• 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.

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.

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.”

“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.