Obesity Care Tag

Children with Obesity Face Elevated Long-Term Health Risks Even with Normal Test Results, Study Finds

Key Takeaways:

• Children living with obesity can face significantly higher risks of future disease even when current clinical tests appear normal
  
• By early adulthood, rates of type 2 diabetes, hypertension and abnormal lipids are markedly higher compared with the general population
  
• Effective obesity treatment in childhood is associated with meaningful reductions in long-term health risks
  
  
  

Rethinking “metabolically healthy” obesity in childhood

Children living with obesity who show no immediate signs of metabolic complications may still be at substantial risk of developing serious health conditions later in life. New research from the Karolinska Institutet, published in JAMA Pediatrics, challenges the long-standing notion that some children with obesity can be considered “metabolically healthy” and therefore may not require intervention.

The findings contribute to an ongoing clinical debate about whether normal blood markers, liver function and blood pressure in childhood are sufficient indicators of long-term health.

“There has been a debate about whether children with normal blood and liver values and normal blood pressure might not need treatment for their obesity. Our study shows that this assumption is incorrect,” says Claude Marcus, professor at the Department of Clinical Science, Intervention and Technology at Karolinska Institutet.

Study design and population

The study followed just over 7,200 children aged 7–17 in Sweden who had initiated obesity treatment. Participants were tracked longitudinally up to the age of 30, allowing researchers to assess long-term health outcomes.

Children were grouped into three categories:

• Those with metabolically healthy obesity (MHO)
  
• Those with obesity and impaired cardiometabolic risk markers (MUO)
  
• A control group drawn from the general population
  

This design enabled a direct comparison of long-term disease risk across different metabolic profiles in childhood.

A clearly increased risk of future disease

Despite appearing clinically healthy in childhood, individuals with MHO demonstrated a substantially elevated risk of developing cardiometabolic diseases by early adulthood.

By the age of 30:

• 9 percent of individuals with MHO had developed type 2 diabetes, compared with 17 percent in the MUO group and 0.5 percent in the control group
  
• High blood pressure was observed in 11 percent of the MHO group, 18 percent of the MUO group and 4 percent of the general population
  
• Abnormal blood lipid levels were present in 5 percent of those with MHO and 13 percent of those with MUO, compared with just 1 percent among controls
  

These findings indicate that even in the absence of early warning signs, children living with obesity carry a significantly increased burden of future disease risk.

“Even children with obesity who show no signs of cardiometabolic impact have a clearly increased risk of future diseases. This means that normal blood pressure and the absence of abnormal blood test results are not sufficient protection against future morbidity,” says Emilia Hagman, associate professor at the same department and the study’s corresponding author.

The role of early treatment

All children included in the study received structured support aimed at improving lifestyle habits. Researchers examined whether treatment response during childhood influenced long-term outcomes.

A strong response to treatment was associated with a reduced risk of developing all studied conditions – including type 2 diabetes, hypertension and dyslipidaemia. Notably, this protective effect was observed in both MHO and MUO groups.

This suggests that early intervention has meaningful and lasting clinical benefits, regardless of a child’s initial metabolic profile.

“Our results suggest that all children with obesity need treatment, even if they appear completely healthy upon examination,” says Claude Marcus.

Data sources and funding

The study drew on data from Sweden’s national quality registry BORIS, alongside several national health data registries.

Funding was provided by multiple organisations, including the Center for Innovative Medicine, the Ollie and Elof Ericsson Foundation and the Freemason Foundation for Children’s Welfare.

Several researchers reported receiving compensation from companies unrelated to this work. A full list of potential conflicts of interest is available in the original scientific publication.

Implications for clinical practice

The findings underscore the limitations of relying solely on current metabolic markers when assessing risk in children living with obesity. Even in the absence of immediate clinical abnormalities, long-term risks remain significant.

For clinicians, this supports a more proactive and inclusive approach to obesity management in paediatric populations – one that does not defer intervention based on apparently normal test results, but instead recognises obesity itself as a key driver of future health risk.

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Larger Organs, More Cells – New Study Clarifies How Obesity May Increase Cancer Risk

Key Takeaways: 

• A new study suggests that larger organ size in people living with obesity increases cancer risk due to a higher number of cells
  
• Organ growth appears to be driven largely by an increase in cell number rather than simply larger cells
  
• Findings indicate that organ size may be a more precise predictor of cancer risk than BMI alone
  
  
  

A longstanding question in obesity and cancer

For many years, researchers have recognised a clear association between obesity and an increased risk of cancer, particularly in organs such as the liver, kidneys and pancreas. However, the biological mechanism underpinning this relationship has remained uncertain.

A research team from City of Hope and its Translational Genomics Research Institute, known as TGen, has now provided a clearer explanation. Their findings suggest that the relationship may be explained by a straightforward principle – larger bodies tend to have larger organs, and larger organs contain more cells.

This increase in cell number creates more opportunities for mutations and, consequently, cancer development.

Study design and key findings

The study, presented in Cancer Research, analysed data from 747 adults across a broad spectrum of body mass index (BMI), ranging from underweight at 18.5 kg/m² to severe obesity above 40 kg/m².

Researchers examined the pancreas, kidneys and liver, identifying a consistent pattern: as body weight increased, organ size increased proportionally.

For every 5-point rise in BMI:

• The liver increased in size by 12%
  
• The kidneys increased by 9%
  
• The pancreas increased by 7%
  

These findings demonstrate a measurable and progressive relationship between BMI and organ enlargement.

More cells, not just bigger cells

To better understand how organs grow, the research team analysed kidney tissue from autopsies and biopsy samples from living individuals. This allowed them to distinguish between two biological processes:

• Hypertrophy – where existing cells grow larger
  
• Hyperplasia – where the number of cells increases
  

First author Sophie Pénisson, PhD, explained the importance of this distinction:

“When an organ increases in size, the question is to know whether it’s because the cells in it become bigger or whether there are more of them [that are] the same size,” Pénisson said. “And the first case is we call hypertrophy, with bigger cells, and hyperplasia is when we have more cells.”

The results showed that approximately 60% of kidney growth was due to hyperplasia, meaning an increase in the number of cells, while the remainder was due to hypertrophy.

A simple but powerful explanation for cancer risk

These findings support the idea that a greater number of cells increases the likelihood of cancer simply by increasing the number of opportunities for mutations to occur.

Senior author Cristian Tomasetti, PhD, illustrated this concept with a simple analogy:

“Think of playing the lottery: The more tickets you buy, the greater your chances of winning,” Tomasetti said. “Similarly, the more cells in an organ, the more mutations and the greater the risk of one cell going awry during division and becoming cancerous.”

Importantly, this mechanism does not replace existing explanations such as inflammation or hormonal disruption. Instead, it works alongside them.

Pénisson elaborated on this interaction:

“If more cells is like having more raffle tickets, she said, ‘if on top of that, there is inflammation – it means you play more often. With greater frequency, again, you increase your risk of developing cancer.’”

Rethinking BMI as a predictor of risk

The study also raises important questions about the use of BMI as a measure of cancer risk.

Although BMI is widely used in clinical practice, the researchers observed considerable variation in organ size among individuals with similar BMI values. Some individuals within a “healthy” BMI range had organ sizes typically seen in severe obesity, while others with higher BMI did not.

The authors wrote:

“We…observe substantial interindividual variation in organ size among people with similar BMI: For example, some individuals in the healthy BMI range have organ sizes expected only in severe obesity, and vice versa. This large variability suggests that organ size itself may be a better predictor of cancer risk than BMI, a possibility we believe warrants further investigation.”

They further concluded:

“Taken together, these findings establish organ hyperplasia as a previously unrecognized contributor to obesity-related kidney, liver, and pancreatic cancer risk, complementing known mechanisms including inflammation, hormonal changes, and metabolic dysfunction.”

Pénisson reinforced this point:

“When an organ doubles in size, it is expected to roughly double its risk of developing cancer,” Pénisson said, noting that BMI does not distinguish between fat mass and lean tissue. “Our work suggests that, at least for some organs, their dimensions may predict cancer risk better than BMI.”

Can weight loss reverse the risk?

An important question arising from these findings is whether reducing body weight can reverse organ enlargement and lower cancer risk.

Tomasetti indicated that this is an active area of research:

“It’s actually something we are working on right now,” Tomasetti said. “But yes, preliminary data seem to indicate that essentially, you are reverting back according to the same process” that caused the weight gain.

He also referenced emerging evidence presented at the American Society of Clinical Oncology, suggesting a link between GLP-1 receptor agonists and reduced cancer risk, although further research is needed to confirm this relationship.

Implications for treatment and prevention

Given the global scale of obesity, affecting more than 2 billion people, these findings may have important implications for prevention strategies and treatment approaches.

Tomasetti suggested that therapies such as GLP-1 receptor agonists could play a broader role:

GLP-1 RAs “are something that should be given to people as a treatment option to reduce the cancer risk, among other things,” including heart disease.

While further research is needed, this study provides a clearer mechanistic link between obesity and cancer risk and highlights the potential importance of organ size as a clinical marker.

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Genetic Risk Scores Offer Improved Prediction of Obesity, Type 2 Diabetes and Long-Term Health Outcomes

Key Takeaways: 

• A new polygenic risk score integrates genetic data from over 8.5 million people to better predict obesity and type 2 diabetes risk
  
• The model goes beyond traditional measures such as body mass index by incorporating multiple aspects of metabolic function
  
• Individuals with higher genetic risk were more likely to develop complications and require interventions such as GLP-1 therapy or bariatric surgery
  
  
  

A more comprehensive approach to metabolic risk

Obesity and type 2 diabetes are complex metabolic conditions influenced by a combination of environmental, behavioural and genetic factors. While traditional clinical measures such as body mass index have long been used to assess risk, they do not fully capture the biological complexity underlying these conditions.

In a new study published in Cell Metabolism, researchers from Mass General Brigham have developed an advanced polygenic risk score designed to improve prediction of both obesity and type 2 diabetes, as well as their long-term health consequences. Polygenic risk scores work by aggregating the effects of many genetic variants across the genome, providing an estimate of an individual’s predisposition to developing a given condition.

“Our intention was to not only capture the risk of being diagnosed with obesity or diabetes, but also to better predict health consequences across the life course by integrating many aspects of metabolic function,” said co-first author Min Seo Kim, MD, MSc. “In the future, this genomic approach could complement established clinical risk factors to inform patient care and preventative strategies.”

Building a next-generation polygenic risk score

The research team constructed two distinct metabolic risk scores – one optimised for obesity and another for type 2 diabetes. Unlike conventional models, these scores incorporate genetic signals linked to 20 different traits associated with metabolic health. These include factors such as fat distribution, insulin regulation and glucose control.

To build these models, the investigators drew on genome-wide association studies conducted across some of the largest biobank datasets globally, encompassing more than 8.5 million individuals. This scale allowed the researchers to capture a broad and diverse range of genetic influences.

Importantly, the model moves beyond reliance on body mass index alone, reflecting a growing recognition that metabolic health cannot be fully understood through weight-based measures in isolation.

Predicting disease progression and clinical outcomes

Beyond predicting the likelihood of developing obesity or type 2 diabetes, the new polygenic risk scores demonstrated the ability to forecast downstream health outcomes.

The researchers found that individuals identified as high risk were more likely to go on to develop complications such as cardiovascular disease and stroke. Even among people who were initially healthy, those with a high genetic risk score were approximately twice as likely to require clinical interventions over time.

Specifically, individuals with higher polygenic risk scores were about twice as likely to receive GLP-1 receptor agonist medications or undergo bariatric surgery compared with those with average risk scores, over a median follow-up period of 5.5 years.

These findings suggest that genetic profiling could help identify people at risk earlier in the disease trajectory, potentially enabling more proactive and targeted care.

Improved performance across diverse populations

A notable strength of the study lies in its use of multi-ancestry genetic data. By incorporating genome-wide association studies from a wide range of populations, including African, East Asian, South Asian and Middle Eastern groups, the researchers were able to develop risk scores that performed better across diverse populations than earlier models.

Historically, many genetic prediction tools have been less accurate in non-European populations due to limited representation in genomic datasets. This study represents a step towards addressing that imbalance and improving equity in precision medicine.

Towards more personalised prevention and treatment

The research team emphasises that this work is part of a broader effort to refine understanding of the genetic subtypes of obesity and type 2 diabetes. Improved classification of these conditions could support more precise patient stratification in clinical trials and, ultimately, more tailored interventions in routine care.

“We want clinicians to be able to think about metabolic conditions in terms beyond body mass index, with a focus more broadly on underlying genetic susceptibility,” said co-senior author Akl Fahed, MD, MPH, of the Cardiovascular Research Center at Massachusetts General Hospital and an interventional cardiologist with the Mass General Brigham Heart and Vascular Institute. “Early identification of people who are likely to have a worse trajectory of poor metabolic health, before they even develop these conditions, can help us improve prevention and clinical interventions. That is how we can cure disease, and that is the bold mission that we are after.”

Implications for clinical practice

While further validation and implementation work will be required, the findings highlight the potential role of genomic tools in enhancing current approaches to metabolic disease prevention and management. By complementing existing clinical risk factors, polygenic risk scores could support earlier identification of people at risk and enable more personalised, proactive care pathways.

As healthcare systems increasingly move towards precision medicine, integrating genetic insights with clinical decision-making may become an important step in improving outcomes for people living with obesity and type 2 diabetes.

CCH insights:

This is exciting research, and a big step towards precision obesity prevention, as it gives us an individual risk score for obesity and diabetes for each patient. However, it is only half the story – ideally we’d also like to be able to determine what type of interventions will work best for each individual (in terms of diet, lifestyle and medicine) in order to optimise their chances of good metabolic health and achieving a healthy weight. Hopefully the ability to do this is not too far away.

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Switching GLP-1 Medications May Improve Long-Term Engagement in Obesity Treatment, Real-World Study Suggests

Key Takeaways:

• Real-world data from nearly 127,000 adults with overweight or obesity found that switching between GLP-1 receptor agonist medications was associated with greater long-term treatment persistence.
  
• Only about one quarter of patients remained on any GLP-1 therapy after one year, highlighting ongoing challenges with long-term adherence.
  
• Researchers suggest that changing medications should be viewed as a normal part of obesity care, rather than as a sign that treatment has failed.
  
  
  

Large real-world study examines how patients use GLP-1 medications

Patients without diabetes who switched between glucagon-like peptide-1 receptor agonist (GLP-1RA) medications for overweight or obesity were more likely to remain engaged with treatment than those who stayed on the same medication, according to new research conducted by investigators at UT Southwestern Medical Center.

The findings were published in JAMA Network Open and provide one of the most detailed real-world analyses to date of how adults with overweight or obesity use these medications over time. The study suggests that switching between drugs within the same therapeutic class is relatively common and may play an important role in sustaining long-term treatment.

The researchers argue that clinicians should not interpret medication changes as treatment failure. Instead, they suggest that switching therapies may represent a pragmatic strategy to maintain continuity of care when patients experience side effects, access issues, or other barriers.

“This study provides one of the largest real-world descriptions to date of how adults with overweight or obesity use and switch GLP-1RAs over time,” said first author Luyu (Amber) Xie, Ph.D., Pharm.D., Assistant Professor in the Peter O’Donnell Jr. School of Public Health and co-Director of the Biostatistics and Data Science Core at UT Southwestern. “It highlights that long-term persistence is low and that switching between medications is a relatively common part of ongoing treatment rather than a sign of failure.”

Tracking medication use in nearly 127,000 adults

To examine treatment patterns, the research team analysed insurance claims data from nearly 127,000 adults in the United States who were living with overweight or obesity and initiated GLP-1RA therapy between 2019 and 2024.

Participants in the study did not have diabetes and were prescribed GLP-1 medications specifically for weight management. The researchers tracked medication use over a 12-month period following treatment initiation in order to understand how patients continued, discontinued, or switched therapies.

The analysis revealed that treatment pathways were rarely straightforward. Instead of remaining on a single medication for the entire year, many patients experienced adjustments to their treatment regimen. These changes were often driven by factors such as side effects, medication availability, insurance coverage, and the introduction of newer therapies.

GLP-1 receptor agonists have become a central component of modern obesity treatment. Medicines in this class include semaglutide, liraglutide, and tirzepatide, all of which act on hormonal pathways involved in appetite regulation and metabolic control. Despite their clinical effectiveness, maintaining long-term adherence has proven difficult for many patients.

Persistence remains a major challenge

The study found that long-term persistence with GLP-1RA therapy remains relatively low.

After one year, only around one quarter of patients remained on any GLP-1 medication. During that same period, approximately one in five patients transitioned from their initial therapy to a different GLP-1RA.

However, the data also revealed an important pattern. Patients who switched medications were more likely to continue treatment overall and demonstrated higher levels of adherence compared with those who remained on their original therapy.

These findings suggest that medication switching may reflect proactive clinical management rather than treatment failure.

“Switching between GLP-1RA medications should be viewed as a normal part of long-term obesity care,” said senior author Sarah Messiah, Ph.D., M.P.H., Professor of Epidemiology and Pediatrics, Associate Dean for Research in the O’Donnell School of Public Health, and Director of the Child and Adolescent Population Health Program. “Persistence should not be judged by staying on a single drug indefinitely, but by maintaining engagement in care and working with clinicians to find sustainable, effective treatment strategies over time.”

Visualising treatment pathways

In addition to analysing persistence and switching rates, the researchers also mapped treatment pathways to illustrate how patients moved between different medications over the course of the study period.

These visualisations showed that newer once-weekly injectable therapies frequently served both as initial treatments and as destinations when patients switched from other medications. This pattern reflects the growing role of these agents in contemporary obesity management.

According to the researchers, these dynamic treatment pathways highlight the evolving nature of obesity pharmacotherapy and reinforce the need for flexible treatment strategies.

“In today’s clinical environment, successful obesity care often involves adapting treatment over time rather than expecting a single medication to meet every patient’s needs indefinitely,” said co-author Jaime Almandoz, M.D., M.B.A., Professor of Internal Medicine in the Division of Endocrinology and Medical Director of UTSW’s Weight Wellness Program.

Setting realistic expectations in obesity care

The findings also underline the importance of setting realistic expectations with patients at the start of treatment.

Clinicians may need to emphasise that finding the most effective long-term medication strategy can involve trial and adjustment. In some cases, more than one medication may be prescribed before a sustainable approach to treatment is established.

By framing medication adjustments as part of routine care, clinicians may help patients remain engaged with treatment and reduce the perception that a change in therapy represents a setback.

Future research on personalised treatment pathways

The authors note that additional research is needed to better understand the factors that shape treatment trajectories in obesity care.

Future work will explore how patient characteristics, specific medications, and the timing of therapy influence patterns of persistence and switching. The goal is to generate insights that can support more personalised and sustainable approaches to treatment.

Study contributors and funding

Additional UT Southwestern researchers involved in the study include Diego Anazco Villarreal, M.D., an Internal Medicine resident; Azucena Herrera Chancay, M.D., an Internal Medicine fellow; M. Sunil Mathew, M.S., Senior Population Science Data Manager; and Jackson Francis, M.P.H., Population Science Project Coordinator.

The research was supported by the UTSW Clinical and Translational Science Award, the National Institutes of Health (1U54TR00236), the Texas Health Resource Clinical Scholar program, and the UTSW Nutrition & Obesity Research Center (NORC).

CCH insight:

This is an interesting study which looks at a very important issue. Obesity is a chronic relapsing disease so ongoing, long-term treatment is necessary. If a patient is struggling with a particular medication, the opportunity to try an alternative is very helpful, and will increase the chances of adhering to treatment. The number of options is gradually increasing, most notably with oral formulations becoming available this year, and new drugs in the pipeline such as petrelintide, which promises slightly less weight loss than Wegovy or Tirzepatide, but minimal gastrointestinal side effects – so far better tolerability. All these developments should help patients find a medication that works for them, enabling long-term treatment compliance and better outcomes.

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Hong Kong Unveils First Territory-Wide Weight Management Strategy to Address Rising Obesity Rates

Key Takeaways:

• Hong Kong has launched its first comprehensive three-year Action Plan on Weight Management, introduced on World Obesity Day (4 March) in response to data showing that more than half of the city’s adults are living with overweight or obesity.
  
• The strategy is built around five pillars and 15 specific objectives, including improved health education, strengthened healthcare services, and environmental changes that support healthier lifestyles.
  
• Officials acknowledge that low awareness and misperceptions about body weight remain major barriers, with many individuals who are overweight believing their weight is “just right”.
  
  
  

Hong Kong launches its first comprehensive weight management plan

Hong Kong has introduced its first territory-wide action plan aimed at improving weight management across the population, marking a significant step in the city’s efforts to address rising levels of overweight and obesity.

The initiative was officially launched on World Obesity Day, 4 March, and will run for three years. It follows findings from the Department of Health’s Population Health Survey conducted between 2020 and 2022, which revealed that more than half of Hong Kong’s adult population are living with either overweight or obesity.

Officials have positioned the plan as part of broader international and national efforts to address obesity. The strategy contributes to China’s national Weight Management Year initiative and aligns with the World Health Organization’s global framework aimed at reducing obesity worldwide.

The new plan aims not only to raise awareness of weight management but also to create conditions that make healthier choices easier for people across the territory.

A framework built around five strategic pillars

The action plan is organised around five core pillars, each designed to address different aspects of weight management across society.

These pillars include:

• Strengthening health education and promotion
  
• Creating a supportive social environment
  
• Enhancing health service delivery
  
• Adopting a life-course approach to health promotion
  
• Continuously monitoring population weight trends
  

Together, these pillars translate into 15 concrete objectives that government departments will pursue during the programme’s three-year implementation period.

The timeline of the plan is also structured in stages. 2026 will focus primarily on raising public awareness, helping people better understand healthy weight and lifestyle behaviours. The second year will concentrate on encouraging positive behavioural change, while the final year will emphasise long-term maintenance, with the goal of embedding healthier habits into everyday life.

Public initiatives begin with a city-wide walking challenge

The first public initiative under the strategy will begin on 21 March, when authorities launch a “10,000 Steps a Day” walking challenge.

The programme will be integrated into the eHealth mobile application’s e+Life platform, allowing participants to track their daily activity digitally. The launch will be marked by a ceremony and public carnival at the West Kowloon Cultural District, intended to encourage participation and raise awareness about physical activity.

Alongside this campaign, the action plan outlines several longer-term measures aimed at promoting healthier lifestyles across the city.

These include:

• Installing weight measurement devices in public housing estates and schools
  
• Integrating weight management education into school curricula
  
• Designing pedestrian-friendly urban environments that encourage walking and other forms of physical activity
  

By combining digital tools, education, and environmental changes, officials hope to create a more supportive ecosystem for healthier behaviours.

A life-course approach to health promotion

According to public health officials, the plan adopts a life-course approach, addressing health and weight management from the earliest stages of life through to older adulthood.

Dr Edwin Tsui, controller of the Centre for Health Protection, explained that the strategy is intended to cover the entire lifespan.

He said the plan takes “a systematic approach covering the full lifespan, from prenatal nutrition to maintaining function in old age.”

Tsui also emphasised the role of primary healthcare as a central component of the initiative, noting that healthcare services will act as the gatekeeper of public health within the strategy.

The plan also encourages collaboration between Chinese medicine and Western medicine practitioners, reflecting Hong Kong’s mixed healthcare landscape. At the same time, authorities intend to use the eHealth digital platform to help residents track and manage their personal health information.

Low awareness and misperceptions present major challenges

Despite the ambitious scope of the initiative, health officials acknowledge that significant barriers remain.

One of the most notable challenges is limited awareness about healthy weight and weight management among the public.

Dr Anne Chee, head of the Non-Communicable Disease Branch at the Department of Health, highlighted this issue during a radio programme. She explained that many individuals living with overweight may not recognise it as a health concern.

Among people who are overweight, she said two-thirds believe their weight is “just right” or even “too thin.”

Chee also noted that many individuals have taken no action to manage their weight over the past year, reflecting gaps in public understanding of healthy weight management.

She further emphasised that some people may not know how to calculate their body mass index, pointing to broader deficiencies in knowledge related to weight and health.

Sustaining behaviour change may prove difficult

Experts outside government have also raised concerns about the challenge of maintaining behavioural change over time.

Sports scientist Professor Lobo Louie from the Education University of Hong Kong warned that while awareness campaigns can be effective, they do not always translate into lasting lifestyle changes.

Louie pointed to the gap between initial engagement and long-term commitment, noting that maintaining motivation may prove difficult for many individuals.

This highlights a broader challenge faced by public health initiatives worldwide – transforming awareness into sustained behaviour change.

Cross-government collaboration to support healthier lifestyles

The action plan is designed as a cross-government initiative, bringing together multiple public agencies.

Departments involved include those responsible for:

• Health
  
• Education
  
• Leisure and cultural services
  
• Urban planning
  

A cross-departmental working group established in October is coordinating these efforts. The group aims to strengthen collaboration not only within government but also with businesses, academic institutions, and community organisations.

Officials hope that this multi-sector approach will create broader societal support for healthier lifestyles.

A voluntary strategy with long-term ambitions

For the moment, the programme relies largely on voluntary participation and public education, rather than regulatory measures.

Whether these measures will be sufficient to reverse current trends remains uncertain. Officials recognise that individual willpower or clinical care alone cannot solve the obesity challenge.

Instead, they emphasise that the wider social and physical environment must also support healthier choices, making it easier for people to adopt and maintain healthy behaviours.Further information about the strategy and related initiatives is available on the Department of Health’s Change4Health website.

CCH insight:

We wish the authorities and people of Hong Kong the best of luck with this programme, but evidence from other countries suggest it is highly unlikely to make a significant reduction in the prevalence of obesity. We know that obesity results from genetic and biological factors driving overeating, made possible by an environment which encourages over-consumption of food. The programme is not attempting to change the population’s biology (by increasing access to anti-obesity medications, for example), nor to restrict the availability of obesogenic foods, so it is unlikely to lead to the kind of changes in behaviour it is aiming for.

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Reducing Parental Stress May Help Lower Childhood Obesity Risk, Yale Study Suggests

Key Takeaways: 

• A Yale study suggests that reducing parental stress may play an important role in lowering obesity risk in young children.
  
• Parents who took part in a mindfulness-based stress management programme showed improvements in parenting behaviours and children’s eating habits.
  
• Children whose parents received the stress-focused intervention were less likely to gain excess weight during follow-up compared with those receiving standard nutrition advice alone.
  
  
  

Childhood obesity continues to rise

Childhood obesity has been increasing in recent years and remains a major public health concern. According to the U.S. Centers for Disease Control and Prevention, approximately one in five children and adolescents in the United States met the clinical definition of obesity in 2024.

Efforts to prevent obesity in children have traditionally focused on encouraging healthier diets and increasing levels of physical activity. However, new research from Yale University suggests that another factor may also be important in shaping children’s health outcomes – parental stress.

A research team led by psychologist Rajita Sinha has found evidence that helping parents manage stress more effectively may reduce obesity risk among young children. The findings were published in the journal Pediatrics.

“It’s the third leg of the stool,” said Sinha. “We already knew that stress can be a big contributor in the development of childhood obesity. The surprise was that when parents handled stress better, their parenting improved, and their young child’s obesity risk went down.”

How parent stress may influence children’s health

Previous research has shown that children are more likely to develop obesity if their parents are living with obesity. However, scientists have increasingly suspected that psychological and environmental factors within families may also influence early childhood weight gain.

Parental stress has emerged as one such potential contributor.

Studies suggest that parents experiencing high levels of stress may be more likely to rely on convenient or fast-food options and less nutritious dietary patterns. These habits can influence the types of foods available in the home and shape children’s developing eating behaviours.

Stress can also affect broader family routines. When parents feel overwhelmed, regular meal patterns may become disrupted, healthier foods may be replaced with more convenient alternatives, and positive parenting behaviours may decline. Reduced patience, decreased emotional responsiveness, and less consistent family structure may all affect children’s wellbeing.

Despite these insights, most childhood obesity prevention programmes continue to focus primarily on nutrition education and physical activity promotion.

According to Sinha, these approaches alone often fail to produce long-lasting behavioural change.

Equipping practitioners with the skills to support lasting change – rather than just deliver initial advice – is the focus of professional training such as the College of Contemporary Health’s Behaviour Change short course, which draws on techniques from psychology and behavioural science.

Sinha is the Foundations Fund Professor in Psychiatry and a professor in neuroscience and child study at Yale School of Medicine.

A randomised trial examining stress reduction

To better understand the potential role of parental stress, the research team conducted a 12-week randomised prevention trial involving 114 parents.

Participants represented diverse ethnic and socioeconomic backgrounds and all had children aged between two and five years old who were living with overweight or obesity.

Parents were randomly assigned to one of two groups:

• Parenting Mindfully for Health (PMH) – a stress-focused intervention programme
  
• Standard counselling focusing on nutrition and physical activity
  

The Parenting Mindfully for Health programme combined several elements. Parents were taught mindfulness techniques and behavioural self-regulation strategies designed to help them manage stress more effectively. The programme also included guidance on healthy eating and physical activity for families.

Both groups attended weekly sessions lasting up to two hours over the 12-week study period.

During the programme, researchers measured parental stress levels, parenting behaviours, and children’s weight. Parenting behaviours assessed included warmth, listening, patience, and positive emotional interactions with children.

Researchers also evaluated children’s dietary patterns, including both healthy and unhealthy food consumption.

Children’s weight was measured again three months after the programme ended in order to assess whether any benefits were sustained.

Stress reduction linked to improvements in parenting and eating habits

The results showed clear differences between the two groups.

Parents who participated in the Parenting Mindfully for Health programme experienced significant reductions in stress levels, alongside improvements in parenting behaviours.

Children in these families also showed reductions in unhealthy food intake.

Importantly, during the three-month follow-up period, children in the PMH group did not experience significant weight gain.

In contrast, the comparison group receiving only nutrition and physical activity counselling showed no meaningful improvements in parental stress or parenting behaviours.

Children in this group experienced greater weight gain during the follow-up period and were six times more likely to move into the overweight or obesity risk category.

Researchers also observed differences in the relationships between stress, parenting, and children’s diet.

Among families in the control group, higher parental stress remained associated with weaker parenting behaviours and lower intake of healthy foods among children.

However, this relationship was no longer statistically significant in families who had participated in the stress management intervention.

“The combination of mindfulness with behavioral self-regulation to manage stress, integrated with healthy nutrition and physical activity, seemed to protect the young children from some of the negative effects of stress on weight gain,” Sinha said.

Building on research into stress and chronic disease

The study builds on broader research conducted at the Yale Stress Center, an interdisciplinary consortium established through a 2007 National Institutes of Health Common Fund initiative.

The centre investigates the biological and behavioural effects of stress, including how stress influences health behaviours and contributes to chronic mental and physical illnesses.

Researchers involved in the current study emphasised that childhood obesity remains a pressing health concern.

“Childhood obesity is such a major issue right now, and the results of this study are highly relevant to the current administration’s priority of reducing childhood chronic diseases,” said Sinha. “When people start moving up the weight scale, their risk of obesity-related illnesses, even in children, is increased.”

The findings suggest that addressing parental stress may represent an additional strategy for preventing early childhood obesity.

Longer-term studies are now underway to better understand the sustained effects of the Parenting Mindfully for Health programme. According to Sinha, results from a larger group of families followed for two years are expected in future research.

Research team and funding

The study was co-led by Wendy Silverman, the Alfred A. Professor in the Child Study Center and professor of psychology, and Ania Jastreboff, the Harvey and Kate Cushing Professor of Medicine and professor of pediatrics.

Additional contributors came from several departments at Yale School of Medicine, including pediatrics, neuroscience, and the Yale Child Study Center.

Researchers from the Bethesda Group, the Chicago School of Professional Psychology, the University of New Mexico, and George Mason University also participated in the study.

The research was supported by funding from the U.S. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

CCH insight:

Childhood obesity is rising and is a major public health concern, so research like this, which improves our understanding of the determinants of childhood obesity, are very valuable. We know that stress causes overeating in many adults, and it is not surprising that it can impact their children too. People experiencing high levels of stress are usually time-poor and will find it very challenging to provide a healthy diet and lifestyle for their young children. The intervention described in the study appears to be effective, but the difficulty will be in scaling it up, at an affordable cost, so it can reach tens or hundreds of thousands of families. Developing an online version would be one way to approach this.

Developing an online version would be one way to approach this. For practitioners wanting to build these skills themselves, CCH’s Behaviour Change Skills CPD short courses (three 2-hour modules, fully online, CPD-accredited) teaches evidence-based techniques from psychology and behavioural science to help patients and families change diet, activity and other health behaviours for good.
Explore Behaviour Change Skills →

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Ultra-Processed Food Intake Linked to Higher Risk of Binge Eating in Adults Living with Obesity

Key Takeaways: 

• Higher consumption of ultra-processed foods was associated with increased symptoms of binge eating, bulimia-related behaviours, and emotional or uncontrolled eating in adults living with obesity.
  
• Individuals consuming the greatest proportion of ultra-processed foods had poorer overall diet quality and significantly lower protein intake.
  
• The findings suggest that addressing eating behaviour patterns alongside dietary composition may be important when supporting people living with obesity.
  
  
  

Rising consumption of ultra-processed foods during nutritional transition

A cross-sectional study published in Archives of Endocrinology and Metabolism has explored the relationship between ultra-processed food (UPF) intake and eating behaviour among adults living with obesity in São Paulo, Brazil.

The research was conducted against the backdrop of a broader nutritional transition that has been occurring in many developing countries. Economic development, demographic changes, cultural shifts, and evolving food systems have led to major transformations in dietary patterns.

While these changes have contributed to reductions in malnutrition and infectious diseases, they have also been accompanied by a marked increase in noncommunicable diseases such as obesity. A key driver of this shift has been the growing consumption of highly processed foods that are rich in fat, sugar, and refined ingredients.

Previous research has linked high consumption of ultra-processed foods to a range of adverse health outcomes, including obesity, overweight, type 2 diabetes, metabolic syndrome, cardiovascular and cerebrovascular disease, anxiety, depression, and increased all-cause mortality.

There is also emerging evidence that ultra-processed foods may influence eating behaviour itself. Some studies suggest that these foods may affect neurobiological and endocrine pathways that regulate appetite, potentially encouraging compulsive overeating.

Disordered eating patterns are also known to occur among individuals living with obesity. These patterns can complicate treatment and may reduce the effectiveness of weight management interventions. Understanding how ultra-processed food consumption interacts with eating behaviour is therefore clinically important.

Study design and participant characteristics

To explore this relationship, researchers recruited adults aged 18 to 59 years living with obesity, defined as a body mass index (BMI) of 30 kg/m² or higher. Participants were recruited both through a clinical obesity treatment service and via social media in São Paulo.

Several exclusion criteria were applied to minimise confounding factors. Individuals were excluded if they were pregnant or had diagnosed eating disorders, cardiac disease, renal disease, obesity caused by genetic disorders, or if they were taking antiepileptic medications or corticosteroids. People who smoked, misused alcohol, or were currently receiving pharmacological treatment for weight loss were also excluded.

Dietary intake was assessed using three non-consecutive 24-hour dietary recalls, including one weekend day. Researchers used the multiple-pass method, a structured interview approach designed to improve the accuracy of dietary reporting.

Foods reported in the recalls were categorised using the NOVA classification system, which groups foods according to the degree of industrial processing. Diet quality was assessed using the Diet Quality Index associated with the Digital Food Guide.

Eating behaviour was evaluated using validated self-administered online questionnaires:

• BITE (Bulimic Investigatory Test Edinburgh) – measuring symptoms and severity of bulimia and binge eating
  
• TFEQ-21 (Three-Factor Eating Questionnaire) – assessing cognitive restraint, emotional eating, and uncontrolled eating
  
• DEBQ (Dutch Eating Behaviour Questionnaire) – evaluating external eating, emotional eating, and restrained eating
  

Associations between ultra-processed food intake and eating behaviours were analysed using generalised linear models.

Prevalence of unusual eating behaviours

A total of 77 adults took part in the study. Of these participants, 78 percent were female.

The mean age of the group was 36 years, and the average BMI was 39.14 kg/m², corresponding to class II obesity.

Participants were divided into three groups based on the proportion of calories derived from ultra-processed foods:

• First tertile – less than 24.1 percent of calories from UPFs
  
• Second tertile – 24.1 percent to 35.4 percent
  
• Third tertile – more than 35.4 percent
  

Only around one quarter of participants displayed what researchers classified as normal eating behaviour.

In contrast:

• Approximately 52 percent exhibited unusual eating behaviour
  
• 23.4 percent reported binge eating
  

Symptoms consistent with unusual eating behaviours were observed across all tertiles of ultra-processed food consumption. However, participants in the highest UPF tertile showed significantly higher symptom scores on the BITE questionnaire compared with those in the lowest tertile.

Despite this difference in symptom scores, severity scores did not significantly differ between groups.

Overall, 40.3 percent of participants had clinically significant symptoms, while 13 percent were classified as having severe symptoms.

Eating style patterns associated with UPF intake

The study also examined several different eating style patterns.

Using the DEBQ questionnaire, researchers found that:

• 37.8 percent of participants had elevated external eating scores
  
• 36.5 percent had elevated emotional eating scores
  
• 25.7 percent had elevated restrained eating scores
  

Results from the TFEQ-21 questionnaire revealed:

• 52 percent had higher emotional eating
  
• 29.3 percent demonstrated increased cognitive restraint
  
• 18.7 percent showed higher uncontrolled eating
  

Higher intake of ultra-processed foods was positively associated with several problematic eating behaviours.

These included:

• Binge eating and bulimia-related symptoms measured by BITE
  
• Emotional eating
  
• External eating
  
• Uncontrolled eating
  

Together, these results suggest that people consuming larger amounts of ultra-processed foods were more likely to display eating behaviours characterised by reduced self-regulation and greater responsiveness to emotional or environmental triggers.

Diet quality and macronutrient intake

Across the overall study population, diet quality was classified as intermediate.

Participants in the highest ultra-processed food tertile had significantly lower diet quality scores than those in the lower tertiles.

Clear dietary differences were also observed between groups.

Participants in the lowest tertile consumed a higher proportion of unprocessed or minimally processed foods, whereas those in the highest tertile consumed more ultra-processed foods.

Interestingly, individuals in the first and second tertiles reported greater intake of processed culinary ingredients, such as oils or sugars used in cooking, compared with those in the third tertile.

The average macronutrient distribution across the entire sample was:

• 20 percent protein
  
• 48 percent carbohydrates
  
• 32 percent lipids
  

Participants in the highest UPF tertile had significantly lower protein intake than those in the other groups. Carbohydrate and lipid intake did not differ significantly between tertiles.

Median total daily caloric intake across the sample was 1,661 kcal. However, participants in the highest UPF tertile reported higher caloric intake than those in the second tertile.

Researchers suggested that lower protein intake associated with higher UPF consumption may influence satiety and appetite regulation, potentially contributing to overeating.

Clinical implications and study limitations

Overall, the study found that more than half of adults living with obesity exhibited unusual eating behaviours.

Higher intake of ultra-processed foods was associated with:

• Binge eating
  
• Bulimia-related symptoms
  
• Emotional eating
  
• External eating
  
• Uncontrolled eating
  

In addition, greater consumption of ultra-processed foods was linked to poorer diet quality and reduced protein intake.

These findings suggest that obesity treatment strategies may benefit from incorporating both dietary assessment and evaluation of eating behaviour patterns. Addressing behavioural drivers alongside nutritional composition could potentially improve weight management outcomes.

However, the authors emphasised several important limitations.

Because the study used a cross-sectional design, it cannot establish cause-and-effect relationships. The research was also conducted within a single clinical population in one urban centre, which may limit the generalisability of the findings.

In addition, dietary recalls and questionnaires were self-reported, which may introduce recall bias or social desirability bias. The relatively small sample size and predominantly female participant group may also affect the applicability of the results to broader populations.

Nevertheless, the study highlights the importance of considering ultra-processed food consumption within a wider behavioural and nutritional context when addressing obesity and supporting individuals in weight management.

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GLP-1 Weight-Loss Drugs Found to Work in Rare Genetic Obesity

Key Takeaways:

• GLP-1–based medicines reduced body weight and improved metabolic health in animals lacking the MC4R receptor, a critical regulator of appetite and body weight
  
• The findings suggest these therapies may work through alternative brain and peripheral pathways, offering potential treatment options for people living with rare genetic obesity
  
• Researchers highlight potential risks linked to lean mass loss, emphasising the importance of long-term monitoring and muscle-preserving treatment strategies
  
  
  

Understanding genetic obesity and loss of appetite control

For individuals born with certain genetic mutations affecting appetite regulation, managing body weight can resemble attempting to stop a vehicle with failing brakes. Despite sustained effort, biological signals governing hunger and energy balance do not respond normally.

One of the most important regulators of food intake is the melanocortin-4 receptor (MC4R), located within the hypothalamus. This receptor plays a central role in maintaining energy balance by responding to hormonal signals that indicate satiety.

When mutations disrupt signalling pathways linked to MC4R, individuals may experience profound dysregulation of appetite. Children affected by these mutations frequently develop severe early-onset obesity, and by adulthood many conventional interventions have produced limited or no sustained benefit.

New research published in the International Journal of Obesity now suggests that widely used GLP-1–based anti-obesity medicines may offer a potential therapeutic approach even when this critical biological pathway is absent.

Testing GLP-1 medicines without MC4R function

The research team investigated whether modern incretin-based therapies could still produce weight-loss effects in the complete absence of MC4R signalling.

To explore this question, scientists used genetically engineered mice lacking the MC4R gene entirely. These animals closely replicate clinical features seen in people living with MC4R pathway deficiency, including:

• Excessive food intake
  
• Rapid fat accumulation
  
• Fatty liver disease
  
• Elevated cholesterol levels
  
• Early insulin resistance
  

Under normal physiological conditions, hunger regulation relies heavily on signalling cascades such as the POMC–MC4R and leptin–MC4R pathways, which transmit satiety signals as the stomach approaches fullness. Disruption anywhere along these pathways can lead to some of the most treatment-resistant forms of obesity recognised in clinical medicine.

The researchers therefore posed a direct question: would GLP-1 therapies still work if MC4R signalling were completely removed?

Three leading anti-obesity drugs evaluated

The study examined three prominent weight-management medicines:

• Semaglutide
  
• Tirzepatide
  
• Retatrutide
  

All belong to the broader class of GLP-1–based therapies, which act on receptors distributed across the brain, pancreas and vagus nerve connecting the brainstem to abdominal organs.

Each drug was administered once daily via injection over a 21-day period.

Despite the absence of functional MC4R signalling, all three treatments produced substantial anti-obesity effects. As the authors reported:

“Our findings demonstrate that all three GLP-1 analogs exhibit significant anti-obesity effects in MC4R KO mice.”

Significant weight and metabolic improvements

Weight reduction occurred across all treatment groups:

• Semaglutide reduced body weight by an average of 19.7 percent
  
• Retatrutide achieved a 24.1 percent reduction
  
• Tirzepatide, which targets both GLP-1 and GIP receptors, produced the largest effect with a 31.6 percent reduction
  

Importantly, these outcomes occurred in animals completely lacking MC4R function.

Food intake declined consistently across groups, accompanied by broader metabolic improvements. Researchers observed:

• Reduced liver injury markers
  
• Lower cholesterol and triglyceride levels
  
• Suppression of liver genes associated with fat production
  

The authors concluded:

“These results suggest that GLP-1 analogs may provide an effective treatment option for patients with MC4R-POMC pathway deficiencies.”

Alternative brain and peripheral mechanisms

The findings indicate that GLP-1 therapies may bypass defective MC4R signalling entirely.

According to the research team:

“GLP-1 analogs appear to exert their anti-obesity effects through central pathways that do not involve MC4R, as well as via peripheral mechanisms involving the vagus nerve.”

This alternative mechanism may explain why the drugs remained effective despite removal of a pathway traditionally considered essential for appetite regulation.

Tirzepatide’s superior performance may relate to its additional action on the GIP receptor, providing dual hormonal signalling that enhances metabolic effects.

Implications for rare genetic obesity disorders

The results carry particular relevance for clinicians caring for people living with rare genetic obesity conditions, including POMC deficiency and Prader–Willi syndrome.

Currently, one approved therapy for some of these disorders, setmelanotide, works by stimulating the melanocortin pathway itself. However, treatment effectiveness depends on partial pathway function, which may limit outcomes in individuals with more severe deficiencies.

GLP-1–based therapies differ in that their effects do not appear dependent on MC4R signalling, potentially expanding treatment possibilities for individuals previously considered difficult to treat pharmacologically.

Lean mass loss and long-term considerations

Alongside reductions in fat mass, researchers observed decreases in lean body mass across all treatment groups. This raises important clinical considerations regarding prolonged therapy.

The authors cautioned:

“Chronic suppression of food intake could lead to muscle loss, potentially resulting in sarcopenia.”

They further noted that:

“Combination strategies, possibly including agents that preserve or increase muscle mass, may help mitigate this effect.”

These findings reinforce growing clinical discussion around muscle preservation during pharmacological weight management.

Early evidence, not yet clinical practice

While the results are encouraging, important limitations remain.

The study:

• Ran for only three weeks
  
• Included only male mice
  
• Lost two animals from the tirzepatide group before completion
  
• Has not yet been replicated in human clinical trials involving individuals with MC4R mutations
  

As such, the findings represent proof of biological concept rather than immediate clinical guidance.

The researchers summarised their conclusion clearly:

“This study provides the first demonstration that GLP-1 analogs can be effective in treating obesity associated with MC4R deficiency.”

A potential shift in understanding obesity treatment

The study contributes to a broader shift in obesity science, suggesting that effective treatment may not depend on restoring a single disrupted pathway. Instead, therapies capable of engaging multiple neural and peripheral systems may overcome even profound genetic drivers of obesity.

For people living with rare genetic forms of obesity, these findings offer cautious optimism that future treatments may succeed where traditional approaches have historically fallen short.

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Obesity-Related Fat Tissue Signals Identified as a Driver of Age-Related Muscle Loss

Key Takeaways: 

• Researchers have identified a biological mechanism linking obesity-related fat tissue to accelerated muscle loss in older adults.
• Tiny particles released by adipose tissue were shown to directly trigger muscle atrophy in ageing human muscle cells.
• Younger muscle appears biologically protected from these effects, highlighting an age-dependent vulnerability that may inform future therapies.
  
  
  

New insight into sarcopenic obesity

Researchers at the University of Birmingham have identified a previously unrecognised biological pathway through which obesity may contribute to muscle loss in older adults. The findings provide important new insight into sarcopenic obesity, a condition in which excess body fat exists alongside reduced muscle mass and strength.

The study, published in the Journal of Cachexia, Sarcopenia and Muscle and conducted through the National Institute for Health and Care Research (NIHR) Birmingham Biomedical Research Centre (BRC), demonstrates for the first time that signals released from adipose tissue can directly induce muscle wasting in human cells.

Sarcopenic obesity is becoming increasingly common as populations age and is associated with frailty, impaired mobility and poorer overall health outcomes. The condition is estimated to affect approximately 11% of the population.

Fat tissue communication with muscle

The research focused on extracellular vesicles – microscopic particles released by fat tissue that act as biological messengers between organs and tissues.

Investigators discovered that extracellular vesicles derived specifically from obese adipose tissue, rather than lean tissue, caused significant thinning of muscle fibres obtained from older adults. This thinning represents a hallmark feature of muscle atrophy.

The harmful effects were traced to molecular cargo carried within these vesicles, particularly miR-150-5p, a microRNA known to regulate gene expression pathways involved in maintaining muscle structure and function.

These findings suggest that obesity does not simply increase fat mass but fundamentally alters how adipose tissue behaves and communicates with other organs, including skeletal muscle.

Age-dependent vulnerability of muscle

A notable finding of the study was that muscle cells derived from younger adults showed resistance to these obesity-related signals.

When exposed to extracellular vesicles from obese adipose tissue, younger muscle cells did not undergo the same degree of thinning observed in older muscle cells. This indicates that ageing muscle becomes biologically more susceptible to inflammatory and metabolic signals associated with obesity.

Speaking about the findings, first author Dr Joshua Price, Postdoctoral Researcher, explained:

“It isn’t just having more fat tissue that matters. Obesity changes how fat tissue behaves and how it communicates with muscle. Ageing muscle is far more vulnerable to these altered signals, which helps explain why muscle loss accelerates with obesity later in life.”

Identifying a potential therapeutic target

The identification of miR-150-5p as a key molecular driver presents a potential opportunity for therapeutic intervention. Researchers found that inhibiting this microRNA could partially reduce the muscle-wasting effects observed in laboratory models.

Overall, the results suggest a dual biological reality – younger muscle demonstrates protective resilience, while ageing muscle becomes increasingly vulnerable to obesity-related signalling pathways.

Senior author Professor Simon Jones, Professor in Musculoskeletal Ageing at the University of Birmingham and lead for the NIHR Birmingham BRC’s Sarcopenia and Multimorbidity research theme, said:

“Through this research, we’ve identified a key molecular pathway by which obesity can accelerate muscle loss in older adults. Importantly, we found that younger muscle appears resilient to these harmful signals, whereas ageing muscle becomes more vulnerable. This reinforces the importance of maintaining a healthy weight and muscle health as we age.”

He added:

“Our findings also open two potential therapeutic avenues: either blocking or modifying the harmful extracellular vesicles released from obese tissue, or developing strategies to make older muscle more resilient, mimicking the protective effects seen in younger muscle.”

Implications for ageing and obesity care

The study strengthens understanding of how ageing and obesity interact at a cellular level to influence physical decline. Rather than viewing muscle loss solely as a consequence of ageing or inactivity, the findings highlight obesity-related biological signalling as an active contributor.

By demonstrating that altered communication between fat and muscle tissue can directly drive muscle atrophy, the research provides a clearer mechanistic explanation for why people living with obesity may experience accelerated functional decline later in life.

The work was delivered through the NIHR Birmingham Biomedical Research Centre, with Dr Joshua Price serving as a BRC-funded postdoctoral research associate within the Sarcopenia and Multimorbidity research theme.

Together, these findings may support future strategies aimed at preserving muscle health in ageing populations, particularly among people living with obesity, where preventing muscle loss is critical for maintaining independence, mobility and long-term health outcomes.

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Parental Weight Before Pregnancy Linked to Higher Risk of Fatty Liver Disease in Adult Offspring, UK Study Finds

Key Takeaways: 

• Pre-pregnancy overweight or obesity in either parent is associated with a significantly increased risk of metabolic dysfunction associated steatotic liver disease (MASLD) in their children by early adulthood.
  
• When both parents were living with overweight or obesity prior to conception, the likelihood of MASLD in offspring by age 24 was more than three times higher.
  
• Much of this increased risk appears to be mediated by excess weight accumulated during childhood and adolescence.
  
  
  

Rising concern over MASLD across generations

Parental weight status before pregnancy may play an important role in shaping long-term liver and metabolic health in the next generation, according to new research published online in Gut. The findings suggest that overweight and obesity in both mothers and fathers prior to conception are linked to a heightened risk of metabolic dysfunction associated steatotic liver disease (MASLD) in their children as young adults.

MASLD, previously known as non-alcoholic fatty liver disease, is now recognised as the most common chronic liver condition worldwide. Researchers note that the disease affects approximately 15% of children and more than 30% of adults globally. The condition is characterised by excess fat accumulation in the liver alongside cardiometabolic abnormalities and may progress to cirrhosis or liver failure in some individuals.

While earlier studies have primarily focused on maternal obesity, uncertainty has remained regarding the contribution of paternal weight and the role of childhood weight trajectories in determining future disease risk.

Large UK birth cohort provides long-term insight

To investigate these questions, researchers analysed data from 1,933 participants enrolled in the UK Avon Longitudinal Study of Parents and Children (ALSPAC), a long-running population study tracking health outcomes across generations.

The study examined associations between parental body mass index (BMI) before pregnancy and the likelihood that offspring would develop MASLD by the age of 24.

MASLD was defined as the presence of elevated liver fat together with at least one cardiometabolic risk factor, such as raised cholesterol levels or elevated fasting glucose.

Both parents provided information on height, weight, BMI and waist circumference before pregnancy. They also completed detailed questionnaires during pregnancy and following childbirth covering a wide range of potential influencing factors, including:

• Age at delivery
  
• Smoking during early pregnancy
  
• Weekly alcohol consumption prior to pregnancy
  
• Employment status
  
• Educational attainment
  

Mothers additionally reported physical activity levels and whether they had previously been diagnosed with diabetes or hypertension at study enrolment.

Tracking early life and adolescent risk factors

Extensive information was also collected about the children, allowing researchers to examine developmental influences across childhood and adolescence. Recorded factors included:

• Sex
  
• Mode of delivery
  
• Gestational age and birthweight
  
• Antibiotic exposure during the first six months of life
  
• Duration of breastfeeding
  

Participants underwent repeated measurements of BMI and waist circumference between the ages of 7–9, 10–12 and 13–17 years. Lifestyle factors in early adulthood, including alcohol and tobacco use, were also assessed.

One in ten young adults developed MASLD

By age 24, MASLD was identified in 201 participants, representing approximately one in ten individuals in the cohort. The remaining 1,732 participants had normal liver findings.

Those living with MASLD were more likely to be male and to have a higher BMI compared with peers without the condition.

After adjusting for multiple potential confounding factors, both maternal and paternal overweight or obesity before conception were independently associated with increased odds of MASLD in offspring.

Each additional kilogram per square metre of maternal BMI increased the likelihood of MASLD by 10%, while each equivalent increase in paternal BMI was associated with a 9% rise in risk.

Most notably, offspring whose parents were both living with overweight or obesity prior to pregnancy had more than three times the odds of developing MASLD compared with those whose parents had a normal BMI.

Childhood weight plays a central role

Further analysis suggested that much of this association operates through weight gain during childhood and adolescence. Researchers estimated that 67% of the increased risk linked to parental overweight or obesity was explained by cumulative excess BMI between the ages of 7 and 17.

Additional analyses incorporating maternal and offspring sugar intake, as well as genetic susceptibility to MASLD, produced similar results, strengthening confidence in the observed associations.

Observational findings with important limitations

The authors emphasise that the study was observational and therefore cannot establish direct causation. Several limitations were also acknowledged.

Parental weight data prior to pregnancy were self-reported, and information was unavailable regarding parental MASLD status or certain underlying health conditions before and during pregnancy. In addition, physical activity levels of offspring in early adulthood were not captured, which may have influenced outcomes.

Implications for preconception health

Despite these limitations, the researchers conclude that their findings highlight the potential importance of parental metabolic health before conception in shaping long-term outcomes for future generations.

They state that the results “lend support to an early life influence of biparental obesity on offspring metabolic health, suggesting efforts to mitigate excess adiposity of both mothers and fathers before conceiving may confer longitudinal benefits to the metabolic outcomes of their future offspring.“

The study adds to growing evidence that prevention of metabolic disease may need to begin not only in childhood, but even before pregnancy, with both parents playing a meaningful role in influencing lifelong health trajectories.

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Mice Study Suggests Tirzepatide Enhances Metabolism by Activating Brown Fat in Addition to Reducing Weight

Key Takeaways: 

• A preclinical mouse study indicates that tirzepatide may improve metabolism not only by reducing appetite, but also by activating brown adipose tissue.
  
• The research suggests that this activation increases energy expenditure and supports improvements in blood glucose and lipid levels.
  
• Findings remain preliminary and require confirmation in human studies before clinical conclusions can be drawn.
  
  
  

A closer look at tirzepatide’s metabolic effects

Tirzepatide has transformed the treatment landscape for people living with obesity and for those with poorly controlled type 2 diabetes mellitus. Despite its established clinical benefits, the precise molecular and cellular mechanisms underpinning its effects are not yet fully understood.

A recent study conducted in mice provides new insight into how the drug may influence metabolism beyond its well-recognised impact on body weight. The findings suggest that tirzepatide directly activates brown adipose tissue, a specialised form of fat involved in energy expenditure. According to the researchers, this discovery helps clarify how the drug works and may inform the development of more comprehensive treatments for obesity and related metabolic diseases.

The study was led by Marion Peyrou, Ramón y Cajal researcher at the Faculty of Biology and the Institute of Biomedicine of the University of Barcelona, the Sant Joan de Déu Research Institute and the CIBER in Physiopathology of Obesity and Nutrition.

A dual-action therapy

Tirzepatide, marketed under the name Mounjaro, is approved for weight management in adults living with obesity or with overweight accompanied by comorbidities. It is also indicated for the treatment of inadequately controlled type 2 diabetes.

Unlike earlier anti-obesity medicines, tirzepatide acts simultaneously on two hormonal receptors – glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). This dual mechanism leads to substantial reductions in body weight, primarily through decreased food intake driven by appetite suppression.

However, appetite reduction alone may not explain the full spectrum of its metabolic effects.

Investigating effects on adipose tissue

To better understand how tirzepatide exerts its actions, researchers conducted a detailed analysis of its effects on different fat depots in an experimental mouse model. Such in-depth tissue analysis is not feasible in humans.

In the study, mice were rendered obese through a high-fat diet and then treated with tirzepatide. Their outcomes were compared with a control group of mice that consumed the same quantity of food but did not receive the drug. This design allowed the researchers to distinguish between effects caused directly by the drug and those resulting solely from reduced caloric intake.

The analysis revealed that tirzepatide activates brown adipose tissue. Unlike white adipose tissue, which primarily stores excess energy and accumulates in obesity, brown adipose tissue specialises in burning calories to generate heat.

“This activation is associated with an increased capacity to burn metabolic energy and with the production of batokines by brown adipose tissue, molecules that are beneficial for metabolism,” says Marion Peyrou.

Metabolic benefits beyond appetite suppression

The activation of brown adipose tissue is particularly significant because it indicates that tirzepatide may exert metabolic benefits independent of weight loss due to appetite reduction.

“This drug not only reduces body weight, but also has beneficial effects on metabolism. Active brown adipose tissue ‘burns’ glucose and fat within the body, which would contribute to its positive effect not only in reducing body weight, but also in lowering blood glucose and fat levels, and improving metabolism,” the researcher points out.

By enhancing the body’s ability to utilise both glucose and lipids, activation of brown fat may contribute to improved glycaemic control and lipid profiles in addition to weight reduction.

Implications for obesity treatment strategies

For several years, activation of brown adipose tissue has been viewed as a promising strategy for tackling obesity and metabolic disorders. However, previous pharmacological attempts to stimulate brown fat have frequently been limited by adverse effects, particularly cardiovascular complications.

“Tirzepatide, although it activates brown adipose tissue, does not have these negative effects; on the contrary, it shows cardiovascular benefits. If our findings are confirmed in humans, it would reinforce the importance of developing therapeutic strategies that not only reduce food intake but also increase energy expenditure and brown fat activation,” explains the researcher.

These findings support the broader principle that obesity treatments may be more effective when they target multiple physiological pathways simultaneously. Addressing both energy intake and energy expenditure could offer a more comprehensive approach to weight management and metabolic health.

“This could help improve weight control and reduce associated disorders, such as type 2 diabetes and other metabolic disorders,” she adds.

Towards more personalised prescribing

A deeper understanding of tirzepatide’s mechanisms may also influence how such medicines are prescribed in future.

“Identifying which patient profiles could benefit most, for example those with more compromised energy expenditure, would open the door to more personalized medicine, based not only on appetite or weight control, but also on overall metabolic status,” she emphasizes.

Such an approach could support more tailored treatment strategies for people living with obesity and metabolic disease, taking into account differences in metabolic function rather than focusing solely on body weight.

The need for caution and further research

Despite the promising findings, the researchers emphasise that the results are based on animal data and cannot yet be directly translated into clinical practice.

“As this is a study conducted on mice, we must be cautious, as there may be significant differences between species in terms of metabolism regulation, adipose tissue distribution and response to drugs. Therefore, we need more clinical evidence on the action of these drugs on fat in humans,” concludes Peyrou.

Further human studies will be required to confirm whether the activation of brown adipose tissue observed in mice also occurs in people receiving tirzepatide and whether it meaningfully contributes to its metabolic benefits.

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GPs Offered £3,000 Incentive to Increase Prescribing of NHS Weight Loss Injections

Key Takeaways:

• GP practices in England will be eligible for a £3,000 annual payment for prescribing the maximum number of eligible patients the weight loss drug Mounjaro.
  
• Access to NHS weight loss injections remains tightly restricted, with eligibility based on BMI and specific health conditions.
  
• Professional bodies stress that prescribing decisions are driven by clinical judgement, not financial incentives, and warn that workload pressures may increase.
  
  
  

New financial incentives added to GP contract

GP practices across England are set to receive annual incentive payments of £3,000 for prescribing weight loss medication to the maximum number of patients who meet NHS eligibility criteria.

The payments will be incorporated into the national GP contract from April. In addition, practices will be able to receive approximately £1,000 per year for referring patients to weight loss support programmes.

Ministers have said the objective is to ensure that people who could benefit from structured weight management and pharmacological support are able to access it within primary care.

However, specialists in obesity care have cautioned that the overall impact of the scheme may be modest. They note that eligibility for NHS weight loss injections remains tightly restricted and that the incentive does not expand access to a broader population.

Focus on Mounjaro within primary care

The new incentive applies solely to Mounjaro, a next-generation injectable treatment for weight management.

Mounjaro became available on the NHS in 2025. Despite this, prescribing rates in general practice have reportedly been lower than expected, with some variation in uptake across different areas.

Another injectable weight loss medication, Wegovy, is also available through the NHS. However, it is not prescribed by GPs and is instead provided through specialist NHS weight management services.

More than one million people are estimated to be using weight loss injections in the UK. The majority, around nine in ten, are paying privately rather than receiving the medication through the NHS.

Government position: access based on need

The Health Secretary, Wes Streeting, described the medicines as potentially transformative for people living with obesity.

He said: “Weight loss drugs can be a real game changer for those who need them. I’m determined that access should be based on need, not ability to pay.

“Outside the NHS, we’ve seen those who can spare the cash buying privately, and the proliferation of rogue prescribers peddling dangerous unlicensed drugs that are putting patients at risk.

“Investing in general practice will help bring this modern medicine to the many, not just the few, and help shift the focus of the NHS from treatment to prevention.“

The government argues that embedding prescribing targets within the GP contract is consistent with longstanding practice. Incentive payments have previously been used to improve dementia diagnosis rates, increase vaccination uptake, and encourage the prescription of statins to reduce cardiovascular risk.

This marks the first time that weight loss injections have been formally included in the GP contract framework, with the £3,000 payment linked to prescribing the maximum number of eligible patients Mounjaro.

Strict eligibility criteria remain in place

Although the incentive has been introduced, NHS access to Mounjaro remains limited.

During the current financial year, GPs have only been permitted to prescribe the medication to people with severe obesity defined as a body mass index over 40, alongside certain weight-related health conditions.

From next year, eligibility is expected to expand to include people with a BMI over 35. By 2028, it is anticipated that 220,000 patients will be receiving Mounjaro through the NHS. Lower BMI thresholds apply for some ethnic groups.

Despite these planned expansions, the roll-out to date has been described as uneven, with variation between practices and regions.

Support from obesity advocates – with caveats

Katharine Jenner, Director of the Obesity Health Alliance, welcomed the move but emphasised its limitations.

She said: “This doesn’t mean weight loss drugs will suddenly be available to everyone who wants them.

“NHS access will remain very limited and focused on those with the greatest clinical need, and these treatments are most effective when combined with sustained support.“

She also stressed the importance of prevention alongside treatment:

“If we’re serious about moving from sickness to prevention, expanded treatment must go alongside stronger action to improve the food environment and prevent obesity in the first place.“

Her comments reflect a broader concern within public health that medication alone cannot address the structural drivers of obesity.

Concerns about equity and workload

Dr Katie Bramall, representing the British Medical Association, questioned whether the scheme would meaningfully reduce inequalities in access.

She said: “While the headlines promise much, in reality there will be no change to NHS England’s eligibility criteria for patients to access injectable weight-loss medication on the NHS.

“These proposals will do nothing over the next year to address the divide between those able to pay and those left waiting unable to afford private self-funded treatments“

Similarly, Professor Victoria Tzortziou Brown of the Royal College of GPs emphasised that prescribing decisions are rooted in clinical appropriateness rather than financial drivers.

She said: “GPs do not withhold treatment or prescribe based on financial incentives. Decisions are guided by clinical judgement and what is safest and most appropriate for individual patients.

“Widening the roll-out of these medications in general practice could end up increasing workload in a way that may not be sustainable and risk raising unrealistic expectations among patients who may not be eligible or for whom these medicines are not suitable.“

Supporting GPs to prescribe these medications safely and confidently – from patient selection through initiation, titration and managing side effects – is the focus of professional training such as the College of Contemporary Health’s GLP-1RAs in Practice: Prescribing, a CPD-accredited online short course.

Her comments highlight the tension between expanding pharmacological options in primary care and managing existing workforce pressures.

A cautious step in a tightly controlled rollout

The introduction of incentive payments signals the government’s intention to embed weight loss pharmacotherapy more firmly within general practice. However, strict eligibility criteria remain in place and access is expected to expand gradually over several years.

While the policy aims to increase NHS provision and reduce reliance on private prescribing, professional bodies and advocacy groups have made clear that the immediate effect will be limited. For now, access continues to be targeted at people with the greatest clinical need, with broader prevention strategies still viewed as essential to addressing obesity at population level.

CCH insight:

It is surprising that GPs need incentivising to prescribe GLP-1 medications like Mounjaro – there is undoubtedly a huge need and demand for these drugs. The reluctance to prescribe them is most likely due to the weight bias that still pervades our society and our health system, the view that people shouldn’t need medication to manage their weight. Referring to these drugs as ‘weight loss jabs’ is not helpful – they are anti-obesity medications. Rather than offer a £3k bonus, GPs should be offered training in understanding obesity as a chronic, relapsing disease, and how GLP-1 medications not only support weight loss but can also improve long-term metabolic and cardiovascular health, and in the long run will save billions of pounds by reducing diabetes and heart disease by reducing diabetes and heart disease. That is precisely why targeted education matters more than a bonus: CCH’s GLP-1RAs in Practice: Prescribing CPD short course (2 CPD hours, fully online, CPD-accredited) equips prescribers with everything they need to use these medications well – from patient selection and initiation to titration, side-effect management and the wider conversation about obesity as a chronic disease.

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