Obesity Care

Visceral Fat and Biological Ageing: New Research Links Deep Belly Fat to Faster Cellular Ageing

Key Takeaways: 

• A study of nearly 4,800 adults aged 45 to 69 from the Busselton Healthy Ageing Study found that higher levels of visceral fat – the fat stored deep within the abdomen – were associated with faster biological and cellular ageing in both men and women.
  
• Among female participants, greater visceral fat was also linked to shorter telomere length, a recognised marker of cellular ageing.
  
• The associations held even after researchers adjusted for overall body fat, body mass index (BMI), waist circumference and lifestyle factors, suggesting visceral fat exerts an effect beyond general measures of body composition.
  
  
  

New research from The University of Western Australia suggests that visceral fat, the type of fat stored deep within the abdominal cavity and wrapped around internal organs, may contribute to faster biological ageing in middle-aged adults independently of overall body weight or general obesity measures. The findings were published in the journal Obesity.

A large population-based analysis

The study was co-authored by Adjunct Associate Professors Jennie Hui and Kun Zhu, both of The University of Western Australia, with the analysis led by Mr Riorden O’Shea, a resident medical officer with the WA Country Health Service. Researchers drew on data from nearly 4,800 participants – 2,614 of them women – aged between 45 and 69 years, all enrolled in the Busselton Healthy Ageing Study.

The team examined how visceral fat related to markers of biological ageing, including indicators of cellular ageing such as telomere length. Telomeres are the repetitive DNA sequences that cap the ends of chromosomes; their progressive shortening over time is widely regarded as a key biological signature of cellular ageing.

The analysis found that greater visceral fat was associated with accelerated biological ageing in both men and women. In women, higher visceral fat was additionally linked to shorter telomere length.

“Our study shows that visceral fat is associated with faster biological and cellular ageing,” said Associate Professor Hui, who is Director of the Busselton Health Study Laboratory. “Understanding what drives faster ageing helps us find better ways to stay healthy for longer.”

An effect that holds after adjusting for other body measures

A central finding of the study is that the link between visceral fat and accelerated ageing persisted even when researchers controlled for other indicators commonly used to assess body composition and adiposity.

“Importantly, these associations remained significant even after accounting for overall body fat, body mass index, waist circumference and lifestyle factors,” Associate Professor Zhu said.

This suggests that visceral fat may have implications for ageing that are not fully captured by routine measures such as BMI or waist circumference – measures that have long been criticised for failing to distinguish between fat stored just under the skin and the metabolically distinct fat located deep within the abdomen.

Why visceral fat behaves differently

Visceral fat is biologically active in ways that subcutaneous fat is not. It secretes inflammatory signalling molecules and contributes to a chronic, low-grade inflammatory state that researchers have increasingly linked to chronic disease and accelerated ageing.

“Visceral fat is metabolically active, secreting a range of pro-inflammatory proteins, which contribute to systemic inflammation and metabolic stress,” Associate Professor Zhu said.

She also noted a practical point that is likely to resonate in clinical settings: visceral fat does not require specialised, costly imaging to assess. “It can be easily measured using imaging technology, which is widely used in routine bone density scans,” she said. This positions visceral fat as a metric that could plausibly be folded into existing clinical workflows without significant additional cost.

The value of long-running cohort data

The findings rest on one of the most established population-health datasets in the world. Established in 1966, the Busselton Health Study is internationally recognised as one of the longest-running population health programmes ever conducted, providing a rich longitudinal dataset that continues to support research into chronic disease and healthy ageing.

Mr O’Shea, who led the analysis, said the project demonstrated the enduring scientific value of sustained cohort studies of this kind. “Access to high-quality longitudinal data allowed us to better understand how clinical risk factors relate to long-term health outcomes,” he said.

Implications for healthier ageing

The findings reinforce a growing body of evidence that abdominal fat distribution – not just total body fat – is an important consideration in healthy ageing. While the study is observational and does not establish that reducing visceral fat will directly slow ageing, the authors argue the results support the case for targeting abdominal fat as part of broader strategies to promote healthier ageing in middle and later life.

For clinicians, the practical takeaway is that visceral fat may warrant attention even in people whose BMI or waist circumference appears unremarkable, and that the imaging tools needed to measure it are already widely available in routine care.

The study, “Visceral fat is associated with accelerated biological and cellular ageing,” is published in Obesity.

Read More

Childhood Obesity Risk May Begin With Fathers, Long Before Birth

Key Takeaways:

• A review in Current Obesity Reports argues that fathers influence their children’s obesity risk through several interacting biological, behavioural, and environmental pathways that begin before conception – not only through the mother.
  
• Paternal obesity is linked to poorer sperm quality and to epigenetic changes in sperm that can alter gene expression in the developing embryo, although some of these changes appear reversible through lifestyle modification before conception.
  
• The authors call for obesity prevention to include fathers explicitly – through preconceptional counselling, perinatal education for both parents, supportive workplace policies, and more research into the paternal role.
  
  
  

A wider lens on obesity research

A recent review published in the journal Current Obesity Reports suggests that fathers shape their children’s risk of obesity through multiple interacting pathways that begin before conception. The authors argue that efforts to prevent and study childhood obesity should focus on fathers as well as mothers.

Childhood obesity continues to rise in the United States, alongside increasing rates of overweight and obesity among adults. Current projections suggest that more than 250 million Americans could be living with overweight or obesity by 2050.

Research shows that children are more likely to develop obesity when one or both parents are affected, and the risk is highest when both parents have obesity. This pattern reflects the complex interplay of genetic, biological, behavioural, and environmental factors that influence obesity risk across generations.

The Developmental Origins of Health and Disease (DOHaD) framework holds that the periconceptional period is critical in setting the foundation for long-term outcomes, including cardiometabolic disease, through exposure to environmental factors. Maternal nutrition, obesity, and metabolism have been studied in detail because they shape the fetal environment.

More recently, the Paternal Origins of Health and Disease (POHaD) framework has been brought under the DOHaD umbrella. The current review examined the biological, psychological, and behavioural pathways through which paternal factors affect children’s health – though not in isolation from family dynamics and other environmental and social factors. The authors stress that paternal influences operate alongside maternal and broader family influences rather than separately from them.

How obesity alters sperm and offspring metabolism

Around 40% to 70% of obesity is heritable, mediated by hundreds of obesity-linked genetic variants. Obesity in fathers can affect the metabolic health of their offspring through several routes.

Paternal obesity influences sperm quality, reducing sperm concentration and motility and increasing the rate of sperm DNA fragmentation. These changes are linked to the adverse effects of obesity on paternal metabolism. The same sperm abnormalities are reflected in a 30% to 66% increase in the risk of infertility among men with obesity, and they raise the risk of pregnancy loss independently of maternal factors.

Obesity is associated with metabolic dysregulation through disrupted endocrine regulation of sperm production, testicular and systemic inflammation, and epigenetic alterations in sperm. Because sperm cells are produced continuously and mature over several months before conception, there is a wide window during which environmental exposures can leave their mark.

These epigenetic changes are heritable and can affect gene expression in the developing embryo, across pathways tied to appetite regulation, insulin signalling, and fat metabolism. In animal studies, a high-fat diet in the father is associated with obesity-related changes in the offspring. Even so, while animal research provides strong evidence for these mechanisms, the equivalent biological pathways in humans remain incompletely understood.

Notably, some obesity-associated epigenetic changes in sperm appear to be reversible through lifestyle modification before conception.

How a father’s habits shape his child’s behaviours

Becoming a father tends to be associated with weight gain and with changes across multiple health behaviours, for better or worse. A healthy preconceptional paternal diet is associated with improved sperm quality and concentration, regardless of age and body mass index (BMI), while a poor-quality diet has the opposite effect.

The quality of a father’s diet, his physical activity habits, his feeding practices, and his parenting style all influence a child’s eating and activity levels – both directly and indirectly through role modelling. The same applies to a father’s physical activity and sedentary habits.

How neighbourhood and food access shape outcomes

A father’s risk of obesity is influenced by many other factors, including income, education, and neighbourhood type.

The residential neighbourhood affects a child’s diet directly, through food access, and indirectly, through its association with food security, socioeconomic status, and the father’s mental health. Food insecurity is linked to higher consumption of high-calorie foods and an increased risk of obesity. Likewise, limited access to safe recreational spaces restricts physical activity and raises obesity risk.

These factors operate at the family level, touching everything from the father’s physiology and parenting style to the child’s developmental environment. Together they interact to compound the increase in obesity risk across generations.

Mental health is particularly important. A father living with depression is less likely to have an engaged or positive parenting style, or to value preventive healthcare for himself or his family. This can worsen a child’s eating and sleep behaviours and increase obesity risk. Children living with a parent experiencing depression are also at greater risk of adverse childhood experiences (ACEs), which may affect their long-term obesity risk.

Why fathers may shape obesity risk from the start

The authors conclude that fathers play an important role in how obesity risk is transmitted across generations – a process that begins preconceptionally and continues through childhood. They note, however, that much of the current evidence is observational, and that further human research is needed to better understand the biological mechanisms linking paternal health and offspring obesity risk.

They suggest that obesity prevention strategies should include preconceptional counselling that addresses fathers as well as mothers; perinatal education aimed at both parents; the inclusion of fathers in obesity prevention methods; workplace policies that support paternal involvement in childcare; and greater priority for research examining the father’s role in transmitting obesity risk across generations.

CCH insights:

At CCH we have been interested in the mounting evidence around the paternal origins of health and disease (POHaD) for some time, particularly in relation to obesity. This review provides a comprehensive summary of the evidence so far for the important role of fathers, not just in terms of their biological intergenerational impact, but also through health-related behaviours and their influence on the child’s environment.

Read More

Beyond the Scales: Why Physical Activity Remains Central to Obesity Care

Key Takeaways:

• Exercise earns its place in obesity care through benefits the scales never show – lower blood pressure, better insulin sensitivity and improved fitness – so it remains worthwhile even when weight changes little.
  
• On its own, activity shifts the scales only modestly, but paired with diet, obesity medications or surgery it protects lean muscle, drives fat loss and makes the results last.
  
• Tools such as the 5A consultation model, wearables and app-based coaching can lift adherence, though their value depends on access, accuracy and how well they fit each person’s life.
  
  
  

How much weight someone loses has long been the headline measure of whether obesity treatment is working. A new scientific statement from the American Heart Association, published in Circulation, makes the case that this measure misses much of what physical activity actually does. Movement, the statement argues, reshapes cardiovascular and metabolic health in ways that a set of weighing scales will never register.

What activity does that the scales cannot capture

Obesity sits at the centre of cardiovascular risk because of the company it keeps: raised blood pressure, disordered blood fats and insulin resistance. With roughly 42% of adults in the United States affected, the stakes are considerable, and treatment has traditionally pursued two linked aims, shedding weight and lowering heart disease risk.

Physical activity contributes to both, but the more interesting finding is how much it achieves on its own terms. Regular exercise lowers blood pressure, sharpens the body’s response to insulin and nudges cholesterol and other lipids in a healthier direction, and it does so whether or not the number on the scales falls. Aerobic and resistance training each deliver. As a rough rule, doing more tends to help weight-related outcomes most, while working harder pays off most for cardiorespiratory fitness.

Why exercise alone is a poor weight-loss strategy

If the goal is purely to lose weight, activity by itself is an inefficient route. Unless someone trains at high volumes, the losses are usually small, and fewer than one person in seven manages a clinically meaningful reduction through exercise alone. The body, in effect, fights back: appetite climbs and metabolism slows, eroding the deficit that training creates.

This is why exercise works best in combination. Adding it to a calorie-reduced diet produces more weight loss and better metabolic results than either approach in isolation. And the composition of that loss matters as much as the total. Eating enough protein and including resistance work helps ensure the weight that goes is fat rather than muscle, preserving the lean tissue that keeps metabolism and strength intact.

Keeping weight off is the harder battle

Losing weight is difficult; not regaining it is harder still, and regain tends to undo the health gains that came with it. Here the evidence points firmly towards higher activity levels, somewhere between 200 and 300 minutes a week, as a marker of people who keep weight off successfully. The catch is that few people sustain that volume.

A more realistic path is to build gradually towards at least 150 minutes a week of moderate-to-vigorous activity, then add more where possible. Even when some weight creeps back, staying active keeps the cardiometabolic benefits in play, which is reason enough to maintain the habit rather than abandon it after a setback.

Where medication and surgery enter the picture

For people whose body mass index is high and for whom lifestyle change has not been enough, obesity medications and bariatric surgery are central options. Both are effective, and both come with real-world limits around cost, availability and side effects. Neither replaces an active lifestyle; the statement frames physical activity as the strategy that should run alongside them.

The newer GLP-1 receptor agonists, including liraglutide, semaglutide and tirzepatide, have transformed what medication can achieve, with some trials approaching the results once seen only after surgery. They work mainly by curbing appetite and slowing the stomach’s emptying, and although side effects are common, they are usually manageable. Beyond weight, liraglutide and semaglutide have been shown to cut major cardiovascular events in certain high-risk groups.

What remains poorly understood is how exercise fits into this newer landscape. Most medication trials simply have not isolated what activity adds, or how the two interact, leaving the ideal exercise prescription for people on these drugs an open question. The issue is sharpened by the fact that a notable share of the weight lost on GLP-1 receptor agonists is lean tissue rather than fat, even if the long-term consequences of that are not yet clear. The handful of studies that do compare medication with and without exercise suggest that adding activity means more fat loss and better fitness, but the field is still waiting for the large, controlled trials that would settle the matter.

Surgery raises related questions. People approaching bariatric procedures tend to be less active to begin with, and there is no agreed playbook for the period beforehand; insurer-mandated pre-surgical activity programmes exist, but the evidence that they change outcomes is thin and inconsistent. Afterwards, the picture is clearer: people who move more lose more weight and fat, hold onto those losses, and gain in fitness and strength, though effects on metabolic risk markers vary and access to structured programmes is frequently lacking.

Turning good intentions into sustained habits

Clinicians are not bystanders in any of this. A widely used framework, the 5A model, gives consultations a useful spine: assess where the person is, advise on the options, agree on goals, assist in pursuing them and arrange follow-up. Worked through properly, each step tends to deepen engagement with both dietary change and activity, making healthy behaviours easier to stick to.

Doing this well means looking past activity levels alone to the psychological, social and medical factors that can stall progress, and gauging how ready and confident someone feels about changing. Counselling tailored to that profile builds motivation and trust, which in turn supports the activity itself. Equipping clinicians to weave physical activity, dietary change and behaviour change into everyday obesity consultations is the focus of practical training such as the College of Contemporary Health’s Obesity Toolbox, a CPD-accredited online short course. Because a short appointment can only do so much, part of the clinician’s job is helping people spot the obstacles in their way, solve them together, and connect with wider support, whether behavioural counselling or a digital programme that keeps them accountable between visits.

Technology is increasingly part of that support. Wearables, apps, text reminders, personalised feedback and self-monitoring all show promise for keeping people moving. The statement is careful, though, to flag the caveats: not everyone has equal access to these tools, the devices vary in how accurately they measure activity, and none of it substitutes for regular reassessment and structured follow-up.

The bottom line for treatment

Physical activity belongs at the heart of comprehensive obesity care, supporting weight loss, helping maintain it and improving health more broadly. Medications and surgery are genuine advances, but exercise adds something they do not fully provide: gains in cardiovascular risk, body composition, fitness and quality of life, many of which arrive independently of any change on the scales.

Delivering that well takes teamwork across clinicians and allied health professionals, and programmes that are not only effective but also affordable and within reach, especially for under-resourced communities where obesity is more common and activity levels lower. Making the wider case for movement, rather than treating it as a weight-loss tool alone, is likely to be what makes obesity treatment hold up over the long run and eases the cardiovascular toll that obesity exacts.

CCH insights:

This study strikes right at the heart of how our understanding of obesity is starting to change – it is not all about body weight and body fat, but about health. Although reducing harmful body fat is an important part of obesity treatment, so is improving cardiometabolic health and other health issues that arise as a result of obesity. And physical activity is a vital tool in delivering these health improvements – helping to reduce blood pressure, regulate blood glucose, reduce cholesterol and improve
muscle mass and function – whether or not it results in weight loss whether or not it results in weight loss. For clinicians looking to put this into practice, CCH’s Obesity Toolbox (1.5 hours, fully online, CPD-accredited) is a quick, practical primer on the essentials of physical activity, dietary change and behaviour change in obesity care – a fast starting point for busy practitioners.

Explore the Obesity Toolbox →

Read More

New Research Shows Obesity May Reshape How Breast Cancer Spreads

Key Takeaways:

• Obesity may alter how early, non-invasive breast lesions progress into invasive cancer, a University of Oklahoma study suggests.
  
• In women with obesity, progression was linked to inflammation, immune cell activity, metabolic changes and raised levels of the enzyme SULF2 – not the rapid cell division seen in women without obesity.
  
• The findings could improve risk prediction for women with DCIS and help reduce overtreatment.
  
  
  

A different route to invasive disease

Obesity may change how early-stage breast cancer becomes invasive, according to a study by University of Oklahoma researchers published in The American Journal of Pathology.

Obesity is already recognised as a risk factor for invasive breast cancer, but researchers have not fully understood how it helps early, non-invasive breast lesions develop into invasive cancer. A clearer picture of this process could strengthen physicians’ ability to predict and treat the disease.

In the study, breast cancers in women without obesity displayed the typical signs of turning invasive, including rapid cell division and an increased ability to invade neighbouring tissue. In women with obesity, however, the researchers identified a different set of biological changes that appeared to help the cancer become invasive.

The cancer environment became more inflamed, with the arrival of immune cells that advanced the growth of the tumour. The tumour cells also appeared better able to survive under stress, and there were changes in cellular metabolism – how the cells use nutrients for energy.

“This could be why women with obesity are at higher risk for invasive breast cancer,” said Bethany Hannafon, Ph.D., co-lead author of the study and an assistant professor in the Department of Obstetrics and Gynecology at the OU College of Medicine. “The changes that the cancer cells are undergoing are allowing them to survive and thrive.”

A cooperative cancer “neighbourhood”

The researchers also found differences in the “neighbourhood” of cells and tissues surrounding the cancer. Epithelial cells, where the tumour originally develops, co-opt other cells around them to create an environment that is even more conducive to cancer growth.

“In women with obesity, there is cooperation between all the cell types, not just the cancer cells, which helps an early pre-cancer to become an invasive breast cancer,” said co-lead author Elizabeth Wellberg, Ph.D., assistant professor in the Department of Pathology at the OU College of Medicine. “That may be an area of future study – can a drug or intervention that targets only one cell type interrupt the whole network of progression toward invasive cancer?”

The role of the enzyme SULF2

The research team additionally discovered higher levels of an enzyme called Sulfatase 2 (SULF2) in the tumour cells of women with obesity, suggesting that it may play an important part in cancer progression. SULF2 will be a further focus of future studies.

Why better DCIS risk prediction matters

Understanding what causes early, non-invasive tumours – known as ductal carcinoma in situ, or DCIS – to become invasive is important because not all women will go on to develop invasive cancer, yet they currently receive the same treatment.

“In women diagnosed with DCIS, about half will later develop invasive ductal carcinoma (IDC) that spreads into surrounding breast tissue. But we currently have no way of determining which women are most at risk. As a result, many women with DCIS receive the same treatments used for IDC, including surgery, radiation and sometimes hormone therapy. Overtreatment is a major concern, but if we had better ways of determining risk, unnecessary treatments could potentially be reduced,” Hannafon said.

While breast cancer survival rates have improved over the past two decades, the number of women diagnosed with invasive breast cancer has not declined – underscoring the need for better ways to predict and prevent disease progression.

A growing public health concern

The rising prevalence of obesity gives the findings added weight.

“Obesity is on the rise – 50% of Americans are expected to be obese by 2030,” said the paper’s first author, Cole Hladik, Ph.D., who worked in Hannafon’s lab while earning his doctorate. “That statistic further highlights the importance of considering a patient’s metabolic health alongside the biology of the tumor itself.”

Read More

Four Weeks of Tomato-Soy Juice Lowered Inflammation in Adults with Obesity

Key Takeaways:

• In a four-week study, a tomato-soy juice rich in lycopene and soy isoflavones significantly reduced three blood markers of systemic inflammation in healthy adults with obesity, while a control tomato juice lacking those compounds did not.
  
• The researchers chose a low-carotenoid tomato juice as the comparison drink, rather than water, so they could isolate the effects of the lycopene and isoflavones rather than the effects of tomato juice in general.
  
• Building on these results and supporting animal data, the team has secured federal funding for a pilot clinical trial examining whether the same juice can ease inflammation in people living with pancreatitis.
  
  
  

A food-based approach to inflammation

Drinking a tomato-soy juice packed with plant compounds previously shown in animal studies to support health lowered pro-inflammatory proteins in healthy adults with obesity after four weeks, according to a new study. The researchers say the findings point to the juice’s potential as a functional food that could help rein in the persistent, unchecked inflammation that underpins a wide range of chronic conditions.

The juice was formulated to deliver high levels of two plant-based compounds, lycopene and soy isoflavones, both of which earlier research suggests have antioxidant and anti-inflammatory properties. Measured against a control tomato juice that lacked these compounds, the tomato-soy juice produced a significant drop in the blood levels of three proteins that serve as markers of systemic inflammation.

“The idea is, can we use food-based interventions to modulate inflammation?” said lead author Jessica Cooperstone, associate professor of horticulture and crop science at The Ohio State University. “And can we test this in a rigorous way so that we can really see this is affecting inflammation, versus just saying something is anti-inflammatory?”

The study was published recently in the journal Molecular Nutrition & Food Research.

What is in the juice

Lycopene is a carotenoid, the class of pigments responsible for the colours of tomatoes and various other vegetables. Soy isoflavones are flavonoids that mimic the action of the hormone oestrogen. Both are phytochemicals, naturally occurring compounds that help plants thrive.

Years ago, drawing on studies that linked diets rich in either tomato products or soy with a reduced risk of prostate cancer, Ohio State researchers developed the tomato-soy juice. It was made using tomatoes bred to contain a high concentration of lycopene – varieties also developed and grown at Ohio State – and then enriched with a soy isoflavone extract.

Subsequent research at the university connected a higher intake of the tomato-soy juice with reduced prostate-specific antigen levels in some men with prostate cancer. Studies conducted elsewhere have likewise suggested that tomatoes and soy, whether eaten separately or together, can influence inflammatory and metabolic pathways tied to obesity and other chronic illnesses.

“There’s been enough compelling evidence that compounds from tomatoes and soy might be modulating inflammation that we decided to test this in people,” Cooperstone said.

How the study was carried out

For the new study, 12 healthy adults with obesity drank two 6-ounce cans of the tomato-soy juice every day for four weeks. Following a washout period, the same participants then consumed the low-carotenoid control tomato juice for a further four weeks.

The choice of comparison drink was deliberate. Rather than pitting the juice against plain water, the team selected a tomato juice stripped of the key compounds so that any difference could be attributed to those compounds specifically.

“The hypothesis is that it’s the lycopene from the tomatoes and the isoflavones from the soy that’s inducing the effect, so we didn’t want to have a control that’s just water,” Cooperstone said.

What the blood tests showed

Before and after each four-week period, the researchers collected blood samples and tested them for cytokines, the pro-inflammatory proteins produced by the immune system. Only the tomato-soy juice produced significant reductions, and it did so in three cytokines: interleukin (IL)-5, IL-12p70 and granulocyte-macrophage colony-stimulating factor (GM-CSF). The juice was also associated with a downward trend in tumour necrosis factor alpha (TNF-a), although that particular change did not reach statistical significance.

Clues from the urine analysis

The team also examined participants’ urine before and after each trial period, looking for changes in metabolites. Metabolites are the molecular products of the biochemical reactions that break down nutrients to generate energy and carry out other essential functions in the body.

The analysis revealed that both the tomato-soy juice and the control tomato juice prompted some of the same shifts in metabolite profiles, indicating that certain tomato-driven effects occurred even in the absence of lycopene. Among the changes specifically induced by the tomato-soy juice, shifts in soy isoflavone metabolites stood out. The researchers note that, while more investigation is warranted, these changes offer further evidence that the food-based intervention is acting on human biology.

“This is probably a function of the fact that there’s more to our intervention agents than just these two compounds,” Cooperstone said. “Ultimately, we want to have a better understanding of how the foods that we eat are relating to our health. And when we really want to be sure, we need to test them in clinical trials. And that’s what we’re doing here.”

Next steps: a pancreatitis trial

On the strength of these results and additional data, Cooperstone and her colleagues have received funding from the National Institute of Diabetes and Digestive and Kidney Diseases for a pilot clinical trial. That trial will test whether consuming the same tomato-soy juice reduces inflammation in people living with pancreatitis.

The team has also gathered evidence from an animal model suggesting that the tomato-soy juice can lessen both inflammation and the severity of chronic pancreatitis. Those findings support the central prediction behind the new clinical trial, namely that the intervention could improve outcomes for people with the condition.

“Care for patients with pancreatitis is palliative, focused on controlling pain and GI symptoms. Our hypothesis is that the tomato-soy juice may serve as an intervention to decrease inflammation and hopefully increase patients’ quality of life,” Cooperstone said.

Funding and contributors

The work was supported by the U.S. Department of Agriculture, the National Institutes of Health, the Lisa and Dan Wampler Endowed Fellowship for Foods and Health Research, and the Foods for Health Initiative at Ohio State.

Co-authors include first author Maria Sholola, along with Jenna Miller, Emma Bilbrey, David Francis and Thomas Mace, all of Ohio State, and Janet Navotny of the USDA. Mace is the lead principal investigator on the pancreatitis trial. Cooperstone, Philip Hart and Kristen Roberts of Ohio State are also principal investigators on that trial.

Source: Eureka Alert!

Read More

Year-Long Trial Finds Rapid Weight Loss Outperforms a Gradual Approach, Overturning a Long-Held Assumption

Key Takeaways:

• In a 52-week randomised trial, adults living with obesity who followed a rapid weight loss programme lost significantly more weight at one year than those on a gradual programme (14.4% versus 10.5% of total body weight), and the gap held throughout the study.
  
• Rapid weight loss was not associated with greater weight regain, directly contradicting the widespread belief that losing weight slowly is necessary to keep it off.
  
• A larger share of people in the rapid weight loss group reached clinically meaningful BMI and waist-to-height targets linked to a lower 10-year risk of obesity-related conditions.
  
  
  

A long-held belief comes under scrutiny

New research presented at the European Congress on Obesity (ECO 2026) in Istanbul, Turkey, indicates that rapid weight loss (RWL) is considerably more effective than gradual weight loss (GWL), both in the amount of weight people lose and in how well that loss is sustained at one year.

For years, conventional thinking has held that rapid weight loss is unhealthy and that shedding weight very quickly raises the chance of regaining it. Yet these concerns rest largely on observational data, historical assumptions, or small studies with methodological limitations. The scientific evidence directly supporting them is limited and inconsistent, and high-quality randomised controlled trial evidence remains relatively sparse.

The study was led by Dr Line Kristin Johnson of the Department of Endocrinology, Obesity and Nutrition at Vestfold Hospital Trust in Tønsberg, Norway, together with colleagues. The centre is a collaborating centre with the European Association for the Study of Obesity (EASO-COM-Centre); EASO leads obesity advocacy and education across Europe and organises ECO.

Setting the treatment targets

A recent large, population-based cohort study concluded that, after weight loss, a body-mass index (BMI) of 27 kg/m² or below and a waist-to-height ratio (WHtR) of 0.53 or below may represent clinically meaningful treatment targets for lowering the 10-year risk of obesity-related complications, namely type 2 diabetes, hypertension, atherosclerotic cardiovascular disease, and hip and knee osteoarthritis.

In this new study, the researchers set out to compare how effectively a rapid weight loss programme and a gradual weight loss programme helped people reach those targets.

How the trial was designed

The 52-week, investigator-initiated, randomised clinical trial was run as a collaboration between the Department of Endocrinology, Obesity and Nutrition at Vestfold Hospital Trust and Roede AS, one of Norway’s leading and most established providers of commercial weight loss programmes.

In total, 284 adults living with obesity (BMI of 30 or above), of whom 257 (90%) were women, were randomised on a one-to-one basis to one of two 16-week, food-based programmes. The rapid weight loss programme reduced energy intake in stages: under 1,000 kcal per day in weeks 1 to 8, under 1,300 kcal per day in weeks 9 to 12, and under 1,500 kcal per day in weeks 13 to 16. The gradual weight loss programme set intake at 800 to 1,000 kcal per day below each participant’s estimated total energy expenditure, with a mean self-reported intake in this group of roughly 1,400 kcal per day.

Estimated energy expenditure was calculated from each participant’s estimated resting energy expenditure and then adjusted according to whether they had low, medium, or high physical activity.

The food composition in both programmes followed current Norwegian dietary recommendations from the Norwegian Directorate of Health. Core advice included eating healthy foods such as vegetables, fruits, whole grains, low-fat dairy products, fish, eggs, lean meat, and other protein-rich foods, while limiting saturated fats and added sugars.

Maintaining the results

After the initial weight loss phase, participants in both groups moved into an identical 36-week weight-regain prevention programme.

Throughout the study, the interventions included weekly in-person group sessions from week 1 to week 16. After that, in-person group meetings took place every 14 days for the first three months, followed by monthly meetings or individual contact via webinars, video, or telephone for the remaining five months.

In these sessions, participants were advised to raise their daily energy intake by 100 to 300 kcal during the first month, until their weight stabilised. From then on, daily intake was adjusted as needed in response to any weight changes across the eight-month maintenance phase. Participants could decide for themselves whether to maintain their weight or aim for further loss, and the majority chose to keep losing weight after the initial 16-week period.

What the trial found

Of the 284 participants, 142 were randomised to the rapid weight loss programme and 142 to the gradual weight loss programme. At baseline, the rapid weight loss group had a mean age of 48.5 years, body weight of 102.4 kg, height of 169 cm, BMI of 35.8 kg/m², waist circumference of 112.5 cm, and WHtR of 0.67. The corresponding figures in the gradual weight loss group were 47.7 years, 103.0 kg, 168 cm, 36.5 kg/m², 112.8 cm, and 0.67.

The primary outcome was one-year percentage total body weight loss (%TBWL). The proportion of participants reaching a BMI of 27 kg/m² or below, or a WHtR of 0.53 or below, after one year were exploratory outcomes.

During the first 16 weeks, the rapid weight loss group lost significantly more weight than the gradual weight loss group, with a mean %TBWL of -12.9% compared with -8.1%, a between-group difference of -4.8%.

At one year, that significant difference was maintained: the mean %TBWL was -14.4% in the rapid weight loss group and -10.5% in the gradual weight loss group, a between-group difference of -3.9 percentage points.

The share of participants achieving a BMI of 27 kg/m² or below was significantly higher in the rapid weight loss group than in the gradual weight loss group at both 16 weeks (13.8% versus 0.8%) and one year (28.3% versus 9.7%). A higher proportion also reached a WHtR of 0.53 or below in the rapid weight loss group, both at 16 weeks (24.2% versus 8.9%) and at one year (33.0% versus 18.4%).

What the researchers say

The authors conclude, “Among adults with obesity, participation in a structured rapid weight loss program resulted in significantly greater weight loss at one year, and higher rates of achieving clinically meaningful BMI and WHtR targets compared with a gradual weight loss approach.

“These findings indicate that, when provided within a controlled and professionally supervised setting, rapid weight loss may represent a more effective method than gradual weight loss for reaching key body weight targets associated with reduced obesity-related health risks.”

Dr Johnson adds, “Our results clearly challenge the prevailing belief that slow and steady gradual weight loss is necessary to prevent weight regain and reduce obesity-related complications.

“By contrast, we show that rapid weight loss is not associated with weight regain, and, more importantly, that a larger proportion of participants undergoing rapid weight loss – compared with gradual weight loss – achieved clinically meaningful treatment targets for reducing the 10-year risk of type 2 diabetes, hypertension, atherosclerotic cardiovascular disease, and hip/knee osteoarthritis.

“These findings are particularly relevant given the urgent need for effective weight-loss and weight-maintenance strategies. As many individuals with obesity cannot access or afford medical or surgical treatments, our results support the potential of effective, commercially available weight-reduction programs to help reduce the growing burden on public health care systems.”

Why it matters

With obesity placing a rising strain on health systems, and with medical and surgical treatments out of reach for many, the trial points to professionally supervised commercial programmes as a potential route to meaningful, lasting results. Its central message reframes a long-standing assumption: under proper supervision, losing weight quickly did not undermine maintenance, and it helped more people reach the targets tied to lower long-term health risks.

CCH insights:

These are impressive results for a diet and lifestyle intervention, with both groups achieving greater than 10% total body weight loss over a period of a year. However, participants received fairly intensive support throughout the entire year of the trial. The important thing is what happens in the next 12 months, after the intervention has stopped – are they able to sustain behavioural changes and weight loss without the support from the programme?

Source: Medical Xpress

Read More

Walking 8,500 Steps a Day May Help Prevent Weight Regain, Study Finds

Key Takeaways:

• New research presented at ECO 2026 suggests that walking around 8,500 steps a day may help people maintain weight loss and reduce the risk of weight regain after dieting.
  
• Researchers found that people who increased and sustained their daily step count were more successful at keeping weight off over the long term.
  
• The study highlights walking as a simple, affordable, and accessible strategy that could support long-term obesity management.
  
  
  

Study explores the role of walking in long-term weight management

New research being presented at the European Congress on Obesity (ECO 2026) in Istanbul, Turkey, taking place from May 12–15, suggests that walking approximately 8,500 steps per day could help people avoid regaining weight after dieting.

The findings, which will also be published in the International Journal of Environmental Research and Public Health, address one of the biggest challenges in obesity care – maintaining weight loss over time.

Although many weight loss programmes encourage people to increase their daily physical activity, including walking, researchers say there has been relatively limited evidence examining whether higher step counts genuinely help people lose weight during dieting or maintain that weight loss afterwards.

The new study aimed to clarify whether walking more each day could reduce the likelihood of weight regain and identify what level of daily activity may be most beneficial.

Preventing weight regain remains a major challenge

Professor Marwan El Ghoch, from the Department of Biomedical, Metabolic and Neural Sciences at the University of Modena and Reggio Emilia in Italy, highlighted the importance of addressing weight regain in obesity treatment.

“The most important – and greatest – challenge when treating obesity is preventing weight regain,” explained Professor El Ghoch.

“Around 80% of people with overweight or obesity who initially lose weight tend to put some or all of it back on again within three to five years.

“The identification of a strategy that would solve this problem and help people maintain their new weight would be of huge clinical value.”

Long-term weight maintenance is widely recognised as one of the most difficult aspects of obesity management. While many people can initially lose weight through dietary changes, sustaining those results often proves far more challenging due to complex biological, behavioural, and environmental factors.

Researchers conducted a large systematic review and meta-analysis

To explore the relationship between walking and long-term weight management, Professor El Ghoch and colleagues from Italy and Lebanon carried out a systematic review and meta-analysis of existing research.

The researchers analysed 18 randomised controlled trials investigating walking and weight management strategies. Fourteen of those studies, involving a total of 3,758 adults, were included in the final meta-analysis.

Participants had an average age of 53 years and an average body mass index (BMI) of 31 kg/m², placing the average participant in the obesity category. The studies included participants from a range of countries, including the United Kingdom, United States, Australia, and Japan.

The trials compared two groups:

• 1,987 participants enrolled in lifestyle modification (LSM) programmes
• 1,771 participants assigned to control groups

The control groups either followed dieting programmes without additional support or received no treatment intervention.

Lifestyle programmes combined diet and increased walking

The lifestyle modification programmes combined dietary guidance with recommendations to increase walking and monitor daily step counts.

These interventions generally included two distinct phases:

1. An initial weight loss phase
2. A longer-term maintenance phase designed to help participants sustain weight loss

Researchers assessed participants’ daily step counts at multiple time points throughout the studies, including:

• At baseline
• After the weight loss phase
• After the maintenance phase

The average duration of the weight loss phase was 7.9 months, while the maintenance phase lasted an average of 10.3 months.

At the start of the studies, physical activity levels were similar in both groups. Participants in the lifestyle modification programmes averaged 7,280 steps per day, while participants in the control groups averaged 7,180 daily steps.

Higher step counts were associated with less weight regain

The researchers found that participants in the control groups did not significantly increase their daily walking levels and did not experience meaningful weight loss during the studies.

In contrast, participants enrolled in the lifestyle modification programmes increased their average daily step count to 8,454 steps by the end of the weight loss phase.

During this period, participants lost an average of 4.39% of their body weight, equivalent to approximately 4 kg.

Importantly, participants were largely able to maintain their higher levels of daily activity throughout the maintenance phase. By the end of the studies, they were still averaging 8,241 steps per day.

They also maintained most of their weight loss over the longer term, with an average sustained weight reduction of 3.28%, or roughly 3 kg.

Further analysis demonstrated a clear association between higher daily step counts and lower levels of weight regain.

Researchers found that people who increased their walking during the weight loss phase and sustained those higher activity levels afterwards were more successful at maintaining weight loss over time.

Walking appeared more important for weight maintenance than initial weight loss

Interestingly, the study found that walking more was not associated with greater weight loss during the initial dieting period itself.

Researchers suggested this may be because calorie reduction and dietary changes tend to have a stronger influence on short-term weight loss than physical activity alone.

However, physical activity appeared to play a more significant role in helping people sustain weight loss once it had been achieved.

This distinction is important because many obesity interventions focus heavily on initial weight reduction, despite evidence showing that long-term maintenance is often the more difficult challenge.

A simple and affordable intervention

Professor El Ghoch said the findings demonstrate that lifestyle modification programmes incorporating walking can support clinically meaningful long-term weight management.

He added:

“Participants should be always encouraged to increase their step count to approximately 8,500 a day during the weight loss phase and sustain this level of physical activity during the maintenance phase to help prevent them from regaining weight.

“Increasing the number of steps walked to 8,500 each day is a simple and affordable strategy to prevent weight regain.”

The researchers suggest that walking may represent a practical and accessible intervention that could be incorporated into obesity treatment programmes without the need for expensive equipment or specialist facilities.

As obesity rates continue to rise globally, strategies that are sustainable, low-cost, and easy to implement may become increasingly important in supporting long-term health outcomes.

CCH insight

The evidence increasingly points to sustained behaviour change – not just the initial loss – as the real challenge in obesity care. CCH’s Obesity Essentials CPD short course (8–10 hours, fully online, CPD-accredited) gives healthcare professionals the practical skills to assess, support and manage patients with overweight and obesity, including how to help them build and maintain the everyday habits, such as regular walking, that keep weight off for good.
Explore Obesity Essentials →

Read More

Obesity Identified as Key Driver of Rising Cancer Rates in Younger Adults

Key Takeaways: 

• A major new study has found that overweight and obesity are likely to be significant contributors to rising cancer rates among younger adults in England.
  
• Researchers found that many traditional behavioural cancer risk factors – including smoking, alcohol consumption and physical inactivity – have remained stable or improved over the past two decades, making them unlikely to fully explain the increase in early-onset cancers.
  
• Although excess weight appears to play an important role, researchers say it cannot entirely account for the rise in cancers such as bowel cancer, suggesting that additional biological, environmental and early-life factors may also be involved.
  
  
  

Study highlights growing concern over early-onset cancer

Being overweight or living with obesity may be a key driver behind rising cancer rates in younger adults in England, according to a major new study led by researchers at The Institute of Cancer Research, London, and Imperial College London.

The analysis, published in BMJ Oncology, examined trends in cancer incidence alongside changes in known behavioural cancer risk factors over nearly two decades. Researchers found that while rates of several cancers among younger adults have continued to increase, many established lifestyle-related risk factors have either improved or remained stable during the same period.

These findings led researchers to conclude that obesity is likely to be one of the most important contributors to the increase in cancer incidence among younger generations in England.

At the same time, the researchers stressed that rising body mass index (BMI) alone does not fully explain the growing number of cancer cases, indicating that additional factors may also be contributing to the trend.

Researchers analysed cancer trends across England

The research team used national cancer registry data from England covering the years 2001 to 2019. The study was conducted by scientists from the Cancer Epidemiology and Prevention Research Unit (CEPRU) at both The Institute of Cancer Research (ICR) and Imperial College London.

Researchers examined incidence trends across:

• 22 cancer types in women
• 21 cancer types in men

From this analysis, they identified 11 cancers that are increasing among adults aged between 20 and 49 years and are associated with known behavioural risk factors.

All of the cancers identified – except oral cancer – are recognised as being linked to excess weight.

For most cancer types, increases seen in younger adults mirrored trends observed in adults aged over 50, where the overall disease burden remains considerably higher. However, bowel cancer and ovarian cancer stood out as notable exceptions because rates were increasing only among younger age groups.

Most traditional risk factors have improved

The study examined trends in several well-established behavioural cancer risk factors, including:

• Smoking
• Alcohol use
• Overweight and obesity
• Physical inactivity
• Red and processed meat consumption
• Low fibre intake

Together, these risk factors accounted for an estimated 40–50 per cent of bowel, endometrial, oral and liver cancer cases in 2019.

However, researchers found that trends for most of these risk factors have either remained stable or improved over time, making them unlikely to substantially explain the recent rise in cancer incidence among younger adults.

According to the analysis:

• Smoking among younger adults has fallen by approximately two per cent annually over the past two decades.
• Alcohol consumption has largely stabilised or declined.
• Physical inactivity has decreased.
• Consumption of red and processed meat has reduced.
• Fibre intake, while still below recommended levels, has gradually improved.

In contrast, rates of overweight and obesity have steadily increased since 1995.

The largest increases in obesity were observed among younger women, where obesity prevalence rose by approximately 2.6 per cent relative increase per year.

Obesity linked to rising bowel cancer rates

The researchers found evidence linking rising BMI to increasing bowel cancer rates among younger adults.

Among younger women, bowel cancer rates associated with BMI rose from 0.9 to 1.6 cases per 100,000 people. In comparison, bowel cancer rates not attributable to BMI increased from 6.4 to 9.6 cases per 100,000 people.

Similar patterns were also observed in men.

However, the authors emphasised that the total number of BMI-linked bowel cancer cases remained lower than the number of cases not linked to BMI. This suggests that although obesity is an important contributor, it cannot fully explain the scale of the increase in bowel cancer among younger adults.

Additional causes may be contributing

The study points to the likelihood that multiple interacting factors are contributing to rising cancer rates in younger generations.

Several suspected contributors have previously been proposed, including:

• Ultra-processed foods
• Antibiotic use
• Air pollution

However, researchers noted that many of these exposures have also shown relatively stable or declining trends in the UK, complicating efforts to identify the main drivers of early-onset cancers.

The authors also highlighted emerging evidence suggesting that obesity-related mechanisms not fully captured by BMI may influence cancer risk. These include:

• Metabolic dysfunction
• Chronic inflammation
• Alterations in the gut microbiome

Further research is needed to determine whether these mechanisms directly contribute to the development of bowel cancer and other cancers in younger adults.

Experts say more research is urgently needed

The researchers called for large-scale, long-term studies capable of tracking exposures across the entire life course in order to better understand what is driving rising rates of early-onset cancers.

Professor Marc Gunter, Co-Director of the Cancer Epidemiology and Prevention Research Unit at Imperial College London, said:

“The changes we’re seeing in cancer incidence, particularly the rates of some cancers in younger adults, don’t have a single cause or a simple answer. They reflect a complex mix of generational effects, gaps in long-term exposure data, and shifts in diagnosis and detection, and show how much more scientists still need to understand about when and how cancer develops across the life course. While rising rates in younger adults are concerning, it remains crucial not to lose sight of cancer trends in older adults, where the absolute burden of disease is still far greater.”

Professor Montserrat García-Closas, Co-Director of the Cancer Epidemiology and Prevention Research Unit and Group Leader in Integrative Cancer Epidemiology at The Institute of Cancer Research, London, said the findings indicate that behavioural changes alone cannot explain current trends.

She said:

“Our findings show that while cancer rates are rising in younger adults, the trends are unlikely to be explained by changes in most known behavioural risk factors. Smoking, alcohol and other behaviours have been stable or improving for two decades, yet early-onset cancers continue to increase – particularly bowel cancer.

“Excess weight is an important contributor, although it cannot fully account for the scale of the rise in bowel and other cancers. This tells us that multiple factors – including early-life exposures – may be acting together. Understanding these patterns is essential for identifying what is truly driving cancer risk in today’s generations. We now need deeper research, better measurement and continued surveillance to uncover the causes behind these worrying trends.

“However, we cannot wait to act. Tackling obesity across all ages, particularly in children and young people, through stronger public health policies and wider access to effective interventions, could slow the rise in cancer and prevent many cancers – and must become a national priority.”

Calls for stronger prevention and public health action

The findings have prompted renewed calls for stronger public health measures aimed at preventing obesity and improving cancer prevention strategies across all age groups.

Professor Kristian Helin, CEO of The Institute of Cancer Research, London, said the study highlights an urgent public health challenge requiring coordinated action across research, prevention and policy.

He said:

“This work highlights a growing public health challenge and the need for urgent action across research, prevention and policy. Although rising cancer rates in younger adults are concerning, the burden remains overwhelmingly higher in older people, which means prevention efforts must span all ages.

“This study makes clear that traditional lifestyle risks alone cannot explain current trends – pointing to the importance of investigating other exposures such as the potential role of the microbiome, while strengthening strategies to address obesity and other established risks. To protect future generations, we must invest in understanding the causes of cancer at all ages and ensure that early diagnosis, screening and prevention strategies keep pace with a changing population.”

CCH insights:

The outcomes of this study are concerning but not entirely surprising, given that obesity rates in children and young people are still rising and obesity is a significant risk factor for many cancers. It adds further support for the call to treat obesity at the earliest opportunity, regardless of the age of the individual. The longer obesity goes untreated the greater the risk of individuals developing serious chronic diseases such as cancer, type 2 diabetes and heart disease.

Read More

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.

Read More

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.

Helping patients hold on to those gains over the long term – and navigate the setbacks a relapsing condition brings – is the focus of professional training such as the College of Contemporary Health’s Behaviour Change Skills: Applying CBT in Practice, a CPD-accredited online short course.

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 will have major implications for long-term obesity care in the future. Because sustaining weight loss is where obesity care so often succeeds or fails, CCH’s Behaviour Change Skills: Applying CBT in Practice CPD short course (2 CPD hours, fully online, CPD-accredited) equips healthcare professionals with cognitive and behavioural techniques to help patients maintain progress, handle setbacks and make change stick.

Explore Behaviour Change Skills: Applying CBT in Practice →

Source: University of Birmingham

Read More

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

Read More

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.

Offering that kind of tailored follow-up draws on a solid grounding in nutrition and weight management – the focus of professional training such as the College of Contemporary Health’s Nutrition & Weight Management Essentials, a CPD-accredited online short course.

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.

CCH insight

As this study shows, supporting women’s weight – particularly those with overweight or obesity – calls for a firm grasp of nutrition and energy balance across the life course. CCH’s Nutrition & Weight Management Essentials CPD short course (10 hours, fully online, CPD-accredited) gives healthcare professionals a solid grounding in the fundamentals of nutrition and the practical methods that help patients achieve and sustain a healthier weight.
Explore Nutrition & Weight Management Essentials →

Read More