Obesity Care

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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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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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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New Cochrane Review Finds Intermittent Fasting Offers No Clear Weight Loss Advantage

Key Takeaways:

• A major Cochrane review found intermittent fasting did not lead to clinically meaningful weight loss compared with standard dietary advice or no structured diet.
  
• Evidence on safety and long-term outcomes remains limited due to small trials, inconsistent reporting, and short follow-up periods.
  
• Experts caution against overinterpreting social media claims and emphasise the need for individualised, long-term approaches to weight management.
  
  
  

Intermittent fasting under scrutiny

Intermittent fasting has become one of the most widely promoted dietary strategies for weight loss, often presented as a superior alternative to conventional calorie reduction. However, a new Cochrane review suggests that these claims may not be supported by robust evidence.

According to the review, intermittent fasting does not appear to deliver greater weight loss than standard dietary advice or even no specific diet plan. The findings challenge the widespread perception that structured fasting schedules offer a unique or clinically meaningful advantage for people who are overweight or living with obesity.

Obesity remains a global public health challenge

Obesity continues to represent a major public health concern worldwide and is now among the leading causes of death in high-income countries. Data from the World Health Organization show that global adult obesity rates have more than tripled since 1975. By 2022, an estimated 2.5 billion adults were classified as overweight, including around 890 million adults living with obesity.

Against this backdrop, intermittent fasting has gained substantial attention. Eating patterns such as alternate-day fasting, periodic fasting, and time-restricted feeding are widely promoted across social media platforms, often accompanied by claims of rapid weight loss and metabolic benefits.

What the review examined

To assess whether intermittent fasting truly offers an advantage, researchers analysed 22 randomised clinical trials involving 1,995 adults across North America, Europe, China, Australia, and South America. The studies evaluated a range of fasting approaches, including alternate-day fasting, periodic fasting, and time-restricted feeding. Most trials followed participants for up to one year.

When outcomes were compared with those of traditional dietary advice or no dietary intervention, intermittent fasting did not result in a clinically meaningful difference in weight loss. In practical terms, fasting-based approaches did not outperform more conventional strategies.

Limited evidence on safety and long-term outcomes

The review also highlighted substantial limitations in the available evidence. Reporting of side effects varied widely between studies, and many trials were relatively small. Inconsistent data collection made it difficult to draw firm conclusions about safety or potential long-term effects.

As a result, the overall certainty of the evidence was judged to be limited.

“Intermittent fasting just doesn’t seem to work for overweight or obese adults trying to lose weight,” said Luis Garegnani, lead author of the review from the Universidad Hospital Italiano de Buenos Aires Cochrane Associate Centre.

Social media enthusiasm outpaces the evidence

Garegnani also warned against the level of enthusiasm surrounding intermittent fasting online. “Intermittent fasting may be a reasonable option for some people, but the current evidence doesn’t justify the enthusiasm we see on social media.”

A further concern is the lack of long-term research. Few studies have examined outcomes beyond relatively short trial periods. “Obesity is a chronic condition. Short-term trials make it difficult to guide long-term decision-making for patients and clinicians,” Garegnani added.

Generalisability remains uncertain

Most of the studies included in the review primarily involved white participants living in high-income countries. Given that obesity prevalence is rising rapidly in low and middle-income countries, the findings may not fully reflect outcomes in more diverse global populations.

The authors note that responses to intermittent fasting could vary depending on sex, age, ethnic background, underlying health conditions, or existing eating behaviours and eating disorders.

Implications for clinical practice

Given the current state of evidence, the review’s authors advise caution when recommending intermittent fasting as a weight loss strategy.

“With the current evidence available, it’s hard to make a general recommendation,” said Eva Madrid, senior author from the Cochrane Evidence Synthesis Unit Iberoamerica. “Doctors will need to take a case-by-case approach when advising an overweight adult on losing weight.”

Overall, the findings reinforce the need for personalised, sustainable approaches to weight management rather than reliance on highly promoted dietary trends.

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Big Breakfast Study Shows Protein Reduces Appetite While Fibre Supports Gut Microbiome Health

 Key Takeaways: 

• Within a calorie-restricted big-breakfast eating pattern, a higher-protein breakfast improved satiety, while a higher-fibre breakfast produced more favourable gut microbiota and short-chain fatty acid profiles.
  
• Both dietary approaches led to clinically meaningful short-term weight loss and improvements in metabolic markers, but with distinct physiological effects.
  
• Fibre-rich breakfasts were linked to greater abundance of beneficial butyrate-producing bacteria, whereas protein-rich breakfasts may better support appetite control and dietary adherence.
  
  
  

Background and rationale

A recent study published in the British Journal of Nutrition examined how breakfast composition influences appetite regulation, energy balance and markers of gut microbiota health when consumed as part of a calorie-restricted, big-breakfast weight-loss diet.

There is growing evidence that meal timing, in addition to dietary composition, plays an important role in healthy weight management. Previous research has shown that people who eat earlier in the day tend to lose more weight than those who eat later. Morning calorie intake has also been associated with improved blood glucose control and lower hunger levels compared with evening intake.

Larger breakfasts have been shown to improve appetite control, while late eating patterns have been linked to increased hunger and greater fat storage. Despite public health advice emphasising the importance of breakfast for weight management, relatively little is known about what people typically consume in the morning. Moreover, evidence explaining how meal timing, calorie distribution and macronutrient composition interact to influence appetite remains limited.

Study design and dietary interventions

The researchers used a randomised crossover design to compare two calorie-restricted weight-loss diets with identical big-breakfast calorie distribution but differing macronutrient profiles. The primary outcomes were appetite, energy balance and gut microbiota composition and metabolites, rather than clinical gastrointestinal outcomes.

Healthy adults with overweight or obesity, aged 18–75 years, were recruited. The protocol consisted of:

• a four-day ad libitum diet
  
• a four-day maintenance diet
  
• a 28-day high-fibre weight-loss diet or high-protein weight-loss diet
  

These phases were separated by a washout period, with participants acting as their own controls. Resting metabolic rate was measured by indirect calorimetry during screening.

The maintenance diet provided 15% of energy from protein, 55% from carbohydrate and 30% from fat, and was set at 1.5 times resting metabolic rate to maintain body weight. Both weight-loss diets were set at 100% of resting metabolic rate to induce a calorie deficit.

Participants consumed three meals per day, with 45% of daily calories at breakfast, 20% at lunch and 35% in the evening. Lunch intake was allowed ad libitum within the provided calorie allowance.

• High-fibre weight-loss diet – 50% carbohydrate, 15% protein and 35% fat, incorporating both soluble and insoluble fibre sources such as lentils, fava beans, buckwheat and wheat bran.
  
• High-protein weight-loss diet – 30% protein, 35% carbohydrate and 35% fat, using foods including fish, poultry, eggs, red meat and dairy.
  
  
  

Measurements and outcomes assessed

Body density, waist and hip circumference, resting metabolic rate, total body water and blood pressure were measured. The thermic effect of food was assessed every 30 minutes for four hours after breakfast. Subjective appetite was evaluated using visual analogue scales.

Blood samples collected after an overnight fast were used to assess glucose, lipid profile and insulin as metabolic biomarkers rather than clinical disease outcomes. Insulin and glucose values were used to calculate HOMA-IR, HOMA-β and the insulin-to-glucose ratio. Total body water was measured using deuterium dilution, and faecal samples were collected to analyse gut microbiota composition.

Weight loss, energy expenditure and metabolic markers

Nineteen participants completed the study, including two women. The mean age was 57.4 years and the mean body mass index was 33.3 kg/m², indicating a predominantly male cohort and limiting generalisability to broader populations.

Energy intake did not differ significantly between the two weight-loss diets. Average weight loss was 4.87 kg with the high-fibre diet and 3.87 kg with the high-protein diet. Both diets significantly reduced fat mass and fat-free mass compared with the maintenance diet, although loss of fat-free mass was greater with the high-fibre approach.

Total body water was reduced following the high-fibre diet but not after the high-protein diet. Waist and hip circumferences, as well as waist-to-hip ratio, were significantly reduced with both weight-loss diets compared with the maintenance diet.

The high-protein breakfast maintained postprandial satiety, whereas the high-fibre breakfast was associated with reduced satiety after meals. Resting metabolic rate declined significantly after both weight-loss diets. The thermic effect of food was lower following the high-fibre diet than after the high-protein or maintenance meals.

Both weight-loss diets improved lipid profiles relative to baseline, with no significant difference between the two approaches. Fasting and postprandial glucose levels were reduced by around 10% following the high-fibre diet and by 8–7% following the high-protein diet compared with the maintenance diet. Fasting insulin, HOMA-IR and the insulin-to-glucose ratio were significantly lower after both weight-loss diets.

HOMA-β decreased significantly more after the high-protein diet than after the maintenance diet, with no significant change observed after the high-fibre diet.

Gut microbiota composition and short-chain fatty acids

Total bacterial load in faecal samples did not differ significantly between the two weight-loss diets. However, microbial diversity was lower following the high-protein diet compared with the high-fibre diet.

Distinct differences in microbiota composition were observed between the dietary patterns, although individual variation remained a major determinant of microbiota profiles and diet explained only part of the observed variability.

The high-fibre diet was associated with a greater abundance of butyrate-producing bacteria, including Anaerostipes hadrus, Roseburia faecis and Faecalibacterium prausnitzii. At the genus level, Bifidobacterium, Faecalibacterium and Roseburia were linked to the high-fibre diet, while Streptococcus was associated with the high-protein diet.

Total short-chain fatty acids and key faecal short-chain fatty acids, including acetate, butyrate and propionate, were significantly lower with the high-protein diet compared with the high-fibre diet.

Interpretation and clinical implications

Overall, the findings suggest that within a calorie-restricted big-breakfast eating pattern, breakfast composition meaningfully influences short-term weight loss, metabolic health markers and gut microbiota characteristics.

Both dietary approaches led to significant weight reduction and metabolic improvements. The high-protein breakfast produced greater satiation, which may support long-term adherence in some people. In contrast, the high-fibre breakfast promoted a more favourable gut microbiota profile and higher short-chain fatty acid production, which may be beneficial for long-term gut health, although this was inferred from microbial and metabolic markers rather than direct clinical outcomes.

The authors emphasised that longer-term studies are needed to determine whether these differences are sustained over time and how they translate into long-term health outcomes.

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Obesity Associated With Higher Risk of Severe Infectious Disease, Large Study Finds

Key Takeaways:

• People living with obesity face a substantially higher risk of hospitalisation or death from a wide range of common infections, with risk increasing alongside body weight.
  
• Weight change matters – moving out of obesity is associated with fewer severe infections, while progression into obesity increases risk.
  
• Global estimates suggest that around one in ten infectious disease deaths worldwide may be linked to obesity.
  
  
  

Obesity and severe infection risk across multiple pathogens

A large population-based study has examined the relationship between obesity and the risk of severe infectious diseases, finding that people living with obesity are significantly more likely to be hospitalised or die from common infections. These include influenza, Covid-19, pneumonia, and gastrointestinal and urinary tract infections. For people living with morbid obesity, the risk was approximately three times higher than for people of healthy weight.

“During the pandemic, obesity was widely linked to a higher likelihood of severe Covid-19. We set out to investigate how broadly this link applies across different types of infections and whether any underlying factors contribute to it. Our findings extend beyond any single pathogen, with similar associations observed for bacterial, viral, parasitic and fungal infections,” says one of the article’s lead authors, Solja Nyberg of the University of Helsinki and the Finnish Institute of Occupational Health.

Notably, HIV and tuberculosis were exceptions, with no evidence that obesity increased the risk of severe disease for these infections. The researchers also found that comorbidities, socioeconomic status, and lifestyle factors such as alcohol consumption and physical activity did not explain the increased infection risk associated with obesity.

Weight matters for infection outcomes

Participants were followed for an average of 13–14 years, with body mass index (BMI) measured at baseline. People living with obesity, defined as a BMI of 30 kg/m² or higher, had a 70% greater risk of hospitalisation or death from any infectious disease compared with people of healthy weight, defined as a BMI of 18.5–24.9. The risk increased progressively with higher body weight.

People living with morbid obesity, defined as a BMI of 40 kg/m² or higher, experienced a risk of severe infection three times that of people of healthy weight.

Importantly, changes in body weight over time were also associated with changes in risk. Participants who lost weight and moved from obesity to overweight or healthy weight experienced 20% fewer severe infections compared with those whose obesity persisted. In contrast, weight gain from overweight to obesity was linked to a 30% higher risk of severe infection.

Possible links with immune system dysfunction

“Obesity is a well-known risk factor for diabetes and other chronic diseases. The links now identified indicate that severe infectious diseases should be added to the same list,” says Mika Kivimäki of the University of Helsinki and University College London, who led the study.

“Obesity seems to weaken the immune system’s ability to manage infections, raising the risk of severe disease,” he explains.

Kivimäki also notes that experimental evidence from studies of weight-loss drugs supports a link between obesity and immune function. Reductions in body weight appear to lower the risk of severe infections alongside other health benefits. However, he emphasises that further research is needed to confirm the biological mechanisms underlying these associations.

Obesity and global infectious disease mortality

The researchers analysed data from large Finnish cohorts and the UK Biobank, tracking participants through national health registers. They also incorporated infectious disease mortality data from the Global Burden of Disease study to assess how obesity contributes to infectious disease deaths across countries and regions.

Their analysis suggests that approximately 0.6 million of the 5.4 million infectious disease deaths recorded worldwide in 2023, equivalent to around 11% or one in ten, were associated with obesity.

In the Nordic countries, the estimated proportions of infectious disease deaths linked to obesity were:

• Finland – 19%
  
• Sweden – 13%
  
• Norway – 11%
  
• Denmark – 12%
  

Among high-income countries, the United States recorded the highest proportion in 2023, at 26%.

Importance of vaccination and prevention

The researchers stress that adults living with obesity should ensure their vaccinations are up to date and take up booster doses when offered to groups at higher risk of severe infection.

They also highlight several limitations of the study. As an observational analysis, it cannot establish causality. In addition, participants in the Finnish cohorts and the UK Biobank are not fully representative of the general population, meaning the findings should be generalised with caution.

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Dietary Melatonin Intake Linked to Lower Rates of Obesity and Depression

Key Takeaways: 

• Higher intake of melatonin from foods was associated with lower prevalence of obesity and depression in a large cohort of Brazilian university graduates.
  
• No significant associations were found between dietary melatonin intake and most cardiometabolic outcomes, including hypertension, metabolic syndrome or type 2 diabetes.
  
• The strongest associations were observed at moderate rather than very high levels of dietary melatonin intake, highlighting the complexity of diet–health relationships.
  
  
  

Background and study context

In a study published in the Journal of Human Nutrition and Dietetics, researchers examined the melatonin content of commonly consumed foods and explored how dietary melatonin intake was associated with a range of health outcomes. The analysis used cross-sectional data from a large cohort of Brazilian university graduates.

Melatonin is a hormone best known for regulating circadian rhythms and sleep–wake cycles. Beyond its endogenous production, melatonin is also present in both animal-based and plant-based foods. Experimental, observational and supplementation studies have linked melatonin to sleep regulation, mood, and metabolic health. Although the concentration of melatonin in foods is considerably lower than in supplements, diets rich in melatonin-containing foods have been shown to increase circulating melatonin levels within physiological ranges.

Previous evidence suggests that increasing melatonin intake through food may deliver doses that align more closely with natural circadian rhythms than pharmacological supplementation, potentially avoiding suprapharmacological exposure. On this basis, dietary melatonin has attracted interest as a marker of broader dietary patterns rather than as a direct therapeutic intervention.

Rationale for examining dietary melatonin

Obesity, depression and sleep disorders represent a substantial and growing public health burden. Prior observational and experimental studies have suggested that melatonin may have protective effects against inflammatory, metabolic and neurobehavioural outcomes. In addition, observational research has reported inverse associations between melatonin exposure and outcomes such as liver cancer incidence and all-cause mortality.

Despite this, relatively few studies have investigated habitual dietary melatonin intake or its associations with chronic conditions in adult populations. The present study aimed to address this gap by estimating melatonin intake from the diet and examining its relationship with multiple health outcomes in a large cohort.

Study design and population

The analysis drew on data from the Cohort of Universities of Minas Gerais (CUME+) study. CUME+ is an open, prospective cohort designed to assess the impact of dietary patterns and nutrition transition on noncommunicable diseases.

At baseline, participants completed a questionnaire administered in two parts. The first part collected information on sociodemographic characteristics, clinical history, lifestyle factors, anthropometric measures and self-reported morbidity.

Dietary assessment and estimation of melatonin intake

The second part of the baseline assessment included a food frequency questionnaire (FFQ), alongside questions on dietary habits, supplement use and cooking practices. Nutrient intake was estimated using established food composition tables.

Dietary melatonin content was estimated based on values reported in the scientific literature for individual food items. These estimates were then adjusted for total energy intake to account for differences in overall food consumption between participants.

Health outcomes and definitions

The health outcomes assessed in the study included obesity, obstructive sleep apnoea (OSA), hypertension, metabolic syndrome (MetS), type 2 diabetes (T2D), sleep duration, dyslipidaemia and depression.

Obesity was defined as a body mass index of 30 kg/m² or higher. Depression and OSA were identified based on self-reported medical diagnoses.

Dyslipidaemia was defined as the presence of at least one abnormal lipid parameter, including total cholesterol of 200 mg/dL or higher, triglycerides of 150 mg/dL or higher, high-density lipoprotein cholesterol below 40 mg/dL for males or below 50 mg/dL for females, or low-density lipoprotein cholesterol of 130 mg/dL or higher.

Cardiometabolic criteria

Metabolic syndrome was defined as central obesity plus any two of the following criteria: elevated triglycerides or treatment for hypertriglyceridaemia, reduced high-density lipoprotein cholesterol or treatment, elevated blood pressure or treatment for hypertension, and elevated fasting plasma glucose or a diagnosis of type 2 diabetes.

Hypertension was defined by the use of antihypertensive medication, a physician diagnosis, systolic blood pressure of 140 mmHg or higher, or diastolic blood pressure of 90 mmHg or higher. Type 2 diabetes was defined as a self-reported or physician diagnosis, use of antidiabetic medication, or fasting plasma glucose of 126 mg/dL or higher.

Sleep duration was categorised as short if participants reported sleeping less than seven hours per day, and normal if they reported seven hours or more per day.

Statistical analysis

Associations between dietary melatonin intake and health outcomes were estimated using logistic and Poisson regression models. Analyses were adjusted for a wide range of potential confounders, including age, sex, family income, binge drinking, smoking status, screen time, physical activity, medication use and sleep duration.

Participant characteristics

The final analysis included 8,320 participants with a mean age of 35.9 years. Most participants were female and reported that they did not smoke. Around one third of the cohort reported short sleep duration.

Dyslipidaemia, depression, obesity and hypertension were the most commonly reported health conditions within the study population.

Melatonin content of foods and dietary sources

Melatonin content was estimated for 119 of the 144 food items included in the FFQ. Reported concentrations ranged from 0 to 169.9 ng per gram of food. Mean daily melatonin intake was estimated at 25,554.7 ng and was significantly higher in males than in females.

The main dietary sources of melatonin in this population were coffee, lentils and beans, and rice. Higher melatonin intake was associated with lower intake of protein, cholesterol, and saturated and monounsaturated fats, alongside higher intake of fibre and carbohydrates. These patterns suggest that dietary melatonin intake may reflect broader differences in dietary composition.

Associations with health outcomes

After full adjustment, no significant associations were observed between dietary melatonin intake and obstructive sleep apnoea, hypertension, metabolic syndrome or type 2 diabetes. Initial associations with sleep duration and dyslipidaemia were attenuated after adjustment for age and sex and did not remain statistically significant.

In contrast, dietary melatonin intake showed an inverse association with both obesity and depression. Participants with daily melatonin intakes between approximately 14,900 and 34,400 ng were less likely to have obesity, while intakes between approximately 14,900 and 25,000 ng were associated with a lower likelihood of depression.

Notably, the strongest associations were observed in intermediate intake quintiles rather than among those with the highest melatonin intake, suggesting a non-linear relationship.

Conclusions and implications

In this cohort of Brazilian university graduates, higher dietary melatonin intake was associated with lower prevalence of obesity and depression, while no significant associations were identified for most other cardiometabolic outcomes or sleep duration.

The findings support existing hypotheses that dietary melatonin may play a role in metabolic and neurobehavioural regulation, potentially through anti-inflammatory pathways. However, the cross-sectional design of the study means that causal relationships cannot be established.

Further longitudinal and experimental research is needed to confirm these associations, determine whether dietary melatonin has an independent effect beyond overall dietary patterns, and clarify the biological mechanisms that may underlie the observed relationships.

CCH insights:

This is an interesting study, but it is difficult to see where this research leads to. If a person is suspected of having obesity, depression or some other condition due to a lack of melatonin, the solution is surely likely to be supplementation of melatonin, not an increase in melatonin-rich foods – because dietary changes are notoriously difficult to adhere to and when we are looking at just one nutrient, supplementation is a much easier option.

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Almost a Quarter of UK GPs Report Obesity in Children Aged Four and Under

Key Takeaways:

• Nearly one in four UK GPs report seeing children aged four and under where obesity is a clinical concern, with cases identified even in infancy.
• Most GPs find conversations about weight with children and parents difficult, citing fear of distress, stigma and complaints.
• The survey also raises concerns about inappropriate private access to GLP-1 weight loss medicines among adults who do not meet eligibility criteria.
  
  
  

Growing concern among family doctors

Almost a quarter of UK general practitioners report seeing children aged four or under who are living with obesity, according to a new survey of family doctors. The findings point to what respondents described as an “alarming” escalation of childhood obesity presenting at ever younger ages.

The research found that almost half of GPs, 49 per cent, have seen boys and girls up to the age of seven with obesity, including a small number of children younger than one year old. These early presentations raise concerns about long-term health consequences and the pressures faced by primary care clinicians in addressing weight sensitively and effectively.

Survey scope and headline findings

The survey, conducted by MDDUS, asked 540 family doctors about their experiences of managing obesity, the rapid growth in the use of weight loss medications, and the implications of widespread overweight and obesity for the NHS.

Almost one in four respondents, 23 per cent, said they had seen children aged zero to four where obesity was a clinical concern. Across childhood more broadly, 81 per cent of doctors reported seeing obesity in children between the age of 12 months and 11 years.

Dr John Holden, chief medical officer at MDDUS, said:
“These findings are an alarming confirmation of the growing crisis of childhood obesity across the country and the very real difficulties this creates in everyday GP consultations.”

Challenges of discussing weight with families

Despite the scale of the issue, most GPs reported significant difficulty in raising concerns about weight with children and their families. Four in five doctors, 80 per cent, said they find it somewhat or very challenging to talk to the parents of a child under 16 living with obesity about their weight and health. Only 10 per cent said they found such conversations easy.

Nearly two thirds of respondents, 65 per cent, also reported difficulty speaking directly with young people themselves about weight, with just 20 per cent describing those discussions as easy.

Doctors cited multiple reasons for this hesitation. Conversations with parents are often constrained by concerns that parents may become upset, reported by 72 per cent, angry, reported by 47 per cent, or may make a complaint, reported by 24 per cent. A further 74 per cent worried that such discussions could cause shame or stigma. Similar concerns were reported when speaking with children, including fears that conversations about weight could contribute to disordered eating behaviours.

Building confidence in these delicate conversations is the focus of professional training such as the College of Contemporary Health’s Behaviour Change Skills: Person-Centred Communication, a CPD-accredited online short course.

The wider determinants of childhood obesity

Respondents highlighted that obesity is shaped by complex and interrelated factors, including poverty, limited access to nutritious food, and fewer safe or affordable opportunities for children to be physically active. These realities, the survey suggests, shape how GPs approach discussions about weight.

Dr Holden said GPs therefore approach these conversations “with care and empathy for families under pressure”. He added:
“When parents feel judged or blamed, conversations can quickly become emotionally charged and, as our members tell us, can lead to complaints from distressed or angry parents.”

Calls for stronger prevention measures

Katharine Jenner, executive director of the Obesity Health Alliance, said the findings underline a failure to protect children early in life.

She said that the high numbers of GPs seeing infants and very young children with obesity “is another sign we’re letting children down before they even start school. If we’re serious about prevention, it has to begin in the earliest years, otherwise the damage follow them through life.”

Jenner called for a stronger focus on prevention, including reformulation of food and drink products to improve their nutritional quality, tighter restrictions on the marketing of products high in fat, salt and sugar, and better support for families facing structural and financial barriers to healthy eating.

Concerns over private access to weight loss drugs

Alongside childhood obesity, the survey also explored GP experiences of adult patients using weight loss medications inappropriately. Doctors reported that some adults who should not be using GLP-1 weight loss drugs are obtaining them through deception from private pharmacies.

These include people with eating disorders, such as anorexia or bulimia, and people already taking other medications that could interact adversely with so-called “fat jabs” and pose risks to their health.

It is estimated that around 1.5 million people in Britain are using GLP-1 medicines for weight loss, the majority having obtained them privately rather than through the NHS, where eligibility criteria are strict.

One GP told the survey that GLP-1s are being “accessed privately pretty indiscriminately by many people whose body mass index is not in the obese category”. Another described a patient with a history of anorexia nervosa who had also obtained the drugs privately. Overall, 67 per cent of family doctors said they had seen patients using GLP-1s despite not meeting eligibility rules.

These findings raise questions about how rigorously private pharmacies are carrying out appropriate checks, including assessments of medical history and potential drug interactions, before supplying weight loss medications.

Implications for the NHS and future care

The vast majority of GPs surveyed said obesity is likely to be a defining public health challenge during their careers, with 92 per cent agreeing with that statement. An even higher proportion, 95 per cent, believe obesity will significantly affect the NHS’s ability to deliver care.

However, views on weight loss injections were more mixed. While 59 per cent of respondents believe such medications will ultimately save the NHS money, 22 per cent disagreed.

Government response

The Department of Health and Social Care did not comment directly on the survey findings. A spokesperson said:
“Every child deserves the best possible start in life, which is why this government is taking decisive action to tackle childhood obesity.

“We are restricting junk food advertising on television before 9pm and online, a move expected to remove up to 7.2bn calories per year from children’s diets; while giving local authorities new powers to stop fast food shops opening outside schools.

“Through our ten-year health plan, we’re shifting the focus from sickness to prevention to create a healthier nation.”

CCH insight:

This study highlights the considerable challenges that primary care practitioners face in addressing obesity in young children. It is a very sensitive issue, and there may also be cultural attitudes that see overweight children as beautiful or healthy. Unfortunately, healthcare professionals in the UK are not trained to deal with obesity and the unique challenges it presents. It requires a very sensitive approach, communicating with parents in a non-judgemental way, highlighting the role of the obesogenic environment and finding ways to support behaviour change at a family level. On the positive side, if this can be achieved, an entire family can benefit from these interventions, not just the child with excess weight an entire family can benefit from these interventions, not just the child with excess weight. Because so much rests on how these conversations are handled, CCH’s Behaviour Change Skills: Person-Centred Communication CPD short course (2 CPD hours, fully online, CPD-accredited) gives healthcare professionals a practical, evidence-based foundation in person-centred communication – helping them raise sensitive issues like weight with patients and families supportively and without judgement.

Explore Person-Centred Communication →

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Genetic Study Establishes Causal Link Between Obesity and Dementia

Key Takeaways: 

• New genetic evidence suggests that higher body weight and elevated blood pressure play a direct causal role in the development of dementia.
  
• The findings indicate that addressing obesity and high blood pressure earlier in life may offer an important opportunity for dementia prevention.
  
• Much of the increased dementia risk associated with higher body weight appears to be driven by high blood pressure, highlighting a potentially modifiable pathway.
  
  
  

Obesity, blood pressure and dementia risk

People living with obesity and high blood pressure may face a higher risk of developing dementia, according to a new study published in The Journal of Clinical Endocrinology & Metabolism. The research adds to a growing body of evidence linking cardiovascular and metabolic health to long-term brain health.

Dementia represents a major and escalating global public health challenge. There is currently no cure, and people living with dementia experience a progressive decline in mental abilities, including memory, thinking and reasoning. Over time, this decline can significantly impair daily functioning and independence.

The most common forms of dementia include Alzheimer’s disease, vascular dementia and mixed dementia. Although these conditions vary in their underlying pathology, all involve progressive damage to nerve cells in the brain, leading to worsening problems with memory, language, problem-solving and behaviour.

Study identifies a causal relationship

The study was led by Ruth Frikke-Schmidt, M.D., Ph.D., Professor and Chief Physician at Copenhagen University Hospital – Rigshospitalet and the University of Copenhagen.

“In this study, we found high body mass index (BMI) and high blood pressure are direct causes of dementia,” said Frikke-Schmidt. “The treatment and prevention of elevated BMI and high blood pressure represent an unexploited opportunity for dementia prevention.”

Researchers analysed genetic and health data from participants in Copenhagen and the UK. Their analysis revealed a clear causal link between higher body weight and an increased risk of dementia.

How Mendelian randomisation strengthened the findings

The researchers were able to establish a direct causal relationship by using a Mendelian randomisation study design, which closely mimics the structure of a randomised controlled trial.

In Mendelian randomisation, naturally occurring genetic variants associated with higher BMI are used as proxies for lifelong exposure to higher body weight. Because these genetic variants are randomly inherited from parents to offspring, their distribution is not influenced by lifestyle, socioeconomic status or other confounding factors.

This process mirrors the random assignment of participants to treatment or placebo groups in drug trials. As a result, any differences in dementia outcomes between individuals with BMI-increasing genetic variants and those without can be more confidently attributed to body weight itself, rather than to external influences.

Using this approach, the researchers were able to demonstrate that higher BMI plays a direct causal role in increasing the risk of dementia.

Blood pressure emerges as a key driver

Further analysis suggested that much of the increased dementia risk associated with higher body weight was driven by elevated blood pressure. This finding points to a potential pathway through which obesity may contribute to cognitive decline.

By implication, preventing or effectively treating obesity and high blood pressure could help reduce the risk of dementia, particularly forms linked to vascular damage in the brain.

“This study shows that high body weight and high blood pressure are not just warning signs, but direct causes of dementia. That makes them highly actionable targets for prevention,” said Frikke-Schmidt.

Implications for prevention and future research

The findings also raise important questions about the timing of weight management interventions. While weight-loss medications have recently been tested in people with early-stage Alzheimer’s disease, these trials have not shown clear benefits for halting cognitive decline once symptoms are established.

“Weight-loss medication has recently been tested for halting cognitive decline in early phases of Alzheimer’s disease, but with no beneficial effect,” Frikke-Schmidt said. “An open question that remains to be tested is if weight-loss medication initiated before the appearance of cognitive symptoms may be protective against dementia. Our present data would suggest that early weight-loss interventions would prevent dementia, and especially vascular-related dementia.”

Together, the results reinforce the importance of addressing obesity and high blood pressure not only to protect cardiovascular health, but also as part of a broader strategy to reduce the long-term risk of dementia.

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Genetic Links Between Obesity and Autoimmune Diseases Identified in Large European Study

Key Takeaways:

• Large-scale genetic analyses have identified a substantial shared genetic basis between obesity and several autoimmune disorders in people of European ancestry.
  
• Dozens of shared genetic loci and genes appear to influence both body weight regulation and immune system function, particularly pathways involved in immune homeostasis.
  
• The findings suggest potential causal links between obesity and certain autoimmune conditions, with implications for future therapeutic strategies.
  
  
  

Overview of the study

A recent study published in the Journal of Translational Medicine has identified important genetic links between obesity and autoimmune disorders, shedding new light on why these conditions often co-occur. The research, led by Jiang and colleagues, focused on individuals of European ancestry and used large-scale genomic datasets to explore how shared genetic factors may influence both excess body weight and immune-mediated disease.

Obesity and autoimmune disorders represent a significant comorbidity burden, yet until now their shared genetic architecture has remained poorly understood. By applying advanced cross-trait genome-wide association study (GWAS) methods, the researchers aimed to uncover pleiotropic genetic variants – genes or loci that influence more than one trait – that may contribute to both conditions.

Study methods and analytical approach

The researchers conducted a comprehensive cross-trait analysis using GWAS summary data for obesity and 17 autoimmune diseases. Genetic correlations between traits were assessed using LD score regression and high-definition likelihood methods, allowing the team to quantify the extent to which obesity and autoimmune conditions share inherited risk.

To identify specific shared genetic loci, the team employed Stratified Pleiotropic Locus Mapping (PLACO), followed by Bayesian colocalization analyses to confirm whether obesity and autoimmune diseases truly shared the same causal genetic variants. Further analyses examined gene-level effects and tissue-specific heritability, while potential drug targets were prioritised using summary-based Mendelian randomisation (SMR).

In addition, immune co-localization techniques and bidirectional Mendelian randomisation were used to explore immunological mechanisms and to clarify potential causal relationships between obesity and autoimmune diseases.

Key genetic findings

The analysis identified eight autoimmune diseases with significant genetic correlations to obesity. In total, researchers discovered 10,324 pleiotropic single-nucleotide polymorphisms (SNPs), which mapped to 52 independent risk loci. Of these, nine loci were confirmed as shared causal variants through colocalization analysis.

Gene-level investigations revealed 133 unique pleiotropic genes. Notably, genes such as CLN3, SH2B1, and MMEL1 were highlighted and found to be enriched in biological pathways related to hematopoietic cell differentiation and immune homeostasis. These pathways are central to both metabolic regulation and immune function, reinforcing the biological plausibility of a shared genetic basis.

Tissue and immune cell involvement

Tissue-specific heritability analyses showed that shared genetic effects were most prominent in immune-related tissues, particularly the spleen, whole blood, and Epstein–Barr virus (EBV)-transformed lymphocytes. This finding further supports the role of immune system regulation in the overlap between obesity and autoimmune disease risk.

Immune co-localization analyses implicated six traits related to IgD+ CD38− B cell subsets as key pathological conduits. These immune cells may represent an important link between metabolic dysfunction and autoimmune processes.

Evidence of causal relationships

Using bidirectional Mendelian randomisation, the study provided evidence that obesity may play a causal role in the development of certain autoimmune conditions, including hypothyroidism, psoriasis, and multiple sclerosis. Conversely, an inverse causal association was observed between type 1 diabetes and obesity risk, suggesting a more complex and condition-specific relationship.

Implications and conclusions

In their conclusions, the authors state:

“This study demonstrates a robust shared genetic foundation between obesity and multiple autoimmune diseases, pinpointing specific pleiotropic loci, genes, and immune cell subsets.”

By identifying shared genetic mechanisms, the research provides a clearer mechanistic framework for understanding why obesity and autoimmune disorders frequently coexist. Importantly, these findings also highlight potential molecular and immunological targets for future therapeutic intervention, with the potential to address both metabolic and autoimmune disease pathways simultaneously.

Overall, the study represents a significant step forward in understanding the complex interplay between body weight regulation and immune system dysfunction, and it opens new avenues for research into integrated prevention and treatment strategies.

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