Obesity Care

Carbohydrate-Rich Diets May Promote Weight Gain Even Without Higher Calorie Intake

Key Takeaways: 

• A new mouse study found that carbohydrate-rich foods such as bread, wheat flour, and rice flour promoted weight gain and fat accumulation even when total calorie intake did not significantly increase.
  
• Researchers observed that the weight gain appeared to be linked more closely to reduced energy expenditure and metabolic changes than to overeating.
  
• Scientists say future human studies will explore how factors such as whole grains, fibre content, food processing, meal timing, and combinations with protein and fat influence metabolic responses to carbohydrates.
  
  
  

Bread and carbohydrates under renewed scrutiny

Bread has served as a central part of human diets for centuries and remains a staple food in many cultures around the world. Foods such as bread, rice, noodles, and other carbohydrate-rich staples continue to form the foundation of everyday meals for billions of people.

However, as rates of overweight and obesity continue to increase globally, researchers are re-examining how modern dietary patterns may influence body weight and metabolic health. While high-fat diets have traditionally received much of the attention in obesity research, scientists are now taking a closer look at the role carbohydrates may play in weight regulation.

A new study led by researchers at Osaka Metropolitan University suggests that certain carbohydrate-heavy eating patterns may contribute to weight gain in ways that are not solely explained by consuming more calories.

The findings were published in Molecular Nutrition & Food Research. 

Obesity research has traditionally focused on fat intake

Obesity is associated with a broad range of chronic conditions and lifestyle-related diseases, including type 2 diabetes, cardiovascular disease, and metabolic dysfunction. Because of this, understanding the drivers of weight gain has become an increasingly important area of scientific research.

Historically, many obesity studies have focused primarily on dietary fat as the main contributor to excess weight gain. This is reflected in the widespread use of high-fat diets in animal research investigating obesity and metabolism.

At the same time, carbohydrate-rich foods remain deeply embedded in daily diets across the world. Despite their prominence, the metabolic effects of staple carbohydrates such as bread, rice, and noodles have not always been explored in the same depth.

Public perceptions around carbohydrates also remain widespread. Beliefs such as “bread makes you gain weight” or “carbohydrates should be restricted” are common, yet researchers say it has remained unclear whether such effects are driven by the foods themselves, overall dietary habits, eating behaviour, or broader metabolic responses.

Researchers investigated how carbohydrate-rich foods affect metabolism

To better understand the relationship between carbohydrates and weight gain, researchers led by Professor Shigenobu Matsumura at Osaka Metropolitan University’s Graduate School of Human Life and Ecology conducted a series of experiments in mice.

The study examined whether mice would preferentially select carbohydrate-rich foods over standard laboratory chow and how those dietary choices would affect body weight, metabolism, and energy expenditure.

The mice were separated into several dietary groups, including:

• Chow
• Chow + Bread
• Chow + Wheat Flour
• Chow + Rice Flour
• High-fat diet (HFD) + Chow
• High-fat diet (HFD) + Wheat Flour

Researchers monitored multiple metabolic indicators throughout the study, including:

• Body weight
• Fat mass
• Energy expenditure
• Blood metabolites
• Liver gene activity
  
  
  

Mice preferred carbohydrate-rich foods

The researchers found that mice consistently showed a strong preference for carbohydrate-rich foods. Animals given access to bread, wheat flour, or rice flour largely abandoned their standard chow diet in favour of these carbohydrate sources.

Importantly, the researchers reported that overall calorie intake did not increase substantially despite this dietary shift. Nevertheless, mice consuming the carbohydrate-rich diets still experienced increases in body weight and fat mass.

Rice flour produced similar effects to wheat flour, suggesting the observed metabolic changes were not specific to wheat itself.

Interestingly, mice in the High-fat diet (HFD) + Wheat flour group gained less weight than those in the High-fat diet (HFD) + Chow group, indicating that the interaction between fat and carbohydrate intake may be more complex than previously assumed.

“These findings suggest that weight gain may not be due to wheat-specific effects, but rather to a strong preference for carbohydrates and the associated metabolic changes,” said Professor Matsumura.

Reduced energy expenditure appeared to play a key role

To investigate why the mice gained weight without substantially increasing calorie intake, the researchers carried out further metabolic analysis using indirect calorimetry and respiratory gas measurements.

The findings suggested that the weight gain was not primarily caused by overeating. Instead, the animals appeared to experience reduced energy expenditure, meaning they were burning fewer calories.

Researchers also identified several metabolic changes in the mice consuming the carbohydrate-rich diets.

Blood analysis showed:

• Increased fatty acid levels
• Reduced levels of essential amino acids

Meanwhile, examination of the liver revealed:

• Greater fat accumulation
• Increased activity of genes involved in fatty acid synthesis
• Increased activity of genes associated with lipid transport

Together, these findings suggest that carbohydrate-heavy dietary patterns may alter how the body processes and stores energy.

Metabolic changes improved when carbohydrates were reduced

The researchers also observed that removing wheat flour from the diet rapidly improved both body weight and several metabolic abnormalities.

According to the authors, this finding suggests that moving away from a highly carbohydrate-focused dietary pattern and towards a more balanced eating pattern may help improve metabolic regulation.

However, the researchers emphasised that additional work is needed to determine how these findings translate to human diets and real-world eating behaviour.

Future studies will explore human dietary patterns

The research team says the next phase of investigation will focus on understanding whether similar metabolic effects occur in people.

“Going forward, we plan to shift our research focus to humans to verify the extent to which the metabolic changes identified in this study apply to actual dietary habits,” stated Professor Matsumura.

“We also intend to investigate how factors such as whole grains, unrefined grains, and foods rich in dietary fiber, as well as their combinations with proteins and fats, food processing methods, and timing of consumption, affect metabolic responses to carbohydrate intake. In the future, we hope this will serve as a scientific foundation for achieving a balance between ‘taste’ and ‘health’ in the fields of nutritional guidance, food education, and food development.”

The researchers noted that future studies examining food quality, fibre content, food combinations, and meal timing may help provide a more nuanced understanding of how carbohydrates influence metabolism and body weight.

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Obesity Leaves a Lasting Imprint on the Immune System, Study Finds

Key Takeaways: 

• Immune cells in people living with obesity can retain a long-term “memory” of excess weight through epigenetic changes
  
• This “obesity memory” may persist for 5–10 years after weight loss and could prolong disease risk
  
• Sustained weight management may gradually reverse these effects, with potential for targeted therapies to accelerate the process
  
  
  

A long-term immune memory of obesity

People living with obesity may carry a lasting biological imprint of excess weight within their immune system, even after successful weight loss. A 10-year study published in EMBO Reports suggests that key immune cells retain a “memory” of obesity, potentially extending the risk of related health conditions for years.

The research, led by Professor Claudio Mauro at the University of Birmingham and supported by the National Institute for Health and Care Research Biomedical Research Centre in Birmingham, focused on helper T cells, also known as CD4+ lymphocytes. These cells play a central role in coordinating immune responses.

The findings indicate that these immune cells undergo lasting changes that continue to influence how the body regulates inflammation and maintains immune balance long after weight has been reduced.

DNA methylation and the “tagging” process

At the centre of this phenomenon is DNA methylation, a biological process in which chemical markers attach to DNA and alter gene activity without changing the underlying genetic code.

In people living with obesity, this “tagging” process appears to leave a durable imprint on helper T cells. These markers can persist for an extended period, with the study suggesting a timeframe of approximately 5–10 years after weight loss.

This sustained epigenetic modification may disrupt normal immune functions, including the removal of cellular waste and the regulation of immune ageing.

As a result, even individuals who return to a clinically healthy weight may continue to experience altered immune function for several years.

Implications for long-term disease risk

The persistence of this immune “memory” may help explain why the risk of certain conditions associated with obesity does not immediately resolve following weight loss.

Professor Claudio Mauro, co-lead author of the study, explained:
“The findings suggest that short-term weight loss may not immediately reduce the risk of some disease conditions associated with obesity, including type 2 diabetes and some cancers.”

He added:
“Instead, ongoing weight management following loss will see the ‘obesity memory’ slowly fade. This may take several years of sustained weight loss maintenance, likely 5–10 years, though this requires further study, to fully reverse the effects of obesity on T cells.”

The study highlights that long-term weight maintenance, rather than short-term weight loss alone, may be critical for reducing risk over time.

Study design and participant groups

To build a comprehensive understanding of how obesity affects immune cells, researchers analysed samples from multiple human cohorts and experimental models.

These included:

• Blood samples from people living with obesity who received weight loss injections
• Individuals with Alström Syndrome, a rare genetic condition characterised by early-onset childhood obesity, alongside matched healthy controls
• Participants undergoing a 10-week exercise intervention, with blood and fat tissue collected
• People with either a healthy weight or obesity undergoing hip or knee replacement surgery due to osteoarthritis

In addition, the team examined:

• Mouse models fed a high-fat diet
• Blood samples from healthy human volunteers

These diverse data sources enabled researchers to investigate both real-world and mechanistic aspects of immune dysregulation in obesity.

Disrupted cellular processes: autophagy and immune ageing

The study identified two key biological pathways affected by obesity-related DNA tagging:

Autophagy

Autophagy is a cellular “clean-up” process in which cells break down and recycle damaged components. The obesity-related epigenetic changes appear to impair this process, potentially leading to an accumulation of cellular waste.

Immune senescence

Immune senescence refers to the ageing of the immune system. The research suggests that obesity-associated changes may accelerate or dysregulate this process, altering how immune cells respond over time.

Together, these disruptions may contribute to prolonged inflammation and impaired immune function.

Potential for targeted therapies

Beyond identifying the problem, the research also points towards potential therapeutic strategies.

Professor Mauro noted:
“Additionally, our study suggests potential therapeutic opportunities to expedite this process, such as repurposing drugs like SGLT2 inhibitors, which have shown promise in reducing inflammation and promoting immune-mediated clearance of senescent cells in obesity.”

Such approaches could complement existing weight loss interventions by addressing the underlying immune alterations that persist after weight reduction.

A molecular record of metabolic history

Dr Belinda Nedjai, senior author from the Wolfson Institute of Population Health at Queen Mary University London, emphasised the broader significance of the findings:
“Our findings show that obesity is associated with durable epigenetic modifications that influence immune cell behaviour. This suggests that the immune system retains a molecular record of past metabolic exposures, which may have implications for long-term disease risk and recovery.”

This concept of a “molecular record” reinforces the idea that the body’s response to obesity is not easily reversed, even when weight is reduced.

Understanding obesity as a chronic disease

Professor Andy Hogan of Maynooth University highlighted how these findings align with the understanding of obesity as a chronic condition:
“We know obesity is a chronic progressive and relapsing disease and our findings provide further understanding of exactly what are the molecular mechanisms potentially driving the risk of relapsing and highlight the challenges facing people living with obesity to successfully manage their weight.”

The research underscores the biological complexity of obesity and the challenges individuals face in achieving and maintaining long-term health improvements.

Looking ahead

Delivered through the NIHR Biomedical Research Centre in Birmingham, this study contributes to a growing body of evidence that obesity leaves lasting effects on the body at a molecular level.

Future research will aim to refine understanding of how these epigenetic changes can be reversed and how targeted treatments might accelerate recovery of normal immune function.

In the meantime, the findings highlight the importance of sustained weight management and long-term support for people living with obesity, rather than a sole focus on short-term weight loss.

CCH insights:

This study provides further support for the characterisation of obesity as a chronic relapsing disease. Clinically significant weight loss is just the first step in obesity treatment – the challenge is to then maintain the weight loss so that health improvements are sustained, despite the biological memory of obesity promoting weight regain. Whether this memory reduces over time will have major implications for long-term obesity care in the future.

Source: University of Birmingham

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Dual Burden of Alcohol Use and Obesity Linked to Rising Liver Disease Risk

Key Takeaways: 

• Around 1 in 10 U.S. adults report both heavy drinking and obesity, creating a compounded risk for liver disease
  
• This overlap is most common in younger and middle-aged adults, suggesting risk accumulates early in life
  
• Integrated, non-judgemental care targeting both conditions together may improve long-term outcomes and reduce progression to advanced liver disease
  
  
  

A growing overlap with serious implications

Heavy alcohol use and obesity are both increasing in the United States, and they are increasingly affecting the same individuals. A new study published in JAMA Internal Medicine explores how often these two major risk factors coincide among U.S. adults and why this overlap has important implications for clinical care and public health policy.

The research was led by Dr Bryant Shuey, a board-certified general internist at UPMC and a clinician-investigator at the University of Pittsburgh Center for Research on Health Care. His work focuses on substance use, chronic disease, and access to care. Drawing on national survey data, the study highlights a critical, and often overlooked, opportunity to intervene earlier in the disease trajectory before severe liver damage develops.

Why examine alcohol use and obesity together?

Dr Shuey explains that this combined risk is increasingly visible in clinical practice:

“In my clinical work, I’ve been seeing more people in their 30s and 40s coming to the hospital with advanced liver disease linked to both alcohol use and metabolic risk factors. Nationally, heavy drinking and obesity are both becoming more common and there has been greater recognition that alcohol and metabolic disease can combine to accelerate liver disease progression. Treatment of both conditions, especially alcohol use disorder, is also lagging, as evident by research by my colleague and study co-author Dr. Eden Bernstein from the University of Colorado. Together, we sought to understand how often risky alcohol use and obesity overlap and what it might mean for prevention and earlier intervention.”

This convergence of risks reflects a broader shift in how liver disease is understood. Rather than being driven by a single cause, many people now present with multiple interacting factors that amplify disease progression.

A significant and early-emerging risk

The study’s central finding is clear:

“The key finding is that about 1 in 10 U.S. adults reported both heavy drinking and a body mass index of 30 or greater in 2023. That’s a substantial share of the population, especially considering how strongly each of these factors contributes to liver disease risk on its own.”

What is particularly striking is how early this overlap appears.

“What stood out most was how early this overlap appears. Rates were highest among young and middle-aged adults, when risk factors for serious liver disease are just beginning to build. These findings suggest that many people are entering adulthood with multiple, reinforcing risk factors for liver disease long before they ever develop symptoms.”

This suggests that prevention efforts may need to begin far earlier than is currently typical, focusing on identifying and addressing risk factors before clinical disease becomes apparent.

How liver disease presents in clinical practice

People living with alcohol-related and metabolically related liver disease may present at very different stages. Some are identified early through routine primary care assessments, while others present later with advanced complications.

Dr Shuey describes this spectrum:

“Patients can show up at different points along the disease course. Some are identified early by their primary care doctor by discussing risk factors like alcohol use and metabolic health and ordering blood work and liver imaging. Others present later, sometimes to the emergency department, with symptoms of advanced liver disease, or cirrhosis, like jaundice, abdominal swelling or gastrointestinal bleeding. Liver disease can lurk for years with no symptoms, so for some, that’s the first time they’re learning they have liver disease. Whether the illness is driven mainly by metabolic disease, alcohol use or a combination of both, if unchecked, the outcome can be the same: progressive liver damage that can lead to cirrhosis and liver failure. That’s why it’s so important to address these risk factors together, not in isolation.”

The silent progression of liver disease underscores the importance of proactive screening and early intervention.

Rethinking care: addressing both risks together

For clinicians, the findings point to the need for a more integrated approach to care.

“We need to routinely screen for both conditions in an empathetic and non-judgmental way and recognize how strongly they interact when it comes to liver disease risk. Clinicians should offer standard evidence-based options to treat both conditions: dietary counseling, motivational interviewing, medications for alcohol use disorder and therapies for metabolic disease such as GLP-1s and related weight loss drugs. There’s growing interest in these medications because they help people reduce their metabolic risk through weight loss and reversing inflammation in metabolic liver disease. Additionally, a smaller trial last year found that GLP-1s may reduce alcohol use among people with alcohol use disorder. While these results should not be overstated, GLP-1s may emerge as an important dual-therapeutic for patients with risky alcohol use and obesity if these findings hold up in larger trials. Ultimately, addressing both risk factors together may be an important strategy to change long-term outcomes.”

This reflects a shift towards dual-risk management, where treatment strategies are designed to address interconnected drivers of disease rather than isolated conditions.

Supporting people without judgement

A central theme in managing these conditions is the importance of person-centred care.

“The most important thing is creating space to talk about these concerns without judgment. I would want to learn about their goals, explore their understanding of the health impacts of alcohol use and metabolic disease, counsel them on treatment options and support them in their decision. For some people, the priority is avoiding serious illness down the road. Others may want to lose weight, drink less or stop drinking altogether. While addressing both conditions simultaneously may be of interest to some patients, others may feel overwhelmed and want to focus on just one. There isn’t a single right goal.”

This highlights the need for flexibility in care plans and respect for individual priorities and readiness for change.

Barriers to care and policy implications

The study also draws attention to wider structural barriers that influence health outcomes.

“Our social conditions shape our health. Improving access to affordable, healthy foods and safe spaces for exercise and activity can go a long way in helping people attain their highest level of health. Bolstering public health messaging about the lesser-known risk of liver disease as a complication of alcohol use and metabolic disease is also critical to helping people make informed decisions. Furthermore, stigma around both weight and alcohol use can discourage people from seeking care in the first place. Fewer than 10% of people with an alcohol use disorder receive treatment, and just 5% are prescribed evidence-based medications that have been demonstrated to reduce alcohol use. Clinicians can be a part of the solution by ensuring they are offering patients standard treatments for alcohol use disorder.”

Access to care remains a major challenge, particularly for those without adequate insurance or financial resources.

“Health care affordability and access to care are major barriers to timely diagnosis and treatment of alcohol- and metabolic-related health issues, particularly for people who are uninsured. Preventing progression to advanced liver disease isn’t just better for patients, it’s far less expensive than treating cirrhosis and its complications. In the U.S., we spend an estimated $135 billion on liver disease every year. We need prevention-focused approaches and more equitable access to care for the populations at highest risk.”

These findings reinforce the importance of prevention-focused policy and equitable healthcare access.

Priorities for future research

Looking ahead, the study highlights several important areas for further investigation.

“We should figure out how to intervene earlier, when obesity and risky alcohol use first begin to overlap, long before advanced liver disease develops. We also need more data on how existing treatments work in patients with multiple, co-occurring risk factors, since many clinical trials have historically excluded these groups.”

There is also a need to better understand how health systems and policy decisions shape outcomes.

“From a policy standpoint, future research should also look at how insurance coverage and access barriers affect outcomes for people at greatest risk. Better evidence in these areas could help guide more effective and equitable prevention strategies.”

A shift towards earlier, integrated prevention

Taken together, the findings point to a clear conclusion: the intersection of heavy alcohol use and obesity represents a growing and under-recognised driver of liver disease. Identifying and addressing these risks earlier, and in combination, may offer a meaningful opportunity to improve patient outcomes and reduce the long-term burden on healthcare systems.

Source: UPMC Life Changing Medicine

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Breastfeeding for Three Months or More Linked to Lower Long-Term Weight Gain in Women

Key Takeaways: 

• Women who breastfeed for at least three months may gain significantly less weight later in life, with differences observed decades after childbirth.
  
• The strongest long-term effect is seen in women who had overweight or obesity before pregnancy.
  
• Breastfeeding appears to influence energy balance, although individual responses vary and support remains essential.
  
  
  

Long-term impact of breastfeeding on weight

Breastfeeding has long been associated with short-term postpartum weight changes, but new research suggests its effects may extend much further. A study conducted by researchers at the University of Oslo indicates that women who breastfeed for at least three months may experience lower weight gain even decades later.

According to the findings, women gained up to 6.5 kilograms less on average later in life if they breastfed for a minimum of three months. This extends the understanding of breastfeeding beyond its immediate postpartum benefits, highlighting its potential role in long-term weight trajectories.

Previous research has largely focused on weight changes in the first one to two years after childbirth. In contrast, this study followed women for up to 50 years after they had stopped breastfeeding, offering a rare insight into lifelong health patterns. The findings are expected to inform further research into maternal cardiovascular risk.

Large-scale study provides robust data

The analysis drew on data from the Women and Health Study, which includes more than 170,000 women in Norway. The results were published in the American Journal of Clinical Nutrition. 

This large cohort allowed researchers to examine how breastfeeding duration relates to weight development across different groups of women, while accounting for factors such as education, physical activity, and smoking.

Strongest effect seen in women with overweight

The most pronounced differences were observed among women who had overweight or obesity in early adulthood, prior to pregnancy.

“We compared women in this group who were otherwise similar in terms of education level, physical activity and smoking. We then found that those who breastfed for three to 15 months gained on average up to 6.5 kilos less from young adulthood to middle age, compared with those who breastfed little,” says Thorbjørn Brun Skammelsrud.

Skammelsrud is completing his doctoral research at the Department of Nutrition, Institute of Basic Medical Sciences at the University of Oslo.

More modest differences in women with normal weight

Among women who had a normal weight in early adulthood, the long-term effect of breastfeeding was still present but less pronounced. Those who breastfed for three to 15 months gained up to 3 kilograms less compared with those who breastfed for shorter periods.

For women who had been underweight before pregnancy, breastfeeding appeared to have little influence on long-term weight outcomes.

Biological mechanisms and individual variation

The study also highlights the complex relationship between breastfeeding and energy balance.

“Breastfeeding increases energy expenditure, so in theory breastfeeding should contribute to weight loss. But precisely because energy expenditure increases, some women will also experience increased appetite when they are breastfeeding,” Skammelsrud explains.

This means that while breastfeeding may support weight regulation at a population level, individual experiences can differ significantly.

Implications for public health

The study included women who had children as early as the 1940s, although the association between breastfeeding and lower weight was strongest among those who gave birth after 1980. This group is considered more representative of current maternal behaviours, particularly in terms of diet and breastfeeding practices.

In Norway, national guidance generally recommends partial breastfeeding for one year or longer, provided both mother and infant are comfortable. Breastfeeding rates in Norway are relatively high compared with many other countries.

“This is positive for public health. At the same time, the study shows that some women may need extra follow-up after giving birth, particularly those with overweight or obesity,” Skammelsrud says.

Supporting women who choose to breastfeed

The findings reinforce the importance of enabling and supporting breastfeeding where desired.

“In this study, we see that breastfeeding for at least three months has a positive effect on women’s weight later in life. It is therefore important that breastfeeding is facilitated, and that women who wish to breastfeed are offered qualified support,” the researcher says.

Ensuring access to appropriate guidance and support may help maximise both short-term and long-term health outcomes for women.

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Whole Milk and Childhood Obesity – New Study Challenges Long-Standing Dietary Advice

Key Takeaways:

• Children who consumed whole-fat milk in early childhood showed lower odds of living with obesity in later childhood compared with those consuming reduced-fat options
  
• The study found no evidence that whole milk increases adiposity, challenging decades of low-fat dietary guidance
  
• Researchers suggest milk fat may influence satiety and overall dietary patterns, although mechanisms remain unclear
  
  
  

Rethinking milk fat and childhood health

New research from the University of Toronto suggests that children who consume whole-fat milk during early childhood may have a lower likelihood of living with obesity in middle childhood than those who drink reduced-fat milk.

These findings contribute to a growing body of evidence indicating that lower-fat milk may not provide the protective effect against childhood obesity that has long been assumed. For several decades, dietary guidelines in many countries have promoted low-fat dairy products. For example, Canada’s Dietary Guidelines in 2019 continued to recommend reduced-fat options, reflecting a broader historical focus on reducing dietary fat intake.

Study overview and design

The study, published in the American Journal of Clinical Nutrition, is described as one of the most comprehensive analyses to date examining the relationship between milk consumption and childhood obesity over time.

Researchers, including former postdoctoral fellow Tara Zeitoun and doctoral student Zheng Hao Chen, analysed data from the CHILD Cohort Study. This large, prospective study tracks health data from thousands of children from before birth through to adolescence.

Caregivers reported the type of milk consumed by children, including skim, one per cent, two per cent, and whole-fat milk. Researchers then assessed a range of outcomes at ages five and eight, including:

• Body mass index (BMI)
• Waist-to-height ratio
• Fat mass
• Preclinical and clinical obesity status
  
  
  

Key findings

Milk consumption was common among participants, with over 90 per cent of children consuming milk before the age of five. Among these:

• 24 per cent consumed whole-fat milk
• Approximately half consumed less than one cup per day
  

Despite relatively modest intake, notable differences emerged. Children who consumed whole milk at age five had significantly lower BMI at age eight. They also had 69 per cent lower odds of living with obesity compared with children who consumed skim milk.

In addition, researchers identified a broader pattern in which higher milk fat content was associated with more favourable adiposity profiles.

Expert insight

Kozeta Miliku, a professor of nutritional sciences at the University of Toronto’s Temerty Faculty of Medicine and a researcher at the Joannah and Brian Lawson Centre for Child Nutrition, emphasised the implications of these findings:

“The most important learning from this study is that whole milk was not associated with higher adiposity or obesity risks risk in children, and may even be linked to healthier growth patterns,”

She also highlighted the limitations of focusing narrowly on fat reduction:

“Switching to lower-fat milk has been about cutting fat in the diet, but that may miss the bigger picture,” says Miliku. “When we think about healthy growth, it’s important to consider the overall nutritional context. Removing fat does not automatically make skim milk a healthier choice for children.”

Implications for public health guidance

The findings raise important questions about long-standing public health recommendations. Prior to 2019, Health Canada advised that children transition from whole milk to reduced-fat milk from the age of two. Similarly, the Dietary Guidelines for Americans 2020–2025 supported reduced-fat dairy intake.

However, recent policy developments suggest a shift in thinking. In the United States, the Whole Milk for Healthy Kids Act has allowed full-fat milk to be reintroduced into school lunches, aligning with updated national guidance that is more permissive of full-fat dairy.

Possible biological mechanisms

While the study did not directly investigate underlying mechanisms, the researchers proposed several hypotheses:

• Milk fat may enhance satiety, potentially reducing the consumption of energy-dense, nutrient-poor foods
• It may influence overall energy balance
• It could play a role in metabolic pathways linked to growth and nutritional status
  

These potential explanations highlight the complexity of dietary patterns and suggest that focusing on single nutrients may overlook broader physiological effects.

The need for further research

Miliku noted that additional research is needed to better understand how milk fat may influence obesity risk and whether any protective effects persist into adolescence and adulthood.

With Canada’s 2019 dietary recommendations offering limited specific guidance on milk consumption for children, the study’s findings may help inform future discussions among parents, clinicians, and policymakers.

A broader view of healthy diets

Miliku concluded by reinforcing the importance of overall dietary quality:

“Whole fat milk can be part of a healthy diet and does not on its own increase obesity risk,” she adds. “And it’s important to think about the overall quality of the diet – the fruits and vegetables, whole grains and protein-rich foods they consume.”

Funding and support

The research was funded by the Canadian Institutes of Health Research and the Joannah & Brian Lawson Centre for Child Nutrition at the University of Toronto, supported through a donation by President’s Choice Children’s Charity.

CCH insights:

This interesting new research will hopefully be the trigger for governments and public health bodies to review and amend their outdated advice to choose low-fat dairy options instead of full-fat. The reductionist approach to nutrition, which considers food just in terms of calories and individual nutrients, is an oversimplification which does not help our understanding of the relationship between food and health. If the best food for children early in life is whole milk, why would it be beneficial for them to suddenly switch to low-fat milk at the age of 2?

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Visual Signals, Healthier Choices – Study Shows Colour-Coded Labels Influence Consumer Decisions

Key Takeaways:

• Colour-coded nutrition labels are more effective than traditional tables in guiding healthier food choices
  
• Red warning signals have a stronger behavioural impact than green positive cues, reflecting a “negative bias” in decision-making
  
• Simple visual labelling systems may support public health efforts to address obesity and poor dietary habits
  
  
  

The growing use of colour-coded nutrition labels

Colour coding on food packaging is becoming increasingly common, particularly as policymakers and manufacturers seek ways to guide consumers towards healthier dietary choices. A recent study conducted by researchers from SWPS University, the University of Wisconsin, and the University of Massachusetts suggests that these visual systems are significantly more effective than traditional nutritional tables.

The findings, published in Current Psychology, indicate that the effectiveness of colour-coded labels lies in how the brain processes signals of benefit and risk. Rather than requiring effortful interpretation, colour cues allow for rapid, intuitive judgements about a product’s healthfulness.

Obesity and the need for clearer nutritional guidance

According to the World Health Organization, overweight and obesity are major contributors to the development of chronic diseases. Over the past three decades, the proportion of children and adolescents in the United States who are overweight or at risk has more than tripled, reaching 37% and 34% respectively.

This trend has been driven largely by reduced physical activity and the increased consumption of foods high in fat and sugar. In response, clearer and more accessible nutritional labelling systems are being explored as tools to help people make more informed food choices.

How traffic light labelling works

One widely adopted approach is the traffic light labelling (TLL) system, originally developed in the United Kingdom. This system uses colours to indicate the levels of key nutrients such as calories, fat, saturated fat, sugar, and salt relative to recommended intake levels.

• Green indicates low levels, typically below 15% of the reference intake
  
• Red signals high levels, typically exceeding 25% of the reference intake

By translating numerical data into easily recognisable visual cues, the system allows consumers to assess a product’s nutritional profile at a glance.

“A picture is worth a thousand words”

The study aimed to explore the psychological mechanisms behind how people interpret these colour-coded labels.

“We decided to investigate the psychological mechanisms behind the reading of color-coded product labels. We drew on theories about verbal and visual information processing, as well as the perception of information in positive and negative contexts. We wanted to bridge a gap. Previous studies focused exclusively on consumer purchasing behavior and analyzed the extent to which color-coded labels influenced the choice of healthy food products,” says Professor Andrzej Falkowski, a business psychologist from the Institute of Psychology at SWPS University and the author of the study.

To examine this, researchers recruited 79 participants in the United States via Amazon Mechanical Turk. Participants were asked to evaluate products such as chicken noodle soup, ranch dressing, and peanut butter. These products were presented either with colour-coded nutrient indicators or with traditional text-based information.

Participants rated each product on a scale from 0 to 10, where 0 indicated “harmful” and 10 indicated “healthy”.

Faster processing, more intuitive decisions

The findings confirmed that visual information is easier for people to process than text. Colour cues are interpreted almost instantly by the brain, requiring minimal cognitive effort.

This enables individuals to make quick, instinctive judgements about whether a product is beneficial, even in time-pressured situations such as shopping. In contrast, traditional nutritional tables require more deliberate analysis, which may reduce their practical usefulness in real-world settings.

The power of red and the role of negative bias

One of the most striking findings was the disproportionately strong influence of the colour red. While green highlights positive attributes, red signals high levels of fat or sugar and prompts caution.

“This result also aligns with existing theories suggesting that negative events exert a stronger influence on behavior than positive ones. It is this ‘negative bias’ that makes color systems so effective. Red causes us to pause and reconsider a purchase,” Professor Falkowski emphasizes.

This asymmetry – where negative signals carry more weight than positive ones – was not observed with traditional labelling formats. Without clear visual cues, participants found it more difficult to distinguish between beneficial and harmful aspects of a product.

Improved consistency in consumer judgements

The study also found that colour-coded labels led to more consistent evaluations across participants. Because the visual system clearly differentiates between risks and benefits, individuals were better able to assess products in a uniform way.

By contrast, traditional descriptors such as “low fat” can be ambiguous and open to interpretation, particularly for those with limited nutritional knowledge. Colour coding, based on universally recognised traffic signals, offers a more accessible and intuitive alternative.

Implications for public health and obesity prevention

The researchers suggest that these findings have important implications for public health policy.

“Given the ongoing global challenges of obesity and poor dietary habits, color-coded labeling represents a simple yet impactful strategy for guiding healthier consumer choices,” Falkowski says.

By enhancing the visibility and clarity of nutritional information, colour-coded systems may encourage people to select healthier options. Over time, such behavioural shifts could contribute to improvements in population health.

The authors conclude that leveraging visual attention mechanisms and simplifying complex nutritional data may be a practical and scalable approach to addressing poor dietary habits and the global rise in obesity.

CCH insights:

The results of this study supports the use colour-coded labelling system as it enables quick health-based decision-making, with minimal time or effort required. And it also revealed that we use the system more to avoid unhealthy ‘red’ foods than to actively choose healthy ‘green’ foods. These outcomes emphasise the complex range of factors that contribute to shopping behaviours and decisions about what people eat. And if we want to encourage people to eat healthily, we need to understand these factors better and consider how best to influence them.

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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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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.

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.

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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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