Obesity Care

Internalised Weight Stigma Places Heavy Emotional Burden on People Seeking Bariatric Care, Indian Study Finds

Key Takeaways:

• More than 71 percent of participants preparing for metabolic and bariatric surgery reported high levels of internalised weight bias, with many expressing self-blame, shame, and reduced self-worth.
  
• Younger individuals and those with a higher BMI reported stronger internalised stigma, which affected emotional well-being, social relationships, and readiness to seek treatment.
  
• Researchers and clinicians stress that obesity is a chronic disease, not a personal failing, and warn that stigma significantly harms mental health and delays access to appropriate care.
  
  

Introduction

A new study has highlighted the profound emotional and psychological toll experienced by people living with obesity who are preparing for metabolic and bariatric surgery. The research found that internalised weight bias is widespread among individuals seeking specialist care, with many reporting depressive symptoms, reduced self-esteem, and deep feelings of self-criticism linked to their weight.

The pilot study, titled The Burden from Within—An Indian Pilot Study on Weight Bias Internalisation, was published in Obesity Surgery, the international journal of the International Federation for the Surgery and Other Therapies for Obesity (IFSO).

Weight stigma beginning in childhood and persisting into adulthood

Lead author Dr Aparna Govil Bhasker, a Mumbai-based bariatric surgeon at the MetaHeal Laparoscopy and Bariatric Surgery Centre, told The Indian Express that stigmatising experiences often begin early in life. She explained that weight-related bullying is common during childhood and continues into adulthood for many people.

“People living with obesity are frequently judged as lazy or lacking willpower. Negative media portrayals, especially weight-based memes and stigmatising content, only deepen these harmful beliefs. Post-pandemic trends show that online negativity toward obesity has grown even stronger,” she said.

Study design and participant profile

To assess the emotional impact of obesity on people seeking surgical intervention, the research team evaluated 142 participants using the validated Weight Bias Internalization Scale (WBIS). Of the total cohort, 78.9 percent were women, and all participants had a body mass index of at least 27.5 kg/m².

Researchers examined total WBIS scores, associations with age, and correlations with BMI to understand how internalised stigma manifests in individuals preparing for metabolic and bariatric surgery.

High prevalence of internalised weight bias

The study revealed striking levels of internalised stigma:

• More than 71.1 percent of participants scored above the neutral benchmark on the WBIS, indicating widespread internalisation of negative weight-based beliefs.
  
• Around 74.6 percent reported feeling depressed about their weight.
  
• More than half felt less attractive because of their weight.
  
• More than one-third questioned their own competence.

The findings indicate that weight stigma does not simply come from external sources. Many participants had come to believe the negative stereotypes directed at them.

Self-judgement, self-hate, and social avoidance

The report found that more than half of the individuals surveyed expressed intense self-criticism, including feelings of self-hatred related to their weight. Many participants described weight as a defining measure of their personal worth.

Social relationships were also severely affected. Approximately 45.8 percent of participants questioned why anyone they considered attractive would want to date them. Half believed they did not deserve a fulfilling social life until they lost weight.

The data also showed that younger participants experienced stronger internalised bias, while those with higher BMI levels demonstrated deeper self-directed stigma.

“This shows that obesity status and internalisation of weight bias affect social interactions, connections, and relationships, which can have a long-lasting impact on the life course of an individual’s personal, emotional, occupational, and financial trajectory,” Dr Govil Bhasker said.

Obesity rising rapidly in India but not recognised as a disease

The researchers noted that obesity rates in India have nearly doubled since 2005. Data from the fifth National Family Health Survey (2019–21) show that 24 percent of women and 22.9 percent of men aged 15 to 49 years live with overweight or obesity.

Despite this rapid rise, obesity is not officially classified as a disease in India. Dr Govil Bhasker argued that the findings underline the deep societal stigma embedded in attitudes toward obesity.

“Patients often feel ashamed, guilty, and discouraged. They endure years of negative comments, judgment, and misinformation, and over time, these negative experiences become internalized. This affects their self-worth and mental health and can delay their decision to seek proper treatment. Obesity is a chronic disease, not a personal failure, and supporting patients emotionally is just as important as helping them medically,” she said. She added that targeted interventions are urgently needed.

Stigma’s broad impact on mental and physical health

Dr Vishakha Jain, Professor of Medicine at AIIMS BibiNagar and one of the study’s co-authors, emphasised that stigma infiltrates every aspect of daily life.

She explained that persistent stigma affects physical health, mental well-being, occupational performance, and social relationships. It can contribute to unhealthy eating patterns and biological stress responses, including increased inflammation.

“Together, these pressures create a cycle of self-blame and prejudice, often making individuals feel undeserving of care,” Dr Jain said.

Conclusion

The study provides compelling evidence that internalised weight stigma is highly prevalent among people preparing for bariatric care in India and that it carries profound psychological, social, and behavioural consequences. The authors urge greater recognition of obesity as a chronic disease and call for emotional as well as medical support for individuals affected.

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Early-life Exposure to Fat-related Food Odours May Shape Lifelong Obesity Risk

Key Takeaways: 

• Early exposure to fat-related food odours during development may prime the brain and body for heightened metabolic responses to high-fat foods later in life.
  
• Sensory cues from a maternal diet, independent of nutritional content or maternal metabolic status, can influence thermogenesis, gene expression, and susceptibility to obesity in adult mice.
  
• Findings suggest a previously underappreciated mechanism of metabolic programming, in which food odours encountered during gestation and lactation can affect lifelong dietary preferences and obesity risk.
  
  

Introduction

A recent study published in Nature Metabolism explores how non-nutritive sensory cues from foods rich in fat, particularly odours, influence the developing brain and metabolic pathways. The research investigates how these early sensory inputs may shape central responses to food cues, metabolic health, and the risk of obesity in adulthood. The findings expand on a substantial body of work showing that early-life nutritional exposure influences later metabolic outcomes, but highlight the specific and previously overlooked contribution of fat-related odours.

Maternal obesity and early nutritional exposure

How maternal diet affects offspring

Developmental exposure to a maternal diet high in calories and fat is a well-recognised risk factor for obesity and metabolic disorders throughout life. Numerous studies have linked maternal high-fat diet (HFD) consumption with outcomes such as excess gestational weight gain, insulin resistance, and increased adiposity in mothers, all of which may contribute to lifelong metabolic vulnerability in offspring.

Despite these strong associations, the specific components of HFDs that drive metabolic programming remain only partly understood. While nutrients themselves contribute directly to energy balance and metabolic pathways, foods also contain non-nutritive sensory elements, including volatile odours. Fetuses and newborns experience these odours during development, meaning that sensory exposure is layered on top of nutritional exposure.

Sensory memories formed early in life

Perinatal olfactory experiences contribute to the formation of sensory memories that influence food preferences and eating habits into adulthood. The authors emphasise that understanding how non-nutritive cues from a maternal HFD influence long-term dietary preferences and metabolic responses is crucial for clarifying early-life drivers of obesity risk.

Study approach

Separating nutritional and sensory influences

To distinguish nutritional caloric components from sensory components, the researchers designed an isonutritional model using a standard normal chow diet (NCD) infused with fat-related odours. This bacon-flavoured diet (BFD) enabled researchers to expose mice to fat-related sensory cues without increasing calorie content.

• BFD: NCD enriched with bacon odours, designed to mimic the odour profile of a standard lard-based high-fat diet (HFDlard).
  
• HFDbutter: A butter fat-based HFD used to represent a non-pork, high-fat option.
  

This design allowed the researchers to isolate the effect of fat-related sensory exposure during development, independent of maternal metabolic changes such as insulin resistance, weight gain, or altered lipid levels.

Odour profile analysis

A detailed chemical characterisation identified 155 volatile compounds across the diets, including aldehydes, ketones, and alcohols. Hierarchical clustering revealed:

• HFD and HFDlard shared high sensory similarity
  
• Both differed significantly from HFDbutter and NCD
  
• BFD’s odour profile closely matched HFDlard, yet its nutritional profile remained identical to NCD
  

These findings confirmed that BFD was an appropriate tool for studying sensory-specific metabolic programming.

Sensory cues and neural activation

Experimental analyses showed that fat-related food odours induced phosphorylation of S6 in olfactory sensory neurons (OSNs), demonstrating that the odours elicited detectable neural activation. Mice perceived BFD as more similar to HFDlard than to NCD, reinforcing that the sensory model accurately represented fat-related olfactory cues.

Early exposure and adult metabolism

Developmental exposure primes obesogenic responses

Control mice exposed only to NCD during development (NCDdev) showed no changes in interscapular brown adipose tissue (iBAT) thermogenesis or hepatic mechanistic target of rapamycin (mTOR) phosphorylation when later exposed to HFDlard odours. In contrast, mice developmentally exposed to BFD (BFDdev) displayed significant increases in both iBAT temperature and hepatic p-mTOR when encountering these odours for the first time in adulthood.

This indicates that early exposure to fat-related odours enhances metabolic responsiveness to high-fat sensory cues later in life.

Independent of maternal obesity

Importantly, these heightened responses occurred without maternal insulin resistance, adiposity, or weight gain. This demonstrates that sensory exposure alone, rather than changes in maternal metabolism, can programme obesity risk.

Sex-specific sensitivity

• Females: Lactation appeared to be the most sensitive developmental window for programming effects.
  
• Males: Required exposure throughout the entire developmental period to exhibit similar heightened metabolic responses.
  
  
  

Responses to different high-fat diets

Eight-week-old BFDdev and NCDdev mice were also exposed to HFDbutter. The aim was to test whether heightened susceptibility required precise sensory matching or whether vulnerability generalised across high-fat diets.

Findings showed that early exposure to fat-related sensory cues increased obesity susceptibility even when adult exposure involved a high-fat diet with different sensory characteristics. This suggests that early sensory programming affects broad metabolic pathways rather than specific flavour-diet associations.

While a perfect sensory match between early and later exposure was not necessary, some degree of sensory similarity still appeared relevant in shaping metabolic outcomes.

Changes in the maternal environment

The study found that feeding mothers BFD altered the volatile odour profile of both amniotic fluid and milk. These changes exposed developing offspring to fat-related sensory information during gestation and lactation, influencing their early sensory learning and shaping later responses to food.

Impairments in thermogenesis and metabolic flexibility

BFDdev mice demonstrated reduced iBAT thermogenesis compared with NCDdev controls. They also exhibited lower expression of thermogenic-related genes in iBAT, including:

• Cidea
• Pparg
  

These findings indicate that developmental exposure to fat-related odours impairs metabolic flexibility and weakens homeostatic responses to hypercaloric diets in adulthood.

Altered neuronal responses to fat

The researchers reported a specific impairment in Agouti-related peptide (AgRP) neuronal responsiveness to dietary fat in BFDdev mice. These neurons help regulate hunger and energy balance. Despite this, responses to major hormonal signals remained unaffected, suggesting that sensory-specific pathways were selectively disrupted.

Conclusion

The study provides compelling evidence that early-life exposure to fat-related food odours can contribute to long-term obesity risk by shaping metabolic and neuronal responses long before an individual consumes high-fat foods. These sensory cues act independently of calorie exposure and maternal metabolic health, highlighting a novel pathway through which obesity susceptibility may be programmed. Although the research was conducted in mice, it underscores the potential importance of early sensory environments in influencing metabolic health across the lifespan.

CCH insights:

This is fascinating research. We already know that the diet of a pregnant woman can influence the dietary preferences and health outcomes of her child, but now it appears odours of certain foods during pregnancy may have similar affects. It adds an intriguing new line of investigation in terms of the Developmental Origins of Health and Disease. However, we must remember this study was in mice, using bacon odours to mimic a lard-based high fat diet, so we are a long way from being able to draw conclusions about real world implications for pregnant women.

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Mice Study Connects Soybean Oil Intake to Liver Changes and Obesity

Key Takeaways: 

• New research in mice suggests that weight gain linked to soybean oil is driven by the metabolic products of linoleic acid rather than the oil itself.
  
• Genetically engineered mice resistant to obesity on a high-fat soybean oil diet produced fewer oxylipins and showed healthier liver function.
  
• Scientists believe differences in human genetics, enzyme levels, and metabolic stress may influence people’s susceptibility to soybean-oil-related metabolic effects.
  
  

A closer look at soybean oil and obesity

Soybean oil is the most widely consumed cooking oil in the United States and is a key ingredient in many processed foods. A growing body of research has associated high intake of soybean oil with weight gain in animals. A new study from the University of California, Riverside (UCR), published in the Journal of Lipid Research, provides fresh insight into why this may occur.

Researchers found that mice consuming a high-fat diet rich in soybean oil gained considerable weight. However, a separate group of genetically engineered mice did not, despite eating the same diet. These altered mice carried a slightly different version of a liver protein that affects the expression of hundreds of genes involved in fat metabolism.

The findings point toward a metabolic mechanism that may help explain differences in weight gain among individuals exposed to similar diets.

“This may be the first step toward understanding why some people gain weight more easily than others on a diet high in soybean oil,” said Sonia Deol, a UCR biomedical scientist and corresponding author of the study.

The role of HNF4α in fat metabolism

In humans, both forms of the liver protein known as HNF4α occur naturally. However, the alternative version typically appears only under certain conditions, such as chronic illness, prolonged fasting, metabolic stress, or alcoholic fatty liver disease. These variations, combined with factors such as age, sex, medication use, and underlying genetics, may influence how different people respond to high levels of soybean oil in their diet.

The UCR team believes that the altered form of HNF4α in genetically engineered mice changes how the body processes linoleic acid, a major fatty acid in soybean oil.

Building on earlier research

The study adds to previous findings from the same research group.

“We’ve known since our 2015 study that soybean oil is more obesogenic than coconut oil,” said Frances Sladek, a UCR professor of cell biology. “But now we have the clearest evidence yet that it’s not the oil itself, or even linoleic acid. It’s what the fat turns into inside the body.”

One of the major metabolic products of linoleic acid is a group of molecules called oxylipins. These compounds are associated with inflammation, fat accumulation, and other metabolic changes.

Oxylipins and their link to weight gain

Mice engineered to produce the alternative form of HNF4α showed markedly lower levels of oxylipins in their livers, despite consuming a high-fat soybean oil diet. They also had healthier liver profiles and enhanced mitochondrial function. Improved mitochondrial activity may help explain their resistance to weight gain.

Researchers pinpointed specific oxylipins derived from both linoleic acid and alpha-linolenic acid (another fatty acid found in soybean oil) that appeared necessary for weight gain in regular mice.

However, the picture is complex. Even though transgenic mice on a low-fat diet showed elevated oxylipin levels, they did not become obese. This suggests that while these molecules contribute to weight gain, they are unlikely to be the sole drivers. Other metabolic conditions must also play a role.

Genetic variation in enzyme levels

Further analysis revealed that the modified mice had far lower levels of two key enzyme families responsible for converting linoleic acid into oxylipins. These enzymes are highly conserved across all mammals, including humans, and can vary significantly from person to person based on factors such as genetics and diet.

The scientists also observed that oxylipin levels in the liver, rather than in the bloodstream, were correlated with body weight. This indicates that standard blood tests may not reliably detect early metabolic disturbances linked to diet.

Soybean oil’s rise in the American diet

Soybean oil consumption in the United States has risen dramatically over the past century. It has increased from around 2 percent of total daily calories to almost 10 percent. Although soybeans provide protein and the oil contains no cholesterol, modern diets deliver far greater quantities of linoleic acid than the body is likely evolved to manage.

In line with this, the UCR study found that soybean oil intake was associated with increased cholesterol levels in mice despite the oil containing no dietary cholesterol. This reflects the complex interplay between dietary fats and internal metabolic pathways.

Questions for future research

The team now aims to understand precisely how oxylipin formation leads to weight gain and whether oils with similarly high linoleic acid content – including corn, sunflower, and safflower oils – trigger comparable effects.

“Soybean oil isn’t inherently evil,” said Deol. “But the quantities in which we consume it is triggering pathways our bodies didn’t evolve to handle.”

Although the researchers have no plans for human trials, they hope the findings will inform future studies and guide public health policy.

“It took 100 years from the first observed link between chewing tobacco and cancer to get warning labels on cigarettes,” Sladek noted. “We hope it won’t take that long for society to recognise the link between excessive soybean oil consumption and negative health effects.”

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Scientists Discover Key Protein Triggering Inflammation Linked to Obesity and Type 2 Diabetes

Key Takeaways:

• Researchers have identified FAM20C as a protein that triggers inflammation and insulin resistance in fat cells, a process linked to type 2 diabetes.
  
• Blocking or removing the FAM20C gene in mice improved insulin sensitivity and reduced inflammation, even without weight loss.
  
• High levels of FAM20C in human fat tissue are associated with insulin resistance, suggesting a potential new therapeutic target.
  
  

Early trigger identified in obesity-related inflammation

Investigators at Weill Cornell Medicine have uncovered an early step in the chain of events that links obesity to inflammation and insulin resistance – key contributors to the development of type 2 diabetes.

Their findings, published on 28 October in the Journal of Clinical Investigation, identify a protein known as FAM20C as a critical “switch” that initiates inflammation within fat cells. The study, conducted in mice, shows that when this protein is removed or blocked, metabolic health improves markedly, even without weight loss.

“By inhibiting or getting rid of FAM20C in fat cells, the mice became healthier even at the same body weight,” said senior author Dr James Lo, the Rohr Family Clinical Scholar and an Associate Professor of Medicine in the Division of Cardiology at Weill Cornell Medicine. “Their fat becomes metabolically healthier, reducing harmful inflammation in fat cells that can lead to chronic diseases like type 2 diabetes, fatty liver disease and heart disease.”

FAM20C: A molecular switch for inflammation

The research team, led by first author Dr Ankit Gilani, a Research Associate in Medicine at Weill Cornell Medicine, discovered FAM20C while screening genes that were switched on in the fat cells of mice with obesity and inflammation. FAM20C belongs to a class of enzymes known as kinases, which work by adding phosphate groups to other proteins – a process that can alter their activity and influence gene expression.

When the researchers increased the production of FAM20C in fat cells, the cells began releasing inflammatory molecules and became resistant to insulin. In contrast, blocking or deleting the gene in mice with obesity had the opposite effect – it reduced inflammation, improved insulin sensitivity, and decreased the accumulation of visceral fat (fat surrounding internal organs), even when total body weight remained unchanged.

“During obesity, when this gene is switched on in the adipose tissue, it causes inflammation,” Dr Gilani explained. “It drives the expression of other inflammatory genes, and then it causes insulin resistance, which can lead to type 2 diabetes.”

Evidence from human fat tissue

To determine whether the same mechanism operates in humans, the researchers analysed visceral fat tissue samples from individuals living with obesity. They found that higher levels of FAM20C were associated with insulin resistance – a key driver of type 2 diabetes – while people with lower FAM20C levels tended to exhibit better metabolic health despite having overweight or obesity.

These findings suggest that the FAM20C pathway could play a pivotal role in determining whether fat tissue becomes inflamed and metabolically harmful or remains relatively benign.

Next Steps: Targeting FAM20C and its downstream pathways

The research team now plans to investigate how FAM20C influences other tissues involved in metabolism and metabolic disease. They are particularly interested in a protein called CNPY4, which is activated by FAM20C and appears to be central to the inflammatory process.

“CNPY4 is going to be a major focus of future research to see how strongly it affects insulin resistance, and whether it could be a target for therapies to treat or prevent insulin resistance,” said Dr Lo, who is also a member of the Weill Center for Metabolic Health and the Cardiovascular Research Institute at Weill Cornell Medicine, and a cardiologist at NewYork-Presbyterian/Weill Cornell Medical Center.

Ultimately, the team hopes to develop small-molecule drugs that can block FAM20C or CNPY4 activity. Such therapies could reduce inflammation, lower visceral fat levels, improve insulin sensitivity, and help prevent or treat type 2 diabetes. Dr Lo noted that these treatments might one day be used alongside weight loss medications, or to support people who continue to experience metabolic inflammation and cardiovascular risk even after losing weight.

Funding and support

This research was supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH), through grants R01DK121140 and R01DK121844.

CCH insights

For a long time now we have known that inflammation in visceral adipose tissue is a major factor in insulin resistance, but it is still unknown why some people with obesity experience this adipose tissue inflammation and subsequent metabolic dysfunction, while other people with obesity do not. This research suggests that the FAM20C protein may contribute to this switch from healthy adipose tissue to inflamed, dysfunctional adipose tissue, and could offer an exciting new therapeutic pathway for type 2 diabetes and other cardiometabolic conditions.

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Weight Training Outperforms Running in Blood Sugar Control, Virginia Tech Mice Study Shows

Key Takeaways:

• Researchers at Virginia Tech found that resistance training was more effective than running in improving glucose tolerance and reducing insulin resistance in mice fed a high-fat diet.
  
• Both endurance and resistance exercise reduced body fat and improved blood sugar regulation, but resistance training yielded stronger metabolic benefits.
  
• The study suggests that strength training could play a particularly valuable role in preventing and managing Type 2 diabetes.
  
  

Weightlifting may offer unique metabolic benefits

Running is widely recognised for its cardiovascular and calorie-burning benefits, but new preclinical findings from the Fralin Biomedical Research Institute at Virginia Tech Carilion suggest that lifting weights may be even more effective for controlling blood sugar and reducing body fat.

Published on 30 October in the Journal of Sport and Health Science, the study compared the effects of endurance and resistance exercise in mice fed a high-fat diet, a common experimental model for obesity, hyperglycaemia, and Type 2 diabetes.

The team, led by Professor Zhen Yan, an exercise medicine researcher and director of the institute’s Centre for Exercise Medicine Research, found that while both running and weight training improved the body’s ability to clear excess glucose from the bloodstream, resistance training had a stronger impact on reducing both subcutaneous and visceral fat, improving glucose tolerance, and lowering insulin resistance.

“We all want to live a long, healthy life,” said Yan. “We all know the benefits of regular exercise. There is plenty of evidence in humans that both endurance exercise, such as running, and resistance exercise, such as weightlifting, are effective in promoting insulin sensitivity.”

Although both types of activity are known to improve metabolic function, the researchers noted that there had previously been no rigorous, controlled comparison between them.

Developing a model for ‘mouse weightlifting’

To address this gap, the Virginia Tech team created a first-of-its-kind preclinical model of resistance training in mice.

In their experiment, the mice lived in custom-built cages where food was available only through a hinged, weighted lid. To eat, the mice had to lift the lid while wearing a small shoulder collar, performing a movement similar to a human squat. The load was gradually increased over time, effectively replicating progressive strength training.

Meanwhile, the endurance group of mice was given unrestricted access to a running wheel, a standard model for voluntary aerobic exercise. Control groups included sedentary mice maintained on either a normal or high-fat diet.

Over an eight-week period, the researchers monitored changes in body weight, fat distribution, and body composition. They measured exercise capacity with treadmill tests, assessed cardiovascular and muscular performance, and evaluated blood sugar regulation. Muscle tissue samples were also analysed to study insulin signalling at the molecular level.

Using their novel resistance training model, the team could directly compare the metabolic outcomes of running and strength exercise under controlled conditions.

“Our data showed that both running and weightlifting reduce fat in the abdomen and under the skin and improve blood glucose maintenance with better insulin signalling in skeletal muscle,” Yan said. “Importantly, weightlifting outperforms running in these health benefits.”

Implications for obesity and diabetes prevention

Obesity and Type 2 diabetes remain among the most pressing public health challenges, driven largely by high-fat diets and sedentary lifestyles. The new study supports existing clinical evidence showing that endurance, resistance, and high-intensity interval training all contribute to better long-term blood sugar control, reduced body mass index, lower blood pressure, and improved overall well-being.

However, this Virginia Tech study fills a critical gap by directly comparing the two types of exercise in a controlled model of diet-induced obesity. The findings may have important implications for exercise recommendations and diabetes prevention strategies.

“The findings also bring good news for people who, for any number of reasons, cannot engage in endurance-type exercise,” Yan explained. “Weight training has equal, if not better, anti-diabetes benefits.”

Exploring new mechanisms and future therapies

The researchers also observed molecular changes in skeletal muscle that may help explain the enhanced benefits of resistance training. These shifts in insulin signalling pathways could, according to the team, inform the development of new drug therapies for managing Type 2 diabetes.

Interestingly, the improvements seen with resistance training were not directly linked to increased muscle mass or superior exercise performance, suggesting that unique metabolic mechanisms may be at work.

Yan emphasised that although pharmacological interventions such as GLP-1 receptor agonists are valuable tools in diabetes management and weight loss, they cannot replace the broad, systemic benefits of physical activity.

“The take-home message is that you should do both endurance and resistance exercise, if possible, to get the most health benefit,” he said.

The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health and by the Red Gates Foundation, with collaborators from the University of Virginia contributing to the work.

CCH insights

This is an interesting study, but it is important to note it was conducted in mice, not humans. Having said that, perhaps the most reassuring thing about these results is that both types of exercise provided metabolic health benefits. The critical thing about physical activity is that any amount and type is better than doing none, and while a combination of endurance and resistance is probably best, if you can only manage one type or the other, it will have a positive impact.

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Childhood Obesity in England Reaches Highest Level Since Pandemic, New Data Reveal

Key Takeaways: 

• One in ten children aged four to five in England are living with obesity, the highest rate since the COVID-19 pandemic.
  
• Teachers warn that poverty, limited access to nutritious food, and cuts to school sport funding are fuelling the crisis.
  
• Nearly all teachers agree that healthy eating improves pupil focus, energy, and behaviour, yet many report children arriving at school hungry.
  
  
  

Childhood obesity at record levels outside pandemic years

Newly released data from the National Child Measurement Programme (NCMP) show that 10.5% of children aged four to five (Reception year) in England are living with obesity – the highest prevalence recorded outside of the pandemic period.

The NCMP, which annually measures the height and weight of primary school pupils, also found that more than one in five pupils in Year 6 (aged 10–11) are living with obesity. The findings indicate that boys are more likely to be overweight or obese than girls.

In Reception year, 13% of children were classified as overweight, meaning that almost one in four children in this age group are either overweight or living with obesity.

Excluding the sharp increase seen during the first year of the COVID-19 pandemic, these figures represent the highest obesity prevalence in Reception year since records began in 2006–07 and mark a rise from 9.6% in 2023–24.

Schools feeling the strain

Lee Parkinson MBE, a primary school teacher from Manchester, said that systemic factors and funding cuts have worsened the situation.

“After the 2012 Olympics, school sport funding was cut, and the promise to ‘inspire a generation’ faded fast due to austerity measures,” he explained.

“Many primary schools lost specialist PE teachers and local competitions, and PE time is often squeezed as pressures on the timetable grow. You cannot separate childhood obesity from poverty either.

“Schools play their part through PE and lessons about healthy lifestyles, but they cannot solve this alone. We need to reinvest in early years support, rebuild affordable community sport, and make healthy choices realistic for all families, not just the privileged few.”

The link between nutrition, learning, and behaviour

A related report on children’s nutrition found that 94% of teachers believe healthy eating improves children’s behaviour. Teachers observed that better nutrition had tangible effects on classroom dynamics – with pupils demonstrating sharper focus, more energy, and improved behaviour.

The report underscored that nutritious food at school is not only essential for health and wellbeing but also for learning outcomes.

Hunger and food insecurity

Research from the Trussell Trust highlighted that around 9.3 million people in the UK, including three million children, experience food insecurity. Currently, one in four children under the age of five are at risk of needing to use a food bank.

Mr Parkinson reflected on the impact of poverty on pupils’ concentration: “Obviously with the poverty element, if children are coming into school hungry it will make it harder for them to concentrate.”

This problem is often exacerbated during school holidays, when free school meals are unavailable. Last summer, one in 12 parents reported that their children had to miss meals due to financial difficulties.

Mr Parkinson added: “I do not know if it is lack of knowledge or the fact that unhealthy food is easier to access or what families can afford. When parents are working long hours and struggling to make ends meet, healthy living becomes another impossible task.”

Teachers filling the gap

The majority of teachers (88%) said they had witnessed children arriving at school hungry, with 66% reporting that they had brought in food from home or purchased healthy food for pupils themselves.

Nearly all teachers surveyed (98%) agreed that nutrition forms a vital foundation for learning. However, 83% said it can be challenging to inspire children to make healthy eating choices, particularly when access to nutritious food is inconsistent outside of school.

Measuring the scale

In total, 1.1 million children across state-maintained schools were measured as part of the NCMP data collection for 2024–25.

Public health experts warn that the findings underline an urgent need for coordinated national action to address the intertwined challenges of obesity, poverty, and food insecurity among children in England.

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Strawberries May Support Glucose Control and Reduce Inflammation in Prediabetes, Study Finds

Key Takeaways:

• Daily intake of freeze-dried strawberries for 12 weeks improved fasting glucose and reduced inflammation in adults with prediabetes.
  
• Antioxidant biomarkers including superoxide dismutase, glutathione, and β-carotene significantly increased during strawberry supplementation.
  
• Findings suggest strawberries could serve as a practical, food-based intervention to prevent progression to type 2 diabetes.
  
  

Strawberries and prediabetes: A promising link

A new randomised controlled trial published in Antioxidants has found that consuming freeze-dried strawberries (FDS) daily may help reduce fasting blood glucose and vascular inflammation in adults with prediabetes. The research also showed marked improvements in antioxidant status, highlighting the potential of strawberries as a simple dietary intervention for metabolic health.

The authors concluded that “strawberries may represent a practical dietary intervention that improves fasting glucose and strengthens antioxidant defence in adults with prediabetes.”

Understanding prediabetes and oxidative stress

Prediabetes represents a critical stage between normal glucose metabolism and type 2 diabetes mellitus (T2DM). It is characterised by mildly elevated blood glucose levels, which contribute to oxidative stress and low-grade inflammation.

High glucose levels increase reactive oxygen species (ROS), impairing insulin function and damaging pancreatic β-cells. Proinflammatory cytokines such as tumour necrosis factor-alpha (TNF-α) further aggravate insulin resistance by interfering with glucose uptake and triggering inflammatory pathways. Over time, these effects contribute to vascular dysfunction and atherosclerosis through increased endothelial adhesion molecules and reduced antioxidant enzyme activity.

Dietary antioxidants – including vitamins, polyphenols, and carotenoids – can neutralise oxidative stress. However, studies using supplements have produced inconsistent results due to differences in absorption and bioavailability. Evidence from clinical trials and meta-analyses indicates that plant-based antioxidants can improve total antioxidant capacity and glycaemic outcomes in people with prediabetes or T2DM.

Berries, particularly strawberries, are rich in polyphenols such as anthocyanins and ellagic acid, which are known to enhance antioxidant enzyme activity and improve insulin sensitivity. Previous studies using FDS have already shown benefits for inflammation and oxidative stress in metabolic disorders, providing a foundation for this new research.

Study design and methodology

Researchers at the University of Nevada, Las Vegas, conducted a 28-week randomised controlled crossover trial involving 25 adults who met the American Diabetes Association’s diagnostic criteria for prediabetes.

Each participant completed two 12-week phases: one with daily FDS intake and another control period without strawberries, separated by a four-week washout. Participants were randomly assigned to begin with either the FDS or control phase.

During the intervention, participants consumed 32 grams of FDS powder per day – equivalent to roughly 2.5 servings of fresh strawberries – containing dietary fibre, polyphenols, flavonols, and anthocyanins. They were instructed to maintain their usual diet and physical activity throughout the trial.

Compliance was carefully monitored using dietary logs, returned powder packets, and plasma ellagic acid levels. Blood samples were collected at baseline, 12, 16, and 28 weeks to measure fasting glucose, antioxidant enzyme activity, total antioxidant capacity, and vascular adhesion molecules using standardised assays. Carotenoid levels were analysed via high-performance liquid chromatography (HPLC).

A mixed-model analysis of variance (ANOVA) was used to evaluate treatment effects while accounting for treatment period, randomisation order, age, sex, fasting glucose, and baseline values. Power analysis confirmed the study was adequately powered to detect meaningful changes in metabolic and antioxidant markers.

Improvements in antioxidant and metabolic markers

Results showed high adherence rates, with more than 85% compliance confirmed by elevated plasma ellagic acid during the FDS phase.

Compared with the control period, strawberry supplementation produced significant improvements in several antioxidant biomarkers, including superoxide dismutase, glutathione (GSH), total antioxidant capacity (AC), and β-carotene. No significant changes were observed in catalase, glutathione reductase, glutathione peroxidase, or α-carotene.

Fasting blood glucose levels also decreased significantly during the FDS period, indicating better glycaemic control. Moreover, markers of vascular inflammation – particularly intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) – were notably reduced. Levels of P-selectin and E-selectin remained unchanged.

Correlation analyses revealed modest inverse relationships between ICAM and GSH, AC, and β-carotene, and between VCAM and AC, suggesting that stronger antioxidant status was associated with reduced vascular inflammation.

Only minor side effects were reported, such as mild gastrointestinal discomfort and headaches.

Implications and limitations

The findings suggest that incorporating strawberries into the diet could help strengthen antioxidant defences, lower inflammation, and improve fasting glucose regulation in people with prediabetes. These benefits may be linked to polyphenols enhancing glutathione synthesis and superoxide dismutase activity, alongside carotenoids and anthocyanins reducing oxidative stress and endothelial dysfunction.

The study’s strengths include its randomised crossover design, objective biomarker measurements, and the use of a realistic dietary dose of strawberries. However, the relatively small and predominantly female sample, the absence of a placebo control drink, lack of participant blinding, and single-site recruitment limit the generalisability of results.

The study was funded by the California Strawberry Commission.

A food-based approach to diabetes prevention

In summary, consuming a daily portion of freeze-dried strawberries for 12 weeks led to measurable improvements in antioxidant capacity, fasting glucose, and vascular inflammation among adults with prediabetes.

While further research in larger, more diverse populations is needed, these results point to strawberries as a simple, accessible dietary strategy that could help prevent the progression from prediabetes to type 2 diabetes in everyday clinical and public health settings.

CCH insights

It is great to have research that shows health benefits from eating strawberries, because nearly everyone loves strawberries and there aren’t many foods that are extremely popular and good for us. However, the amount of freeze-dried strawberries consumed in this study would set you back about £20 per week – not a huge amount, but during a cost-of-living crisis might not be feasible for many people. This study was, unsurprisingly, funded by the California Strawberry Commission, and it begs the question whether eating other berries or certain other foods might not have a similar effect – but credit to the strawberry industry for making the effort to do the research.

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Age and Sex Shape Obesity’s Impact on Major Diseases, Large Genetic Study Finds

Key Takeaways: 

• A time-resolved genetic analysis of over 360,000 UK Biobank participants shows that obesity’s health risks vary substantially across age and between men and women.
  
• Higher BMI was causally linked to greater risk of type 2 diabetes, coronary artery disease, atrial fibrillation, and osteoarthritis, but the timing and intensity of these effects differed by condition.
  
• The study’s novel genetic approach revealed that preventive interventions such as statin or blood pressure treatment may temporarily dampen obesity-related cardiovascular risk in midlife.
  
  

Understanding obesity’s changing health risks

Nearly one billion adults globally live with obesity, making it a key driver of type 2 diabetes (T2DM), coronary artery disease (CAD), atrial fibrillation (AF), and osteoarthritis (OA). Yet researchers have long struggled to pinpoint when in life excess body weight does the most harm.

Most studies average risk across all adults, masking crucial age-specific patterns. Body mass index (BMI) remains the standard measure of obesity, but its health impact may shift as metabolism, hormones, behaviour, and medical care evolve through life. Moreover, traditional epidemiological studies cannot always distinguish correlation from causation.

Genetic studies using Mendelian randomisation (MR) can infer causal effects, but conventional MR assumes that risks remain constant over time. In a new paper published in Science Advances, researchers introduced a time-resolved MR framework that tracks how obesity’s effects on major diseases change with age and differ between sexes.

Study design and methods

The researchers analysed data from 361,906 unrelated adults of European ancestry within the UK Biobank, a large population-based health resource. Participants had linked genetic and medical record data, and follow-up continued until a median age of around 70 years, capped at 76 to avoid sparse data at older ages.

BMI at study entry was standardised within sex-by-age groups. The primary outcomes were first occurrences of T2DM, CAD, AF, and OA, identified using International Classification of Diseases (ICD-10) codes.

To establish causal relationships, the team employed MR using polygenic scores (PGS) as instruments. They performed genome-wide association studies (GWAS) for BMI in two independent subsamples (each ~180,953 participants) to identify genome-wide significant genetic variants.

To minimise reverse causation, disease-specific BMI PGS were filtered using the Steiger method, which excluded variants that explained more variation in disease outcomes than in BMI itself. The researchers then modelled time-to-event data using Aalen’s additive hazard model, estimating both cumulative (“life-course”) and age-specific (“momentary”) effects.

Sensitivity analyses accounted for potential biases, including lipid-lowering treatment among CAD-free participants, blood pressure (SBP) as an alternative exposure, and cohort selection effects.

Distinct patterns across diseases

Across adulthood, higher BMI was causally associated with increased rates of all four conditions, but with striking differences in timing and trajectory.

• Osteoarthritis (OA): BMI-related risk rose early in life, becoming significant over 20 years before risk for AF increased. This suggests that musculoskeletal strain and inflammatory pathways linked to obesity manifest relatively early.
  
• Atrial Fibrillation (AF): The risk associated with BMI intensified later in adulthood, suggesting that atrial and metabolic factors accumulate over time.
  
• Type 2 Diabetes (T2DM): The effect of BMI increased steadily from midlife but plateaued between ages 60 and 70, indicating that preventive measures or clinical interventions may mitigate risk during this period.
  
• Coronary Artery Disease (CAD): The most distinctive pattern emerged here – a U-shaped curve. Risk decreased markedly around ages 50 to 70 before rising again in older age. This midlife dip was not explained by study participation patterns but appeared more pronounced among individuals on lipid-lowering medication such as statins, suggesting that treatment may blunt BMI-related cardiovascular risk during this window.
  

When the researchers replaced BMI with systolic blood pressure (SBP) as the exposure, AF risk displayed a similar midlife trough, consistent with the effect of antihypertensive therapy. However, no comparable trough appeared for CAD, reinforcing the role of statins rather than blood pressure control in midlife coronary risk reduction.

Sex differences in risk

Sex-stratified analyses revealed generally stronger BMI effects in men for T2DM, CAD, and AF. Osteoarthritis was an exception: both sexes exhibited similar BMI-related risk until about age 60, after which the association appeared to decline slightly in women, although the results carried uncertainty due to diverging confidence intervals.

A particularly notable finding concerned T2DM. Women displayed a distinct, temporary reduction in BMI-related diabetes risk beginning around age 60 and lasting roughly a decade, whereas men’s risk continued to rise. This “female trough” was not accounted for by menopause timing or the use of hormone therapy, suggesting that behavioural or clinical factors – such as greater engagement with weight management or preventive health care – could play a role.

Genetic and methodological insights

Clustering of BMI-associated genetic variants revealed multiple mechanistic pathways underlying obesity’s effects. Different genetic clusters contributed distinct temporal risk patterns for CAD and T2DM. For instance, “high-risk” clusters largely accounted for the CAD trough and the sex differences seen in T2DM.

Importantly, the researchers verified that the strength of genetic effects on BMI declines with age, underscoring the need for age-sensitive models. Simulation studies confirmed that their time-resolved MR method accurately captured dynamic effects even when the genetic influence on BMI varied over time.

Adjustments for potential selection bias slightly reduced the overall magnitude of effects but preserved key age-related patterns, including the midlife risk reductions.

Clinical implications

The findings emphasise that the timing of prevention matters as much as the magnitude of obesity itself. Sustained high BMI elevates the risk for several major diseases, but the most effective period for intervention differs by condition and by sex.

For example:

• Lipid-lowering treatment in midlife may attenuate BMI-related CAD risk.
  
• Blood pressure control could moderate AF risk later in life.
  
• Women may experience a unique window in their 60s when obesity-related diabetes risk temporarily subsides.
  

The authors conclude that prevention strategies should be tailored to life stage and sex, targeting the periods when intervention can avert the greatest number of disease events.

They also note limitations, including the assumption of an immediate biological response to BMI changes and the reduced precision of genetic instruments for early-life BMI. Nonetheless, their time-resolved MR framework offers a powerful new approach for uncovering dynamic, age-specific health risks that static analyses may obscure.

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Obesity-Linked Lipids Drive Aggressive Breast Cancer Growth in Mouse Models

Key Takeaways: 

• New research from the University of Utah reveals that lipids – fat molecules elevated in people living with obesity – can accelerate tumour growth in aggressive forms of breast cancer.
  
• The findings suggest that lipid-lowering therapies may slow cancer progression and that high-fat diets such as ketogenic regimens may worsen outcomes in some patients.
  
• Researchers caution that weight loss without addressing lipid levels is insufficient protection against obesity-associated cancers like triple-negative breast cancer.
  
  
  

Lipids identified as key driver in obesity-related breast cancer

A new study from the University of Utah’s Huntsman Cancer Institute (HCI) has found that lipids, a hallmark of obesity, play a significant role in fuelling tumour growth in an aggressive form of breast cancer. The research, funded by the National Cancer Institute and conducted using preclinical mouse models, highlights how lipid metabolism may be a crucial therapeutic target for individuals living with obesity who have or have survived breast cancer.

The findings suggest that breast cancer patients and survivors with obesity could benefit from therapies that lower lipid levels. Conversely, high-fat dietary approaches, such as the ketogenic diet, may have unintended adverse effects by increasing lipid availability to cancer cells.

“The key here is that people have underestimated the importance of fats and lipids in the all-encompassing term that is obesity,” explained Dr Keren Hilgendorf, assistant professor of biochemistry and investigator at HCI. “But our study shows that breast cancer cells are really addicted to lipids, and the abundance of lipids in patients with obesity is one of the reasons that breast cancer is more prevalent and more aggressive in these patients.”

Focus on triple-negative breast cancer

The study focused on triple-negative breast cancer (TNBC) – a fast-growing and difficult-to-treat subtype that lacks receptors for oestrogen, progesterone, and HER2. TNBC is more common in women under 40 and in Black women, and it accounts for approximately 10 to 15 per cent of all breast cancer cases. This form of cancer is particularly prone to recurrence and metastasis.

A high level of lipids in the blood, known as hyperlipidaemia, is a frequent feature of obesity. Dr Hilgendorf and her colleagues, Dr Amandine Chaix and Dr Greg Ducker, both from HCI, examined how lipid levels influence tumour growth using specialised mouse models.

Lipid levels alone drive tumour growth

The researchers used two sets of models: one group of mice was fed high-fat diets, while another was genetically engineered to develop hyperlipidaemia without other typical markers of obesity, such as elevated blood glucose or insulin levels. In both cases, tumours grew faster when lipid levels were high.

“The idea is that lipids, which form the surface membrane of the cell, are like building blocks,” explained Dr Chaix, assistant professor of nutrition and integrative physiology. “If a cell receives the signal to proliferate and more building blocks are available, the tumour is going to grow more easily. We see that a high amount of lipids enables this proliferation.”

Importantly, when lipid levels were lowered – even in the presence of high glucose and insulin – breast cancer cell growth slowed down.

Potential implications for treatment and prevention

While the research was conducted in mice, the results point to potential therapeutic strategies for people with obesity and breast cancer.

“We think this has therapeutic implications, because if you could just lower the lipids – which we already know how to do in patients, for example, with lipid-lowering medication – that could be a way to decelerate breast cancer growth,” said Dr Hilgendorf. “If we can target these high levels of fat in the blood, the cancer sufferers, because the lipids are no longer feeding the cancer. But while our results in mice were striking, there are clear limitations in directly projecting these findings onto human patients. More research using human samples and patients will be necessary to confirm our hypotheses.”

Rethinking weight management in cancer care

These findings may also influence how clinicians guide people with obesity and breast cancer in managing their weight. While weight loss is commonly recommended to reduce recurrence risk, there is limited guidance on the best dietary approaches.

Some individuals turn to ketogenic diets, which are high in fat and low in carbohydrates, to induce ketosis – a state where the body uses fat rather than carbohydrates for energy. However, the new findings raise concerns about such diets in this patient group.

“For patients who are diagnosed with breast cancer and have an elevated BMI [body mass index], we would advise them to consult their physician and develop a weight-loss plan as part of their treatment,” said Dr Ducker, assistant professor of biochemistry. “If you have high cholesterol levels to start with, think about a weight-loss plan or potential pharmaceuticals that could lower your lipid levels. As our study shows, diets like keto that are very high in fat can have serious unintended side effects – even causing the tumour to grow.”

Beyond breast cancer: Broader implications

The research team believes that lipid-driven tumour growth may not be limited to breast cancer alone. Elevated lipid levels could also contribute to tumour progression in other cancers linked to obesity, such as ovarian or colorectal cancers.

The next stage of the research will investigate how anti-lipid drugs could improve the effectiveness of chemotherapy and explore the mechanisms through which lipids feed cancer cells.

Dr Chaix, Dr Ducker and Dr Hilgendorf emphasised that their results apply specifically to triple-negative breast cancer, and that ketogenic diets might still hold benefits for other forms of cancer. Nevertheless, their findings underscore the need for careful, evidence-based dietary guidance for people with obesity affected by cancer.

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Precision Medicine Poised to Redefine Obesity Prevention and Treatment

Key Takeaways:

• Researchers at the Pennington Biomedical Research Center highlight how precision medicine could revolutionise the prevention, diagnosis, and treatment of obesity by tailoring interventions to an individual’s biology and environment.
  
• Significant barriers remain, including limited large-scale clinical trials, underrepresentation of diverse populations, and challenges in integrating personalised tools into clinical practice.
  
• Experts call for robust biomarkers, inclusive research, and policy support to make precision obesity care accessible and evidence-based.
  
  
  

A blueprint for personalised obesity care

A new report led by researchers at the Pennington Biomedical Research Center underscores the rapidly growing potential of precision medicine to transform how obesity is prevented, diagnosed, and treated. Published in Obesity in September, the paper titled “Precision Prevention, Diagnostics and Treatment of Obesity” brings together insights from the recent Pennington–Louisiana Nutrition Obesity Research Center (NORC) scientific workshop.

The workshop, held in April 2024, convened experts to review evidence on tailoring obesity interventions to a person’s unique biological, behavioural, environmental, and social characteristics. The resulting report presents both the opportunities and obstacles in implementing precision-based strategies in obesity care.

Understanding the multifactorial nature of obesity

The authors emphasise that obesity is not a one-size-fits-all condition. Instead, it is shaped by a complex interplay of factors including genetics, epigenetics, metabolic phenotypes, microbiome composition, and environmental exposures. These elements influence why individuals gain or lose weight differently and why some respond better to certain interventions than others.

The review highlights how understanding these factors could enable clinicians to identify subgroups of people with obesity who would benefit from specific preventive or therapeutic strategies. This approach marks a shift from broad public health recommendations towards tailored, data-driven care.

Diagnostic innovation: Towards greater precision

The report calls for improved diagnostic tools—including the development of reliable biomarkers, imaging technologies, and phenotypic classifications—to better characterise the different subtypes of obesity and related risk profiles.

By accurately identifying an individual’s obesity phenotype, clinicians may be able to predict treatment response more effectively and target interventions that align with a person’s unique biology and lifestyle. Such advances could help move beyond the current trial-and-error approach in weight management.

Treatment personalisation and the path ahead

Emerging research indicates that personalising diet, physical activity, pharmacotherapy, and behavioural interventions according to an individual’s biological and psychosocial characteristics may improve both efficacy and long-term sustainability of outcomes.

However, the authors caution that while enthusiasm for precision-based treatment is growing, more robust clinical evidence is essential before these approaches can be fully integrated into standard care.

“Despite tremendous interest in precision-based treatment, the field is still relatively young,” said Dr Corby Martin, Co-Chair of the symposium and Director of the NORC Human Phenotyping Core. “We need rigorous clinical trials to empirically determine if precision treatment is indeed better than current practices. Unfortunately, few such trials exist, and those that do are not always supportive.”

Persistent gaps and barriers

The report identifies several key challenges hindering progress in precision obesity medicine:

• Limited large-scale clinical trials validating precision approaches.
  
• Insufficient diversity in study populations, leading to reduced generalisability of findings.
  
• Inadequate cost-effectiveness data, making implementation difficult within healthcare systems.
  
• Integration challenges when introducing precision tools into routine clinical settings.
  

Addressing these barriers will be essential for translating the promise of precision medicine into meaningful clinical and public health outcomes.

Recommendations for future research and policy

To advance the field, the authors recommend:

• Conducting diverse and inclusive research to ensure results are representative across ethnicities, genders, and socioeconomic groups.
  
• Developing and validating robust biomarkers and imaging tools for more accurate diagnosis and monitoring.
  
• Running comparative effectiveness trials to determine whether precision interventions outperform current standard treatments.
  
• Implementing programmes and policies that make precision obesity care both accessible and affordable.
  

The report suggests that precision-based approaches could enhance obesity prevention by identifying people at risk earlier and tailoring lifestyle or environmental interventions to reduce progression. Moreover, by customising treatment to a person’s biological and behavioural profile, clinicians could minimise side effects, avoid ineffective treatments, and improve outcomes.

A continuing commitment to obesity research

For more than 25 years, the Pennington–Louisiana Nutrition Obesity Research Center (NORC) has convened over 100 scientists annually to explore emerging topics in obesity and nutrition science.

“Supporting 1.5-day workshops such as the ‘Precision Prevention, Diagnostics, and Treatment of Obesity’ brings top scientists and clinicians from around the world to Pennington Biomedical,” said Dr Leanne Redman, NORC Director, LPFA Endowed Chair in Nutrition, and Associate Executive Director for Scientific Education. “These reports provide a blueprint for the current state of the science and avenues for future research.”

Building a collaborative future

Dr John Kirwan, Executive Director of Pennington Biomedical, commended the team’s contribution:

“This team’s efforts in advancing precision medicine to diagnose, prevent, and treat obesity are truly commendable. At Pennington Biomedical, our work is built on strong partnerships across Louisiana and throughout the United States, strengthened through centres and institutes like the Pennington–Louisiana NORC. We are proud to collaborate with leading research institutions, universities, and healthcare systems nationwide to advance obesity research.”

As the science of precision medicine matures, the report provides a clear framework for how personalised approaches may one day redefine obesity prevention and treatment, improving outcomes for individuals and populations alike.

CCH insight:

Precision approaches to obesity prevention and treatments could massively improve outcomes for people with, or at risk of, obesity. The complex nature of the condition, with its broad range of biological, behavioural, psychological, social and environmental determinants and risk factors, means every patient is unique and requires a personalised intervention. However, this complexity of obesity also makes it difficult to characterise an individual’s obesity phenotype and predict responses to interventions – so there is still a long way to go, a lot more research is needed.

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Exercise Shown to Reduce Artery Hardening After Weight Loss in Adults With Obesity

Key Takeaways:

• Regular exercise after weight loss significantly reduces inflammation and improves blood vessel health in adults living with obesity.
  
• The GLP-1 receptor agonist liraglutide helped participants maintain weight but did not show the same protective effects against artery hardening.
  
• Researchers emphasise exercise as an essential factor for maintaining cardiovascular health after weight reduction.
  
  

Exercise and heart health after weight loss

Maintaining weight loss through regular exercise, rather than relying solely on the glucagon-like peptide-1 receptor agonist (GLP-1RA) liraglutide, appears to protect against atherosclerosis in adults living with obesity, according to new research from the University of Copenhagen. Atherosclerosis—hardening and narrowing of the arteries due to inflammation and fat deposits—is a major underlying cause of cardiovascular disease (CVD).

The findings were presented at the Annual Meeting of the European Association for the Study of Diabetes (EASD) 2025 in Vienna (15–19 September).

“Our findings reveal that regular exercise is crucial to helping people living with obesity get the full cardiovascular benefits after a substantial weight loss,” said Dr Rasmus Sandsdal, lead author of the study from the University of Copenhagen, Denmark.

Understanding the risk

Cardiovascular disease remains the leading cause of death globally. It often begins with atherosclerosis, in which chronic inflammation and lipid accumulation cause the arteries to stiffen and narrow. If left unchecked, these plaques can rupture and trigger life-threatening events such as heart attacks and strokes.

Obesity contributes to chronic low-grade inflammation and endothelial dysfunction—a condition in which blood vessels lose their ability to contract and relax properly—both of which accelerate atherosclerosis.

While both exercise and GLP-1RAs are known to lower cardiovascular event risk in people with obesity, their specific effects on the development of atherosclerosis during weight loss maintenance have remained unclear—until now.

The study design

The Danish research team conducted a randomised placebo-controlled trial involving 215 adults aged 18–65 years (63% female) living with obesity (BMI 32–43 kg/m²) but without diabetes or other serious chronic conditions.

All participants began an eight-week low-calorie diet (800 kcal per day) using the Cambridge Weight Plan. Of these, 195 participants who achieved at least a 5% reduction in body weight (average loss of 12% or 13.1 kg) entered a one-year maintenance phase. They were randomly assigned to one of four groups:

1. Exercise (150 minutes/week of moderate-to-vigorous activity) plus placebo
   
2. Liraglutide treatment (3.0 mg per day)
   
3. Exercise combined with liraglutide
   
4. Placebo only
   

Researchers measured several key biomarkers at three points—before dieting, at the start of weight maintenance, and after one year. These included inflammatory markers (interleukin-6 [IL-6] and interferon-γ [IFN-γ]), endothelial function markers (intercellular adhesion molecule [ICAM-1], vascular adhesion molecule [VCAM-1], and tissue plasminogen activator [tPA]), and carotid artery intima-media thickness [cIMT], an indicator of arterial wall health measured by ultrasound.

Exercise reduced inflammation and improved arterial health

After one year, participants in both the exercise and liraglutide groups successfully maintained their weight loss. However, significant differences emerged in their cardiovascular health profiles.

Those who exercised—whether or not they also received liraglutide—had notably lower levels of inflammatory biomarkers compared with non-exercising participants. On average, IL-6 levels were 21% lower, and IFN-γ levels were 27% lower.

Exercise also had a favourable effect on endothelial function, reflected in a 6% reduction in VCAM-1, 8% reduction in ICAM-1, and 12% reduction in tPA compared to those who did not exercise. Moreover, carotid artery thickness decreased by an average of 0.024 mm, indicating reduced arterial hardening.

In contrast, treatment with liraglutide alone did not yield any measurable improvements in inflammatory or endothelial biomarkers, nor did it affect carotid artery thickness.

“Regular exercise seems to confer a protective effect against the development of atherosclerosis in people trying to maintain weight loss,” said Dr Sandsdal. “Since both exercise and GLP-1RA treatment were successful at keeping weight off, it seems that exercise plays an important role in mitigating cardiovascular risk factors in a weight-independent manner.”

Implications for long-term health

Exercise offers multiple benefits beyond weight control, including improvements in body composition, cardiorespiratory fitness, and metabolic health. Together, these contribute to better long-term cardiovascular outcomes.

“The most important message from our findings is that, for those trying to maintain weight loss, exercise is crucial in improving long-term health,” said Professor Signe Sørensen Torekov, corresponding author from the University of Copenhagen. “Given the substantial societal and economic costs of obesity-related cardiovascular disease, these findings underscore regular exercise as a critical component of weight management and heart health.”

Study limitations and future research

The authors acknowledged several limitations. The study’s sample size was relatively small, and adherence to structured exercise in real-world conditions may be lower than in a supervised trial setting.

Future studies, they suggested, should explore longer-term interventions and evaluate newer GLP-1 receptor agonists—potentially more potent than liraglutide—in combination with consistent exercise to assess whether similar or enhanced cardiovascular benefits can be achieved.

CCH insight:

We have long known that exercise is important for cardiovascular health, so the results of this study should not be a surprise – exercise provides cardiovascular benefits whether or not you are taking a GLP-1 medication. It is also important to remember that GLP-1 receptor agonists are meant to be taken as an adjunct to a healthy diet and lifestyle, including exercise. This is not just about weight management, but also about maximising health benefits and minimising the risk of developing diseases associated with obesity – such as cardiovascular disease.

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Severe Obesity Accelerates Lung Ageing by Altering Tissue Structure, Study Finds

Key Takeaways:

• Researchers at the University of Bonn have shown that severe obesity causes structural and molecular changes in lung tissue that mimic those of natural ageing.
  
• Obesity leads to the accumulation of fat within lung connective tissue cells, disrupting their normal function and reducing lung elasticity.
  
• These findings help explain why people living with obesity often experience breathing difficulties and may face a higher risk of lung-related complications.
  
  
  

Obesity found to accelerate ageing in the lungs

A research team led by Professor Dr Veronika Lukacs-Kornek from the ImmunoSensation2 Cluster of Excellence at the University of Bonn and the Institute for Molecular Medicine and Experimental Immunology (IMMEI) at the University Hospital Bonn (UKB) has discovered that severe obesity causes the lungs to age prematurely. The findings, published in Cell Reports, shed new light on how excessive body weight affects lung function and structure at the molecular level.

The study explored how the lungs respond to nutritional challenges associated with obesity, revealing that excess body fat significantly remodels the extracellular matrix (ECM) – the protein-based “scaffolding” that provides the lungs with their shape, strength, and stability. These alterations in lung architecture closely resemble those typically observed during the natural ageing process, suggesting that obesity accelerates the biological ageing of lung tissue.

Multi-omics analysis reveals profound structural changes

To investigate these effects, the researchers employed state-of-the-art multi-omics techniques – a set of advanced tools that allow for the simultaneous study of proteins, lipids, and genes. This integrative approach enabled the team to map how obesity influences the lungs at multiple biological levels.

By combining molecular analyses with microscopic imaging and functional experiments that tested how lungs perform, the team was able to capture a comprehensive picture of obesity’s impact. They compared the lungs of obese and lean mice, examined human lung fibroblasts (connective tissue cells), and studied the overall composition of lung tissue to identify both molecular and functional differences.

Fat accumulation and loss of elasticity in lung tissue

The results showed that in obesity, lung fibroblasts – the cells responsible for maintaining the connective tissue – begin to accumulate fat, becoming more mobile and displaying early signs of premature ageing. At the same time, the matrisome, which refers to the entire collection of ECM proteins, undergoes significant changes.

These changes disturb the delicate balance of protease inhibitors, enzymes that regulate tissue maintenance and repair. As a consequence, the lungs become less elastic and more prone to stiffness. This reduced elasticity helps explain why people living with obesity often experience shortness of breath and other respiratory difficulties.

“Interestingly, these changes are similar to those normally seen in older people – pointing to obesity as a driver of accelerated lung ageing,” the authors noted.

Overcoming complex research challenges

Studying the lung’s connective tissue presented major technical challenges. The fibroblastic stroma – the supportive framework of the lungs – comprises numerous cell types with highly specialised roles, making it difficult to isolate and analyse. Furthermore, the extracellular matrix itself is notoriously complex: many of its proteins are insoluble and possess intricate structures that resist standard laboratory analysis.

To address this, the team had to develop novel analytical methods that could overcome these limitations and enable the simultaneous study of multiple molecular components within the tissue. This innovative approach has allowed researchers to better understand how obesity-induced changes at the cellular level translate into functional impairments in lung performance.

Implications for understanding obesity-related lung disease

The study provides compelling evidence that obesity accelerates biological ageing processes in the lungs, underscoring the broader systemic impact of excess body weight beyond metabolic and cardiovascular complications.

By demonstrating that obesity alters both the composition and function of lung tissue, the findings open new avenues for exploring how weight management and metabolic interventions might help preserve lung health and mitigate premature ageing in people living with obesity.

CCH insight:

This is an interesting study. It shows that shortness of breath in people with obesity is not simply a case of poor cardiorespiratory fitness or due to mechanical difficulties due to accumulation of adipose tissue in the chest – it actually involves structural changes to lung tissue, similar to biological aging. It would be interesting to compare the lung tissue of people with obesity who have a sedentary inactive lifestyle with that of people with obesity who are active and physically fit, to see if exercise and better cardiorespiratory fitness can prevent these tissue changes and premature aging of the lungs.

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