Obesity Care

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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Many People with Severe Obesity Face Medical Discrimination, Study Finds

Key Takeaways:

• A new study reveals that over 40% of clinics in the United States refused to schedule an appointment for a hypothetical patient with severe obesity.
  
• More than half of practices surveyed lacked the basic facilities or equipment required to provide appropriate care to patients with a body mass index (BMI) of 60 or greater.
  
• Researchers warn that discrimination and inadequate resources may contribute to poorer health outcomes, including delayed cancer detection, among people living with severe obesity.
  
  

Widespread discrimination in clinical settings

People living with severe obesity frequently encounter discrimination and barriers when seeking medical care, according to a new study published in the Annals of Internal Medicine. Researchers reported that about 2 in 5 (41%) clinics refused to schedule an appointment for a hypothetical patient weighing 465 pounds.

One receptionist at an orthopaedic surgeon’s office stated: “We’ve reached our limit for bariatric patients at this site,” without offering further explanation.

The study highlights a critical issue in access to care: beyond outright refusals, more than half of clinics (52%) did not have the equipment or facilities necessary to provide basic medical care for patients with very high body weights. Severe obesity is defined as a BMI of 40 or higher, with extremely severe obesity considered a BMI of 60 or greater.

Lack of facilities and equipment

Many clinics lacked essential infrastructure, including examination tables or chairs that could safely support higher weights, wide enough doorways and hallways for patient mobility, and appropriately sized medical gowns.

Dr Tara Lagu, senior author of the study and adjunct lecturer of medicine and medical social sciences at Northwestern University Feinberg School of Medicine in Chicago, emphasised the harmful impact of such deficiencies:

“Patients living with severe obesity are likely already struggling with shame and difficulty navigating the world. To tell a patient that they can’t be examined on a table, or can’t wear a gown, or need to stand during an appointment makes what should be a safe place and the experience of seeing a doctor humiliating and degrading. We need to acknowledge, as a profession, that all people deserve better than this.”

Affected population and health risks

According to the researchers, approximately 1 in every 270 Americans – close to 1 million adults – lives with extremely severe obesity (BMI ≥ 60). These individuals are two to three times more likely to experience significant health problems compared with the general population.

Despite this increased risk, previous studies have shown that people with obesity are less likely to receive preventive health services such as cancer screenings. Dr Lagu explained:

“Obesity affects cancer screenings, and failure to screen can result in later cancer detection. We’re always attributing worse outcomes in higher-weight patients to weight itself, but more and more studies are now pointing to worse care, lack of care or being care avoidant as possible reasons for these delays.”

Study design and findings

To investigate barriers to care, researchers used a “secret shopper” approach, in which callers attempted to schedule an appointment for a hypothetical patient weighing 465 pounds. They contacted 300 clinics across four metropolitan areas – Boston, Cleveland, Houston, and Portland, Oregon. The study covered five specialties: dermatology, endocrinology, obstetrics and gynaecology, orthopaedic surgery, and ear, nose, and throat (ENT).

Lead researcher Dr Molly Hales, a physician at University of Chicago Medicine, noted that the caller questions were intentionally designed to suggest possible urgent medical needs:

“We designed some of the questions our callers asked to be red flags for a receptionist to think, ‘I should really schedule this person,’ because the questions suggested the patient might have cancer and need an urgent workup.”

Despite this, only 59% of clinics overall were willing to schedule the appointment. ENT specialists were least likely to agree, with only 48% offering an appointment, while endocrinologists were most likely to accept and to have suitable facilities.

Humiliating workarounds

Even among clinics that agreed to see the hypothetical patient, around 1 in 6 (16%) suggested workarounds that could be humiliating, such as requiring the patient to stand during the exam or to use a sheet instead of a gown.

Dr Hales observed:

“Our numbers likely underestimate the magnitude of the problem. Likely, very few high-weight patients who are scheduling appointments know to even ask if they can be accommodated based on their weight, and they might be hesitant to ask these questions or advocate for themselves because of the social stigma.”

Potential solutions

The researchers highlighted that a Clinical Environment Checklist has been developed to guide outpatient clinics in ensuring they can provide appropriate care for patients with obesity. However, it has not been widely adopted.

Dr Hales noted:

“They designed the checklist to be used by general outpatient clinics and tested it in both primary care and subspecialty settings, so it’s a good resource for clinics in determining where there are opportunities for improvement.”

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Green Tea Shows Significant Benefits for Glucose Metabolism and Muscle Health in Mice with Obesity

Key Takeaways: 

• Green tea extract significantly improved insulin sensitivity, glucose tolerance, and muscle preservation in mice with obesity, even when they continued consuming a high-calorie diet.
• The study controlled for temperature effects, providing clearer evidence that green tea’s metabolic benefits are independent of cold-induced energy expenditure.
• Findings suggest a potential role for green tea as a safe, accessible adjunct to obesity treatment in humans, though exact dosing for people remains to be established.
  

Ancient beverage, modern research

Green tea, long valued for its medicinal and antioxidant properties, continues to attract scientific interest for its impact on metabolic diseases such as obesity and type 2 diabetes. A recent study led by Professor Rosemari Otton from the Interdisciplinary Graduate Programme in Health Sciences at Cruzeiro do Sul University in São Paulo, Brazil, offers new insights into how green tea affects metabolism.

Otton, who has dedicated over 15 years to the study of green tea, explained that her initial curiosity stemmed from the popular belief that green tea promotes weight loss. The findings of her latest research, published in Cell Biochemistry & Function, reinforce the potential of green tea as a therapeutic adjunct in managing obesity.

Study design and green tea administration

The research team first fed mice a high-calorie diet for four weeks, including both a fat-rich diet and a “cafeteria diet” to replicate a Western-style eating pattern. “We give them chocolate, filled cookies, dulce de leche, condensed milk… In other words, the same type of food that many people consume on a daily basis,” said Otton.

After this induction phase, the mice continued on the high-calorie diet for 12 weeks, with some receiving a standardised green tea extract at 500mg per kilogram of body weight via intragastric gavage. This method ensured precise dosing. “If we put it in water, for example, we’d have no way of knowing how much the animal actually ingested,” Otton explained.

For humans, this dose would equate to approximately 3 grams of green tea daily — roughly three cups. However, Otton cautioned that not all commercial products meet required standards:

“Ready-made tea bags do not always guarantee the quantity or quality of the compounds. The ideal for consumption would be to use standardised green tea extract, like those found in compounding pharmacies. This is a concentrated way of using the plant, with a guarantee of the presence of flavonoids, which are the health-beneficial compounds present in the green tea plant.”

Controlled conditions for reliable results

A distinctive feature of the study was the use of a thermoneutral environment at 28°C, eliminating confounding effects caused by chronic cold exposure. Mice are typically kept at around 22°C in animal facilities, a temperature that triggers energy expenditure to maintain body heat.

“Excessive cold activates compensatory regulatory mechanisms in the animals’ bodies, causing them to expend more energy to stay warm. This can mask the real effects of any substance,” Otton explained. “By maintaining thermoneutrality, we were able to see the effects of green tea in a ‘clean’ way, without environmental interference.”

A previous study published in European Journal of Nutrition (August 2022) found that obese mice treated with green tea lost up to 30% of their body weight — a reduction Otton described as highly significant:

“If a person loses 5% to 10% of their body weight, that’s already a lot. So this result in animals is very significant.”

Preservation of muscle health

One of the most striking findings of the latest study was the preservation of muscle fibre morphology. Obesity often leads to a reduction in muscle fibre diameter, but green tea helped maintain muscle structure.

“One way to assess muscle function is to look at fibre diameter. If it increases, we have more active muscle components. Green tea managed to maintain this diameter, showing that it protects muscle against the harmful effects of obesity,” Otton said.

Genetic and metabolic insights

The study also explored gene expression related to glucose metabolism. Green tea treatment enhanced the expression of genes such as Insr, Irs1, Glut4, Hk1, and Pi3k, all of which play a role in glucose uptake and utilisation in muscle tissue. Additionally, the activity of lactate dehydrogenase (LDH), an enzyme vital for glucose metabolism, was restored.

Otton noted that green tea appeared to have a selective effect:

“It makes obese animals lose weight but keeps lean animals at a balanced weight. This shows that the tea seems to need an environment with excess nutrients to act, which supports the hypothesis that it acts directly on fat cells.”

Synergy of bioactive compounds

Green tea contains dozens of bioactive compounds, and attempts to isolate them have proven less effective than using the whole extract.

“We’ve tried to separate these compounds and study their effects individually, but the whole extract is always more effective. There’s a synergy between the compounds that we can’t reproduce when they’re isolated,” Otton explained.

One mechanism under investigation involves adiponectin, a protein secreted by fat cells that regulates inflammation and metabolism. In mice genetically modified to lack adiponectin, green tea showed no effect — pointing to adiponectin as a key mediator of its benefits.

Translating findings to human health

Despite these promising findings, Otton cautioned that safe and effective doses for humans have yet to be established, owing to variability in extracts and individual responses. She stressed the importance of long-term, habitual consumption rather than expecting rapid results:

“The ideal is chronic consumption, as we see in Asian countries. In Japan, for example, people consume green tea every day, throughout their lives, and obesity rates are low. But this is different from drinking tea for five months and expecting a miraculous weight loss effect.”

Otton also emphasised the importance of accessible and safe treatment options:

“The idea is to have safe, natural, effective, and high-quality compounds. The Camellia sinensis plant offers this. We’re still studying all the compounds involved, but there’s no doubt that green tea, as a plant matrix rich in flavonoids, has important therapeutic potential.”

The road ahead

Finally, Otton underscored the need for caution when translating animal research to clinical practice:

“What we see in animals doesn’t always reproduce in humans. But if we want to make this translation to real life, we need to think about all the details, such as ambient temperature. It’s these precautions that increase the validity of our data. We’re far from having all the answers, but we’re getting closer and closer.”

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Fasting may influence metabolism and immunity differently depending on body type, study finds

Key Takeaways:

• New research shows that people living with obesity respond differently to fasting compared to lean individuals, particularly in how their immune systems react.
• A 48-hour fasting study found that lean participants’ immune cells adapted by burning more fat, while those with obesity maintained higher levels of pro-inflammatory signals.
• Researchers say the findings highlight the complex interaction between nutrition, metabolism and immune function, and stress the need for further investigation.
  

Growing interest in fasting and ketogenic diets

Fasting has become a popular dietary trend, especially among those seeking to manage weight. Increasingly, fasting is paired with ketogenic or very low-carbohydrate diets, which aim to shift the body’s energy use from carbohydrates to stored fat, producing ketones as an alternative fuel source.

Dr Hashim Islam, Assistant Professor in the School of Health and Exercise Sciences at the University of British Columbia Okanagan (UBCO) and a member of the Centre for Chronic Disease Prevention and Management, explains that while fasting and low-carbohydrate diets can be beneficial, their effects are not uniform across all body types.

“These diet trends continue to grow in popularity. But our study found that people with obesity may respond to fasting differently than leaner individuals, especially in how their immune systems react,” says Dr Islam.

Fasting and immune health

Fasting has attracted significant attention in recent years, partly because of its coverage in mainstream media. Beyond public interest, scientists value fasting for its potential to alter metabolic processes in beneficial ways.

Lead author Dr Helena Neudorf notes that fasting forces the body to switch from burning glucose to burning fat, a process that produces ketones. “Fasting may improve health by changing metabolism to strengthen the immune system and reduce chronic inflammation, which is linked to many diseases,” she says.

However, the team was particularly interested in whether fasting has distinct effects on people living with obesity compared with lean individuals.

Study design and methods

To investigate, the researchers recruited participants with obesity and lean counterparts. Each group underwent a 48-hour fasting period, during which blood samples were collected before, during and after the fast.

The samples were analysed for hormones, metabolites, metabolic rate, inflammation markers and the activity of T cells – white blood cells that are crucial for fighting infections but can also drive chronic inflammation.

The study was a collaborative effort between Dr Islam’s group and Professor Jonathan Little’s research group at UBCO’s Centre for Chronic Disease Prevention and Management. The findings were published in iScience. 

Key findings

The results indicated that fasting did not affect all participants equally.

• In people living with obesity: T cells remained more pro-inflammatory, continuing to produce inflammatory signals even after fasting. These participants also showed a smaller increase in ketones and lower levels of important chemical reactions associated with immune regulation, such as ketones binding to amino acids or proteins.
  
• In lean participants: Immune cells adapted more readily to fasting by shifting to fat metabolism. This led to a stronger movement towards a balanced, anti-inflammatory state compared with their counterparts living with obesity.
  

“We also found the immune cells in lean participants adapted to fasting by burning more fat. This didn’t happen in those living with obesity,” explains Dr Neudorf. “Overall, their shift toward a more balanced, anti-inflammatory state was weaker in this particular group.”

Implications and future research

The findings suggest that while fasting may carry health benefits, these benefits may be blunted in people living with obesity. Dr Islam stresses that the implications of this are not yet fully understood.

“People living with obesity may respond differently to an isolated two-day fast compared to those who are leaner, but we don’t yet know if this is good or bad,” he says. “Our study shows the complex relationship between nutrition, metabolism and immune function, and that more research is needed to see how fasting can be used as a therapeutic tool for people with different body types.”

CCH Insight

This study is a good reminder that there is no one diet that suits everyone. We are all biochemically unique, due to a range of personal factors such as genetics, the makeup of our gut microbiome and our state of health, so it is always a good idea to be skeptical about ‘shiny new diets’ that appear to be the answer for weight loss or longevity. In this study, fasting appears to benefit people of a healthy weight, but not those living with obesity. Considering that one of the keys to good health and maintaining a stable, healthy body weight is to adopt healthy dietary habits that works for you and you can sustain, it is arguable that regular fasting could be unhelpful for people with obesity, who may be prone to binges or irregular eating patterns.

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Global study reveals obesity has overtaken being underweight among the world’s young

Key Takeaways:

• For the first time in recorded data, there are more children and adolescents living with obesity than those who are underweight, according to UNICEF.
• Nearly one in ten young people aged 5–19 years – around 188 million globally – are now affected by obesity, driven largely by the rise in consumption of ultra-processed foods.
• UNICEF is calling for urgent government action to protect children’s diets, restrict the influence of the ultra-processed food industry on policymaking, and make nutritious foods affordable and accessible.
  

A historic shift in global child health

For the first time, the number of children and adolescents worldwide living with obesity has surpassed the number who are underweight. This milestone, highlighted in a major study by UNICEF, underscores a profound transformation in global nutrition and public health.

The study found that approximately one in ten young people aged between 5 and 19 years – an estimated 188 million individuals – are now living with obesity. This represents a sharp increase compared with the early 2000s. Researchers attribute this shift primarily to the replacement of traditional diets with ultra-processed foods that are inexpensive, calorie-dense, and nutritionally poor.

Redefining malnutrition

Historically, malnutrition in children was almost synonymous with underweight and hunger. Today, the definition is broader, encompassing not only wasting and stunting but also the growing prevalence of overweight and obesity.

Children are classified as overweight when their weight significantly exceeds the healthy range for their age, sex, and height. Obesity is recognised as the more severe form of overweight and is associated with an elevated risk of type 2 diabetes, cardiovascular disease, and some cancers in later life.

Good nutrition throughout childhood – including adequate intake of fruit, vegetables, and protein – is vital for healthy growth, cognitive development, and mental wellbeing. Yet many of these traditional sources of nourishment are being replaced by foods laden with sugar, starch, salt, unhealthy fats, and artificial additives.

UNICEF’s Executive Director, Catherine Russell, warned that the dangers posed by this trend must not be underestimated. She described obesity as “a growing concern” that has significant implications for the health and development of children.

Rising obesity, declining underweight

The UNICEF-backed study, which analysed data from over 190 countries, highlights two diverging global trends. Between 2000 and 2022, the proportion of children aged 5–19 years who were underweight declined from nearly 13 per cent to 9.2 per cent. At the same time, obesity rates rose steeply from 3 per cent to 9.4 per cent.

This means that almost one in ten children worldwide is now living with obesity. When combining overweight and obesity, the figures are even more striking: one in five school-aged children and adolescents – around 391 million globally – is above a healthy weight.

Although underweight remains a pressing concern in children under the age of five, particularly in low and middle-income countries, obesity is increasingly the dominant nutritional challenge for those aged 5–19. The only regions where underweight still exceeds obesity are sub-Saharan Africa and South Asia.

Geographic hotspots and global distribution

The prevalence of childhood obesity is particularly acute in certain regions. Pacific Island nations have some of the highest rates, including Niue (38 per cent), the Cook Islands (37 per cent), and Nauru (33 per cent).

High-income countries are not exempt. In Chile, 27 per cent of 5–19-year-olds live with obesity, while in the United States and the United Arab Emirates the figure stands at 21 per cent.

“This double burden of malnutrition – the existence of both stunting and obesity in the same populations – requires targeted interventions,” Catherine Russell explained. “Nutritious and affordable food must be available to every child to support their growth and development. We urgently need policies that support parents and caretakers to access nutritious and healthy foods for their children.”

The call to action

The UNICEF report highlights the potentially devastating health and economic consequences of inaction. By 2035, the global economic burden of overweight and obesity is projected to exceed US$4 trillion (£2.95 trillion) per year.

To mitigate these risks, UNICEF has called upon governments to implement robust policies. These include:

• Restricting unhealthy foods – such as removing ultra-processed products from school canteens and regulating food labelling and marketing to children.
  
• Introducing fiscal measures – for example, taxing sugar-sweetened beverages and other unhealthy products, while incentivising healthier options.
  
• Encouraging reformulation – compelling food manufacturers to reduce unhealthy ingredients such as excess salt, sugar, and harmful fats.
  
• Safeguarding policy from industry influence – ensuring that ultra-processed food and drink producers are excluded from developing or implementing public health policy. Any lobbying efforts would need to be transparently reported.
  

A global imperative

The findings mark a pivotal moment in global health, emphasising the urgent need for a coordinated response. The steady replacement of traditional diets with ultra-processed foods has triggered a nutrition crisis that spans continents and income levels.

Without decisive policy action, the health outcomes for millions of children and the economic burden for societies will only worsen. UNICEF’s call is clear: protecting children’s diets from the pervasive influence of ultra-processed food industries and ensuring access to affordable, nutritious foods must become a global priority.

CCH Insight:

These statistics highlight an interesting phenomenon occurring in some developing countries, such as India, China and Nigeria. As these countries develop economically, they are grappling with the dual challenge of undernourished, underweight children in poor, mostly rural areas, and childhood obesity amongst the more affluent, who have adopted a western, processed food diet, mostly in urban areas. Due to the populous nature of these countries, global childhood obesity rates are likely to continue to rise for many years to come, unless a concerted effort is made to regulate food processing, as suggested by the authors. Unfortunately, the food industry is a very powerful lobby, that makes these kind of policies very difficult to adopt.

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