solution, but their actions tell a different story — one focused on protecting profits and resisting effective regulation.”
Urgent Need for a Unified Global Response
The authors call for a global public health movement to protect policy-making from industry interference, end ties between industry and health organizations, and strengthen networks advocating for reduced UPF consumption.
Professor Karen Hoffman, University of the Witwatersrand, South Africa, says, “Just as we confronted the tobacco industry decades ago, we need a bold, coordinated global response now to curb the overproportionate power of UPF corporations and build food systems that prioritize people’s health and well-being.”
They argue that transforming food systems requires a new vision that elevates local food producers, preserves cultural food traditions, promotes gender equity, and ensures that economic benefits flow to communities rather than to distant shareholders.
Dr. Phillip Baker concludes, “We are currently living in a world where our food options are increasingly dominated by UPFs, contributing to rising global levels of obesity, diabetes and mental ill-health. Our Series highlights that a different path is possible — one where governments regulate effectively, communities mobilize, and healthier diets are accessible and affordable for all.”
The Lancet Series on Ultra-Processed Foods and Human Health, was supported by funding from Bloomberg Philanthropies.

Our fat cells, known as adipocytes, do far more than store extra body weight. They serve as an important energy reserve for the body. Inside each adipocyte, fat is packed into lipid droplets that can be tapped when fuel is needed — for example, during the hours between meals. To release this stored energy, the body relies on a protein called HSL, which functions much like a switch. When energy is running low, hormones such as adrenaline activate HSL, prompting it to free fat that can then supply various organs.
Without HSL, it would be reasonable to expect fat to build up, as though the body had lost access to its energy supply. Surprisingly, this is not what happens. Research involving both mice and patients with mutations in the HSL gene shows that the lack of this protein does not lead to excess fat or obesity. Instead, affected individuals experience a loss of fat mass, a condition known as lipodystrophy.
Although obesity and lipodystrophy appear to be complete opposites, both involve fat cells that do not function properly. As a result, each condition can contribute to metabolic disturbances and cardiovascular problems.
HSL Found in an Unexpected Location Inside Fat Cells
To understand this surprising behavior, a team led by Dominique Langin, professor at the University of Toulouse within the I2MC, took a closer look at where HSL is found inside adipocytes. The protein is well known for its role at the surface of lipid droplets, where it helps break down stored fat. However, the study revealed that HSL also resides inside the nucleus of fat cells. “In the nucleus of adipocytes, HSL is able to associate with many other proteins and take part in a program that maintains an optimal amount of adipose tissue and keeps adipocytes ‘healthy’,” explains Jérémy Dufau, co-author of the study, who completed his doctoral thesis on this topic.
The researchers also found that nuclear HSL levels are tightly controlled. Adrenaline, which activates the form of HSL located on lipid droplets, also encourages the protein to leave the nucleus. This process occurs naturally during fasting. In contrast, obese mice show elevated levels of HSL within the nucleus, suggesting a shift in this regulatory system.
A Revised Understanding of HSL’s Role in Metabolism
“HSL has been known since the 1960s as a fat-mobilizing enzyme. But we now know that it also plays an essential role in the nucleus of adipocytes, where it helps maintain healthy adipose tissue,” says Dominique Langin. This additional responsibility helps explain why the absence of HSL results in lipodystrophy, and it offers new insights into metabolic disorders such as obesity and related health complications.
This discovery appears at a critical time. In France, one in two adults is overweight or obese, and globally the number reaches two and a half billion people. Obesity increases the risk of a range of diseases, including diabetes and heart problems, and often reduces overall quality of life. Continued scientific research is crucial to improving prevention efforts and patient care.

8 hours agoShareSaveNoor NanjiCulture reporterShareSavePA MediaThe Princess of Wales has called for an end to the “stigma” surrounding addiction, and urged people to offer “empathy and support” to those dependent on alcohol, drugs or gambling.Catherine, who sent the message to mark Addiction Awareness Week, said “significant progress” has been made to better understand addiction, but warned more needs to be done.The princess is the patron of The Forward Trust, a charity that tries to break the cycle of addiction and is behind the campaign running from 23-30 November.Catherine, who has also campaigned on mental health issues, draws parallels between the two conditions in her message.She said addiction was “not a choice or a personal failing, but a complex mental health condition that should be met with empathy and support”.She added: “But still, even now in 2025, people’s experience of addiction is shaped by fear, shame and judgement. This needs to change.”The stigma surrounding those who face addiction allows it to thrive behind closed doors, impacting families and communities, and ultimately ruining lives.”The princess said that many people will know someone who is struggling with addiction.”Now is the moment to show our compassion and love to help them, or their friends and family, to reach out to organisations like The Forward Trust for support,” she said.”Recovery is hard, but with the right treatment it is possible. And this begins with a conversation, a listening ear and showing we care.”Catherine launched the first Addiction Awareness Week in 2021 on behalf of the trust and its Taking Action on Addiction campaign.She concluded her message by urging people to have open conversations to bring addiction and the harm it causes “out of the shadows”.PA MediaIt is not the first time Catherine has spoken out on the issue of addiction.In 2022, she gave her personal support to people struggling with addictions, telling them shame should not stop them getting help and urging a more compassionate public attitude towards the condition.Former England and Arsenal captain Tony Adams, who spent 11 years in addiction, has also recorded a video to launch a series of films demonstrating the power of open conversations in the journey to recovery.In the film, he reveals that a conversation with his mother-in-law Barbara was the catalyst to getting help.Adams, who is now chairman of trustees at the Forward Trust, said: “If you are struggling with an addiction or a mental health issue, then please reach out and get the appropriate help. The greatest thing I ever did was to say, ‘I can’t do this’.”The charity provides services including helping with employment and addressing the problems of addicts and addictions in prison.Before the Princess of Wales became the Forward Trust’s patron, she had twice visited the charity’s substance misuse services at HMP Send, a women’s prison in Surrey.The trust has also called for greater recognition of the scale of gambling inside prisons.

8 hours agoShareSaveFergus WalshMedical editorShareSaveChu familyA three-year-old boy has astounded doctors with his progress after becoming the first person in the world with his devastating disease to receive a ground-breaking gene therapy.Oliver Chu has a rare, inherited condition called Hunter syndrome – or MPSII – which causes progressive damage to the body and brain.In the most severe cases, patients with the disease usually die before the age of 20. The effects are sometimes described as a type of childhood dementia.Due to a faulty gene, before the treatment Oliver was unable to produce an enzyme crucial for keeping cells healthy. In a world first, medical staff in Manchester have tried to halt the disease by altering Oliver’s cells using gene therapy.Prof Simon Jones, who is co-leading the trial tells the BBC: “I’ve been waiting 20 years to see a boy like Ollie doing as well as he is, and it’s just so exciting.”At the centre of this remarkable story is Oliver – the first of five boys around the world to receive the treatment – and the Chu family, from California, who have put their faith in the medical team at Royal Manchester Children’s Hospital.A year after starting the treatment, Oliver now appears to be developing normally.”Every time we talk about it I want to cry because it’s just so amazing,” says his mother Jingru.The BBC has followed Oliver’s story for more than a year – including how scientists in the UK first developed the pioneering gene therapy and how the medical trial they are conducting almost didn’t get off the ground due to lack of funds.Stem cell removal – December 2024We first meet Oliver and his dad Ricky in December 2024 at the clinical research facility at Royal Manchester Children’s Hospital. It’s a big day.Since being diagnosed with Hunter syndrome in April, Oliver’s life – like that of his elder brother, Skyler, who also has the condition – has been dominated by hospital visits.Skyler had shown some late development in speech and coordination, but this had initially been put down to being born during Covid.Ricky tells me his sons’ diagnosis came as a complete shock.”When you find out about Hunter syndrome, the first thing the doctor tells you is ‘Don’t go on the internet and look it up because you’ll find the worst cases and you’ll be very, very disheartened’.””But, like anybody, you look it up and you’re like, ‘Oh my goodness, is this what’s going to happen to both my sons?'”Children are born apparently healthy, but around the age of two they start to show symptoms of the disease. These vary and can include changes to physical features, stiffness of the limbs and short stature. It can cause damage throughout the body, including to the heart, liver, bones and joints and in the most serious cases can lead to severe mental impairment and progressive neurological decline.Hunter syndrome almost always occurs in boys. It’s extremely rare, affecting one in 100,000 male births in the world.Until now, the only medicine available for Hunter syndrome was Elaprase, which costs around £300,000 per patient, per year and can slow the physical effects of the disease. The drug is unable to cross the blood-brain barrier and so does not help with cognitive symptoms.But today, Oliver is being hooked up to a machine and having some of his cells removed – the first crucial step in trying to halt his genetic disorder in this one-off treatment.”His blood is being passed through a fancy machine that is collecting a specific type of cell called stem cells which will be sent to a lab to be modified and then given back to him,” Dr Claire Horgan, consultant paediatric haematologist explains.Oliver’s cells are tweaked Oliver’s cells are carefully packaged and sent to a laboratory at Great Ormond Street Hospital (GOSH) in London.In Hunter syndrome, a genetic error means that cells are missing the instructions for making an enzyme, iduronate-2-sulfatase (IDS), essential for breaking down large sugar molecules which over time accumulate in tissues and organs.Scientists insert the missing IDS gene into a virus, which has its genetic material removed so that it can’t cause disease.A similar method has been used in other gene therapies, such as the treatment for another rare inherited condition, MLD.Dr Karen Buckland, from the Cell and Gene Therapy Service at GOSH, explains: “We use the machinery from the virus to insert a working copy of the faulty gene into each of the stem cells.”When those go back to Oliver, they should repopulate his bone marrow and start to produce new white blood cells and each of these will hopefully start to produce the missing protein [enzyme] in his body.”There still remains the issue of how to get enough of the missing enzyme into the brain.To overcome this, the inserted gene is modified so that the enzyme it produces crosses the blood-brain barrier more efficiently.Infusion day – February 2025We next meet Oliver back at the clinical research facility at Royal Manchester Children’s Hospital.This time he’s with his mum Jingru, while Ricky has stayed in California to look after Skyler.There is a sense of anticipation as a member of the research team opens a large metal cryopreservation tank where Oliver’s gene edited stem cells are frozen, having been transported back from GOSH.A small, clear infusion bag is removed and slowly brought to body temperature in a tray of liquid.After multiple checks, a nurse draws the clear fluid containing around 125 million gene-modified stem cells, into a syringe.Oliver is used to hospitals, but is fretful, and wriggles as the research nurse slowly injects the treatment, about a cup full, into a catheter in his chest.Jingru holds Oliver steady in her arms. After 10 minutes, the infusion is done.An hour later, a second, identical infusion is made. Oliver continues to watch cartoons on a portable screen, oblivious to the potential importance of what’s just happened.And that’s it. The gene therapy is complete. It seems to be all over rather quickly, yet the ambition here is huge: to stop Oliver’s progressive disease in its tracks, in a one-off treatment.After a couple of days, Oliver and Jingru fly back to California. Now the family, and the medical team must wait to see if the gene therapy has worked.Early signs of progress – May 2025In May, Oliver is back in Manchester for crucial tests to see if the gene therapy is working. This time the whole family is here.We meet in a park in central Manchester and it’s immediately clear that things are looking good.Oliver is more mobile and inquisitive than I’ve seen him. Admittedly, he now has the freedom to play and is out of hospital, but he appears brighter and healthier.Ricky is thrilled: “He’s doing really well. We have seen him progressing in his speech, and mobility. In just three months he has matured.”The really big news is that Oliver has been able to come off the weekly infusion of the missing enzyme.”I want to pinch myself every time I tell people that Oliver is making his own enzymes,” says Jingru. “Every time we talk about it I want to cry because it’s just so amazing.”She tells me he is “so different” from before the treatment, is talking “a ton” and is engaging more with other children.It is lovely to finally meet five-year-old Skyler who is very protective and caring towards his younger brother.”My wish upon the star is for Skyler, to be able to get the same treatment,” says Ricky. “It feels like Oliver has got a reset in his life, and I want the same thing for Skyler, even though he’s a bit older.”Initially it was thought that Oliver was too old for the trial, as the treatment cannot reverse existing damage, but tests showed he was still largely unaffected.Skyler seems to take delight in the world around him, and is keen to hold my hand and chat as we walk to the park.Ricky explains that Skyler has delayed development in speech and motor skills, but is undergoing infusion therapy, which gets the treatment to his body, but not his brain.’Eternally grateful’Oliver returns to Manchester every three months for a few days of follow-up tests.In late August, further checks confirm the gene therapy is working.Oliver is clearly thriving, and to date is now nine months post treatment.Prof Jones, whom Oliver calls Santa because of his white beard, is beaming: “Before the transplant Ollie didn’t make any enzyme at all and now he’s making hundreds of times the normal amount.”But more importantly, we can see he’s improving, he’s learning, he’s got new words and new skills and he’s moving around much more easily.”However, Prof Jones exercises a degree of caution: “We need to be careful and not get carried away in the excitement of all this, but things are as good as they could be at this point in time.”On the rooftop garden at the hospital, Oliver plays with his dad.”He’s like a completely different child. He’s running around everywhere, he won’t stop talking,” says Ricky.”The future for Ollie seems very bright and hopefully this means more kids will get the treatment.”In all, five boys have been signed up for the trial, from the US, Europe and Australia. None are from the UK as patients here were diagnosed too late to qualify.All the boys will be monitored for at least two years. If the trial is deemed a success, the hospital and university hope to partner with another biotech firm in order to get the treatment licensed.Prof Jones says the same gene therapy approach is being applied to other gene disorders.There are similar treatments on trial in Manchester for MPS type 1 or Hurler syndrome and MPS type 3 or Sanfilippo syndrome.Ricky and Jingru say they are “eternally grateful” to the Manchester team for allowing Oliver to join the trial.They say they are astonished by his progress in recent months.Oliver’s now producing the missing enzyme and his body and brain are healthy.”I don’t want to jinx it, but I feel like it’s gone very, very well,” says Ricky.”His life is no longer dominated by needles and hospital visits. His speech, agility and cognitive development have all got dramatically better.”It’s not just a slow, gradual curve as he gets older, it has shot up exponentially since the transplant.”The trial that almost never wasResearchers at the University of Manchester led by Prof Brian Bigger had spent more than 15 years working on creating the gene therapy for Hunter syndrome.In 2020 the university announced a partnership with a small US biotech company Avrobio, to conduct a clinical trial.But three years later the company handed back the licence to the university, following poor results from another gene therapy study and a lack of funds.The first-in-human trial, which would soon help Oliver, was in jeopardy before it had even begun.Prof Jones: “We had to move very quickly to try to save the whole idea and find another sponsor and another source of funding.”It was then that British medical research charity, LifeArc, stepped in, providing £2.5m of funding.CEO Dr Sam Barrell said: “A huge challenge for the more than 3.5 million people in the UK living with rare conditions, is getting access to effective treatments – currently 95% of conditions have none. “The Chu family are relieved the trial didn’t come to a halt and now hope Skyler may one day benefit from the same gene therapy as his brother.”I would walk to the end of the earth, backwards, forwards, upside down, barefoot, to make sure my kids have a better future,” says Ricky.Additional reporting Nat Wright and Brijesh Patel

The third stage of the Covid-19 Inquiry begins hearing evidence on Monday focusing on the measures taken to support workers’ incomes and keep businesses afloat when the pandemic struck.It will focus on what action the UK government, devolved administrations in Scotland, Wales and Northern Ireland, and local authorities took, how well schemes were designed and what was done to minimise fraud and waste.According to the Treasury £140bn was spent on support for businesses, much of it going to pay people’s wages when they were forced to stay at home.Last week the report on the second phase of the inquiry, into political decision-making, found the government had done “too little, too late”.The Covid Inquiry, chaired by Baroness Hallett, is expected to look at ten areas in total, and provide lessons for managing future pandemics.This next module, expected to last until just before Christmas, will examine the unprecedented economic intervention rolled out when the first lockdown was announced in March 2020.The largest scheme, the Coronavirus Job Retention Scheme, known as furlough, covered 11.7 million jobs between March 2020 and September 2021, at a cost of £70bn, paying a portion of employees’ wages to ensure they still had an income even if they could not go to work, and to keep businesses going so that they could reopen later.There was also a support scheme for self-employed people, loan schemes for businesses and business rates relief.At the time there was widespread praise for the prompt roll-out of support, especially in the travel and hospitality sectors where businesses were shuttered overnight. But questions were also raised over the scale of the programme, the strength of safeguards against fraud and error, and whether it delayed people taking up new work roles.This phase of the inquiry will also look at the additional funding provided for public services such as the railways to keep them running during lockdowns, and support for the voluntary and community sector.It will examine decisions on benefits, sick pay and support for vulnerable people.However, this part of the inquiry will not look at how the pandemic affected the economy as a whole.Baroness Coffey, the former work and pensions secretary, is due to appear on Wednesday, as well as Will Quince, the former welfare delivery minister.The first item on Monday will be an impact film featuring personal testimony from people affected, and opening submissions from lawyers for the inquiry itself and core participants. Labour market expert Mike Brewer, one of five experts commissioned to write reports on different aspects of the governments’ economic policy response, will be the first witness to give evidence on Tuesday morning. Also appearing are: Former Treasury officials James Benford and Dan York-SmithRepresentatives of the charities Child Poverty Action Group, Long Covid Support and Disability UKFormer Downing Street special adviser Ben WarnerFormer director general for analysis of the Covid-19 Taskforce, Robert Harrison.Rishi Sunak, who was chancellor of the exchequer during the pandemic, has confirmed that he will appear in a couple of weeks’ time.On Friday, he told Matt Chorley’s programme on BBC Radio 5 Live that the government and scientific community were “operating in a highly uncertain environment”. “I think we do need to view the decisions taken through that lens. “But it’s important that lessons [are] learned so that we can be better prepared if there’s ever another pandemic.”Last week the inquiry published a highly critical report on core decision-making during the pandemic, which described a “toxic and chaotic” culture at the centre of the UK government.Michael Gove, who was a cabinet minister at the time, told BBC Radio 4’s Today programme he wanted to “apologise to all those who lost loved ones during the pandemic – and to many others who made huge sacrifices”.The public hearings for this section of the inquiry – known as Module 9 – are scheduled to run for four weeks, ending on 18 December.

Former Prime Minister David Cameron has revealed he has been treated for prostate cancer.Lord Cameron, 59, told the Times newspaper his wife Samantha insisted that he go for a check-up after being inspired by a BBC radio interview with entrepreneur Nick Jones, who was campaigning for more men to be tested after being diagnosed himself.He had a prostate specific antigen (PSA) test earlier this year, followed by an MRI scan and a biopsy which confirmed the diagnosis. He was treated with focal therapy, which targets the area where the tumour is present using methods such as ultrasound waves to destroy cancel cells.Prostate cancer is the most common cancer in males in the UK, with around 55,000 new cases every year.Lord Cameron told the newspaper he wanted to use his platform to support a call by Prostate Cancer Research, a charity which counts Mr Jones – founder of private members’ club chain Soho House – as a trustee, for screening to be offered to high risk men.The cancer is most common in older age – among men over 75. Cases in the under-50s are rare. It is also more common in black men.”I don’t particularly like discussing my personal intimate health issues, but I feel I ought to,” Lord Cameron said.”Let’s be honest. Men are not very good at talking about their health. We tend to put things off.”But he said: “I sort of thought, well, this has happened to you, and you should lend your voice to it.”Lord Cameron, prime minister between 2010 and 2016 and later foreign secretary in Rishi Sunak’s government, told the Times: “I would feel bad if I didn’t come forward and say that I’ve had this experience. I had a scan. It helped me discover something that was wrong. It gave me the chance to deal with it.”There is currently no screening programme for prostate cancer in the UK because of concerns about the accuracy of PSA tests.But the peer’s intervention comes days after a major prostate cancer screening trial began in the country. It is aimed at finding the best way to detect the disease.Around one in eight men will develop prostate cancer in their lives, according to Prostate Cancer UK, with research showing it has overtaken breast cancer as the most commonly diagnosed form of the disease in the UK.

Researchers at Rutgers Health and collaborating institutions have uncovered why a widely used leukemia medication eventually stops helping most patients and have also identified a possible strategy to reverse this resistance.
The team pinpointed a protein that enables cancer cells to alter the shape of their mitochondria, the structures that generate cellular energy. This remodeling shields the cells from venetoclax (brand name, Venclexta), a common therapy for acute myeloid leukemia that often becomes less effective over time.
When scientists blocked this protein in mice carrying human acute myeloid leukemia, the experimental compounds restored venetoclax activity and extended the animals’ survival.
The study, published in Science Advances, highlights an unexpected form of drug resistance and offers a potential new direction for treating one of the most lethal blood cancers in adults.
How Altered Mitochondria Help Leukemia Cells Survive
“We found that mitochondria change their shape to prevent apoptosis, a type of cell suicide induced by these drugs,” said senior study author Christina Glytsou, an assistant professor at Rutgers’ Ernest Mario School of Pharmacy and Robert Wood Johnson Medical School and a member of the Rutgers Cancer Institute’s Pediatric Hematology and Oncology Research Center of Excellence (NJPHORCE).
Venetoclax can push many acute myeloid leukemia patients into remission by triggering cancer cell death. However, nearly all patients eventually develop resistance. The five-year survival rate remains 30 percent, and the disease claims about 11,000 lives in the United States each year.

OPA1 Identified as a Key Driver of Resistance
Through electron microscopy and genetic screens, Glytsou’s team determined that treatment-resistant leukemia cells produce unusually high amounts of OPA1, a protein that organizes the inner structure of mitochondria. Cells with elevated OPA1 develop tightly packed, more numerous folds in their mitochondrial membranes, known as cristae, which trap cytochrome c. Under normal conditions, cytochrome c escapes from the mitochondria to initiate cell death.
Researchers verified these findings in samples from leukemia patients. Individuals who had relapsed after therapy had significantly narrower cristae than newly diagnosed patients, with the most dramatic differences appearing in those previously treated with venetoclax.
Blocking OPA1 Restores Drug Sensitivity
To determine whether inhibiting this structural reshaping could restore treatment response, the team tested two experimental OPA1 inhibitors. In mice transplanted with human leukemia cells, adding the OPA1 inhibitors to venetoclax at least doubled survival time compared with venetoclax alone.
The combined approach was effective across multiple leukemia subtypes, including those with p53 mutations that are typically linked to poor outcomes and strong drug resistance.

Additional Weaknesses Revealed in Resistant Cells
The results also suggest that OPA1 inhibitors may have benefits beyond restoring standard cell death pathways. Experiments showed that cells lacking OPA1 rely heavily on the nutrient glutamine and become susceptible to ferroptosis, an iron-driven form of cell death that results from lipid damage.
Importantly, mouse studies indicated that these compounds did not interfere with normal blood cell development, which is essential when considering new leukemia treatments for people.
Early-Stage Work With Broad Potential
The research remains in its early stages. The OPA1 inhibitors, created by collaborators at the University of Padua in Italy, are still lead compounds and will require further refinement before clinical testing can begin.
“There is still some time to go through,” Glytsou said, noting that a third generation of compounds may be needed to improve solubility and other drug properties.
Even so, Glytsou believes this work points toward a promising therapeutic direction for stubborn leukemia cases and possibly other cancers as well. She is also a member of the cancer institute’s cancer pharmacology and cancer metabolism and immunology research programs.
OPA1 is overexpressed in several cancer types and is linked with poor outcomes and therapy resistance in breast cancer, lung cancer and other malignancies.
Rutgers Cancer Institute, in partnership with RWJBarnabas Health, is New Jersey’s only National Cancer Institute-designated Comprehensive Cancer Center.

Researchers at Tulane University, working with teams from eight additional institutions, have identified a previously unknown way that nerve cells send messages. This discovery could change how scientists understand pain and may guide the development of safer and more effective treatments.
The work was co-led by Matthew Dalva, director of the Tulane Brain Institute and professor of cell and molecular biology in the School of Science and Engineering, together with Ted Price at the University of Texas at Dallas. Their study shows that neurons can release an enzyme outside the cell that activates pain signals following an injury. The findings, reported in Science, also shed new light on how brain cells strengthen their connections during learning and memory.
External Enzyme Linked to Pain Activation
“This finding changes our fundamental understanding of how neurons communicate,” Dalva said. “We’ve discovered that an enzyme released by neurons can modify proteins on the outside of other cells to turn on pain signaling — without affecting normal movement or sensation.”
The researchers identified this enzyme as vertebrate lonesome kinase (VLK). They found that neurons use VLK to communicate in the space surrounding the cells, where it alters nearby proteins in ways that can influence how signals travel between nerve cells.
VLK’s Role in Cell Signaling and Drug Development
“This is one of the first demonstrations that phosphorylation can control how cells interact in the extracellular space,” Dalva said. “It opens up an entirely new way of thinking about how to influence cell behavior and potentially a simpler way to design drugs that act from the outside rather than having to penetrate the cell.”
The team discovered that active neurons release VLK, which increases the activity of a receptor involved in pain, learning and memory. When researchers removed VLK from pain-sensing neurons in mice, the animals did not experience normal post-surgical pain, yet their movement and sensory abilities remained intact. When VLK levels were increased, pain responses intensified.

Implications for Pain, Learning and Neural Plasticity
“This study gets to the core of how synaptic plasticity works — how connections between neurons evolve,” said Price, director of the Center for Advanced Pain Studies, professor of neuroscience at the University of Texas at Dallas’ School of Behavioral and Brain Sciences and a co-corresponding author of the study. “It has very broad implications for neuroscience, especially in understanding how pain and learning share similar molecular mechanisms.”
Dalva noted that the results point toward a safer strategy for altering pain pathways by focusing on enzymes such as VLK instead of blocking NMDA receptors. NMDA receptors help regulate communication between neurons but can cause significant side effects when disrupted.
Pathway May Simplify Future Drug Design
The findings also offer one of the first examples of how to influence interactions between proteins on the cell surface without entering the cell itself. Dalva said this could make drug development easier and reduce unintended effects, since the therapeutic agent would work outside the cell.
Next steps include determining whether this mechanism affects only a small set of proteins or represents a wider biological process that has gone largely unnoticed. If it proves to be widespread, it may reshape treatment strategies for neurological and other diseases.

Large Collaborative Effort
The research was carried out in partnership with colleagues at The University of Texas Health Science Center at San Antonio, The University of Texas MD Anderson Cancer Center, the University of Houston, Princeton University, the University of Wisconsin-Madison, New York University Grossman School of Medicine and Thomas Jefferson University.
“Our findings were only possible through this kind of collaboration,” Dalva said. “By combining Tulane’s expertise in synaptic biology with the strengths of our partners, we were able to reveal a mechanism that has implications not just for pain, but for learning and memory across species.”
The project was supported by grants from the National Institute of Neurological Disorders and Stroke, the National Institute on Drug Abuse and the National Center for Research Resources, all part of the National Institutes of Health. Co-first authors include Dr. Sravya Kolluru, Dr. Praveen Chander and Dr. Kristina Washburn, all members of The Dalva Lab at Tulane.

Cancer biology, drug safety studies and aging research may all benefit from a fluorescent sensor created at Utrecht University. The new technology gives scientists the ability to watch DNA damage and repair unfold inside living cells in real time. This development, described in Nature Communications, enables types of experiments that were not previously possible.
DNA in our cells faces continual harm from sunlight, chemicals, radiation and even the normal processes that keep the body functioning. Most of this damage is corrected very quickly. When these repairs fail, the resulting errors can play a role in aging, cancer and several other diseases.
For years, researchers struggled to directly observe these repair events as they occurred. Many traditional approaches required killing and preserving cells at different time points, producing only isolated snapshots instead of a continuous view.
A New DNA Damage Sensor for Living Cells
Scientists at Utrecht University have now introduced a sensor that changes this situation. Their tool allows researchers to watch damage appear and fade inside living cells and also inside living organisms. According to the study published in Nature Communications, this capability opens the way to experiments that were previously out of reach.
Lead researcher Tuncay Baubec describes the approach as a method for looking inside a cell “without disrupting the cell.” He notes that common tools such as antibodies and nanobodies often bind too tightly to DNA, which can interfere with the cell’s own repair systems.
“Our sensor is different,” he says. “It’s built from parts taken from a natural protein that the cell already uses. It goes on and off the damage site by itself, so what we see is the genuine behavior of the cell.”
How the Fluorescent Sensor Works

The system relies on a fluorescent tag attached to a small domain taken from one of the cell’s own proteins. This domain briefly recognizes a marker that appears only on damaged DNA. Because the interaction is gentle and reversible, the sensor highlights the affected region while leaving the cell’s repair work untouched.
Biologist Richard Cardoso Da Silva, who helped design and evaluate the tool, recalls the moment he recognized its potential. “I was testing some drugs and saw the sensor lighting up exactly where commercial antibodies did,” he says. “That was the moment I thought: this is going to work.”
A Continuous View of DNA Repair
The contrast with older methods is striking. Instead of running many separate experiments to capture different moments, researchers can now watch the entire repair sequence as a single continuous movie. They can track when the damage appears, observe how rapidly repair proteins arrive and see when the cell resolves the issue. “You get more data, higher resolution and, importantly, a more realistic picture of what actually happens inside a living cell,” says Cardoso Da Silva.
The research team also tested the sensor outside the lab dish. Collaborators at Utrecht University used the tool in the worm C. elegans, a widely used model organism. The sensor performed equally well and revealed programmed DNA breaks that occur during the worm’s development. For Baubec, this demonstration was essential. “It showed that the tool is not only for cells in the lab. It can be used as well in real living organisms.”
The potential applications extend beyond watching repair occur. The sensor’s protein domain can be connected to other molecular components, allowing scientists to map the locations of DNA damage across the genome or determine which proteins gather around a damaged region. Researchers can also reposition damaged DNA inside the nucleus to test how its location influences repair. “Depending on your creativity and your question, you can use this tool in many ways,” says Cardoso Da Silva.

Better Tools for Medical and Drug Research
Although the sensor is not a treatment, it could significantly improve medical research. Many cancer therapies work by inflicting deliberate DNA damage on tumor cells, and early drug development often requires precise measurements of how much damage a compound creates.
“Right now, clinical researchers often use antibodies to assess this,” Baubec says. “Our tool could make these tests cheaper, faster and more accurate.” The team also sees potential uses in clinical settings, such as studying natural aging or detecting exposure to radiation or other mutagenic factors.
The innovation is already attracting interest. Several laboratories contacted the team before publication, eager to use the sensor in their own repair studies. To support this demand, the researchers have made the tool available without restrictions. Baubec notes, “Everything is online. Scientists can use it immediately.”

Researchers at Baylor College of Medicine have identified a natural process in the brain that can remove existing amyloid plaques in mouse models of Alzheimer’s disease while also helping preserve memory and thinking ability. This process relies on astrocytes, star shaped support cells, which can be guided to clear out the toxic plaque buildup commonly seen in Alzheimer’s. When the team increased the amount of Sox9, a protein that influences many astrocyte functions during aging, the cells became more effective at removing amyloid deposits. The findings, reported in Nature Neuroscience, suggest that strengthening astrocyte activity could one day help slow cognitive decline linked to neurodegenerative disorders.
“Astrocytes perform diverse tasks that are essential for normal brain function, including facilitating brain communications and memory storage. As the brain ages, astrocytes show profound functional alterations; however, the role these alterations play in aging and neurodegeneration is not yet understood,” said first author Dr. Dong-Joo Choi, who conducted this work while at the Center for Cell and Gene Therapy and the Department of Neurosurgery at Baylor. Choi is now an assistant professor at the Center for Neuroimmunology and Glial Biology, Institute of Molecular Medicine at the University of Texas Health Science Center at Houston.
Focusing on Sox9 as a Key Regulator
For this project, the investigators set out to understand how astrocytes change with age and how those changes relate to Alzheimer’s disease. Their attention centered on Sox9, a protein that influences a wide network of genes involved in astrocyte aging.
“We manipulated the expression of the Sox9 gene to assess its role in maintaining astrocyte function in the aging brain and in Alzheimer’s disease models,” explained corresponding author Dr. Benjamin Deneen, professor and Dr. Russell J. and Marian K. Blattner Chair in the Department of Neurosurgery, director of the Center for Cancer Neuroscience, member of the Dan L Duncan Comprehensive Cancer Center at Baylor and principal investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital.
Testing the Approach in Symptomatic Alzheimer’s Models
“An important point of our experimental design is that we worked with mouse models of Alzheimer’s disease that had already developed cognitive impairment, such as memory deficits, and had amyloid plaques in the brain,” Choi said. “We believe these models are more relevant to what we see in many patients with Alzheimer’s disease symptoms than other models in which these types of experiments are conducted before the plaques form.”
In these models, the researchers either increased or removed Sox9 and then monitored each mouse’s cognitive performance for six months. During this period, the animals were tested on their ability to recognize familiar objects and locations. After the behavioral studies were completed, the team examined the brains to measure plaque accumulation.

Higher Sox9 Levels Improve Plaque Removal and Memory
The results showed a clear difference. Lowering Sox9 led to faster plaque buildup, reduced structural complexity in astrocytes and diminished plaque clearing. Raising Sox9 had the opposite effect, increasing the cells’ activity, supporting plaque removal and preserving cognitive performance. The protective benefits suggested that strong astrocyte engagement may help slow the cognitive decline associated with neurodegenerative disease.
“We found that increasing Sox9 expression triggered astrocytes to ingest more amyloid plaques, clearing them from the brain like a vacuum cleaner,” Deneen said. “Most current treatments focus on neurons or try to prevent the formation of amyloid plaques. This study suggests that enhancing astrocytes’ natural ability to clean up could be just as important.”
Future Potential and Ongoing Research Needs
Choi, Deneen and their colleagues note that additional research is needed to understand how Sox9 behaves in the human brain across time. Still, these results point toward the possibility of developing therapies that harness astrocytes’ natural cleaning abilities to combat neurodegenerative disorders.
Sanjana Murali, Wookbong Kwon, Junsung Woo, Eun-Ah Christine Song, Yeunjung Ko, Debo Sardar, Brittney Lozzi, Yi-Ting Cheng, Michael R. Williamson, Teng-Wei Huang, Kaitlyn Sanchez and Joanna Jankowsky, all at Baylor College of Medicine, also contributed to this work.
This research was supported by National Institutes of Health grants (R35-NS132230, R01-AG071687, R01-CA284455, K01-AG083128, R56-MH133822). Additional funding came from the David and Eula Wintermann Foundation, the Eunice Kennedy Shriver National Institute of Child Health & Human Development of the National Institutes of Health under Award Number P50HD103555 and from shared resources provided by Houston Methodist and Baylor College of Medicine.