Obesity Care

How Losing Around 80 Minutes of Sleep a Night Could Drive Weight Gain and Inactivity

Key Takeaways: 

• Adults who cut their nightly sleep by about 80 minutes over six weeks gained roughly one pound (around 0.45 kg) on average and became more sedentary, Columbia University researchers found.
  
• Modest over six weeks, but the team estimates that sustaining this mild sleep loss for a year could cause clinically meaningful weight gain – a pattern affecting around 30% of adults.
  
• Related work in the same participants linked mild sleep restriction to greater insulin resistance and heart inflammation, pointing to a wider risk of type 2 diabetes and heart disease.
  
  
  

Why modest sleep loss deserves attention

Trimming a little sleep each night may carry more weight for your health than you might realise. Researchers at Columbia University Vagelos College of Physicians and Surgeons found that adults who shortened their nightly sleep by about 80 minutes over a six-week period gained an average of one pound and spent more of their waking hours being inactive.

The findings add to a growing body of evidence suggesting that consistently getting enough sleep may play an important role in preventing weight gain and in lowering the risk of obesity-related disease. Rather than pointing solely to diet and exercise, the results place sleep alongside them as a factor worth taking seriously.

“Our study shows that getting adequate sleep may help reduce the risk of weight gain and obesity-related conditions like heart disease and diabetes,” says Marie-Pierre St-Onge, a professor of nutritional medicine in Columbia’s Department of Medicine and Institute for Human Nutrition and the study leader. “People tend to gain weight over the course of their adulthood, and obesity is a major risk factor for heart disease. But focusing on eating a healthier diet and getting more physical activity to offset weight gain is simplistic and can be difficult to maintain.”

Looking beyond extreme sleep deprivation

Much of the earlier research connecting poor sleep with obesity has centred on severe sleep deprivation, frequently restricting people to as little as four hours of sleep a night. Those studies indicated that extreme sleep loss can heighten appetite and encourage overeating – behaviours that in turn contribute to weight gain.

The difficulty is that such severe restriction is hard for most people to sustain for more than a few days, which limits how far the results can be applied to everyday life. Very few people live with four hours of sleep for weeks at a time, so the relevance of those findings to the wider population has remained uncertain.

“These studies only show us what happens under the most extreme conditions and don’t tell us if mildly sleep-deprived people, like a lot of Americans who get 5 or 6 hours of sleep a night, will gain weight,” St-Onge says.

To reflect real-world habits more closely, the researchers set out to examine the effects of chronic, mild sleep loss – a pattern estimated to affect around 30% of adults.

Six weeks of less sleep led to measurable changes

The study involved 95 adults who typically slept between seven and eight hours each night. During one six-week phase, participants delayed their usual bedtime by 90 minutes, which shortened their nightly sleep. During a separate six-week phase, they kept to their normal sleep schedule, allowing each participant to serve as their own comparison.

Across both phases, participants wore wrist monitors that tracked sleep and physical activity. The researchers also measured body weight, waist circumference, body composition, and fasting levels of several hormones involved in regulating appetite, building a detailed picture of how the body responded to the change.

“While the one-pound weight gain observed with modest sleep curtailment is not overwhelming, it is important to remember this is occurring over just six weeks,” says Faris Zuraikat, assistant professor of nutritional medicine in Columbia’s Department of Medicine and Institute for Human Nutrition and first author of the study. “Our study was designed to mimic sleep patterns that most adults experience chronically. When extrapolated to a full year, we would expect that losing less than an hour and a half of sleep per night could result in clinically meaningful weight gain.”

Less sleep also meant more sitting

Alongside the change in weight, the researchers found that participants became less active during the sleep-restriction phase. On average, sedentary time rose by 17 minutes per day. Among men and postmenopausal women, inactivity climbed by nearly 30 minutes each day.

Notably, this increase in sitting held up even after accounting for the extra waking hours that come with shorter sleep – so the added inactivity was not simply a matter of being awake for longer.

“Even when we accounted for the fact that they were awake longer when sleep was shortened, participants spent more time being inactive than when they got adequate sleep,” Zuraikat says. “This is notable, as people who are more sedentary have elevated risk for chronic diseases.”

Earlier research suggests broader health effects

The same group of participants has featured in several related studies, which together suggest that the consequences of mild sleep loss may extend well beyond weight. In one earlier investigation, women with increased cardiometabolic risk who reduced their sleep by about 80 minutes each night for six weeks developed greater insulin resistance – an important risk factor for type 2 diabetes. The effect was particularly pronounced in postmenopausal women.

A separate study found that men and women with an elevated risk of heart disease developed an influx of inflammatory cells in the heart after undergoing mild sleep restriction, hinting at a possible mechanism linking short sleep to cardiovascular harm.

“Though more research is needed to further understand how sleep restriction leads to weight gain, all of our findings suggest that insufficient sleep increases the risk of obesity-related conditions like type 2 diabetes and heart disease,” St-Onge says.

“Now we need to understand the health effects of improving sleep in those who fail to get adequate sleep on a regular basis.”

About the study

The study, titled “Skimping on Sleep and Its Impact on Body Weight and Composition: A Pooled Analysis of Randomized Trials,” was published on 6 July in Annals of Internal Medicine.

The authors are Faris Zuraikat, Samantha Scaccia, Justin Cochran, Bin Cheng, Keith Diaz, Seth Creasy (University of Colorado), Brooke Aggarwal, Sanja Jelic, and Marie-Pierre St-Onge. The authors report no conflicts of interest.

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Air Pollution May Raise Obesity Risk in Children by Affecting Impulse Control

Key Takeaways:

• New peer reviewed research suggests early exposure to PM2.5 air pollution may contribute to childhood obesity by affecting children’s impulse control.
  
• Babies exposed to higher PM2.5 levels during their first year of life were more likely to show later difficulties with inhibitory control, which were linked to higher body fat and BMI between ages four and eight.
  
• Researchers say individual steps such as HEPA filtration may help reduce exposure, but wider policy action is needed to limit PM2.5 pollution.
  
  
  

Study links PM2.5 exposure with later weight gain

Exposure to common air pollution may contribute to childhood obesity by disrupting children’s ability to control impulses, according to new first of its kind peer reviewed research.

The study, led by researchers at Mount Sinai’s Icahn School of Medicine, focused on particulate matter 2.5, known as PM2.5. This pollutant is made up of microscopic solid or liquid particles suspended in the air. Common manmade sources include traffic emissions and the burning of fossil fuels.

PM2.5 is considered a probable carcinogen and has been linked to a range of health problems, including dementia and strokes. Previous research has also shown that PM2.5 has obesogenic properties, meaning it may disrupt metabolism and is associated with weight gain.

Impulse control identified as a possible pathway

Researchers said the new study is the first to identify impulse control as a potential pathway linking early PM2.5 exposure with childhood obesity.

The study found that babies exposed to higher levels of PM2.5 during their first year of life were more likely to develop difficulties with impulse control later in childhood. Those behavioural changes were then associated with higher body fat and higher BMI among children aged between four and eight.

“A lot of the obesity research primarily focuses on – and is being shaped by – diet and physical activity, and a lot may not include environmental exposures, including air pollution,” said Jamil Lane, a co-author with Mt Sinai’s Icahn School of Medicine.

“Our study is novel in that we are showing that high levels of air pollution early in life may cause more difficulty with self-regulation, which contributes to weight gain.”

Why early life exposure matters

The researchers examined data from 434 children born largely between 2007 and 2008 in Mexico City. The children are part of a longitudinal health study.

The authors modelled ambient PM2.5 exposure during pregnancy and during the children’s first year of life. Lane described this early period as a “very sensitive window” for brain development.

The children were later assessed for impulsivity and measures linked to obesity. According to the study, the group with the highest PM2.5 exposure showed a pattern of high impulsivity, reflecting significant deficits in inhibitory control.

How brain development and eating behaviour may be connected

Poor inhibitory control is already well established as being linked to obesity. Bob Wright, a study co-author and environmental epidemiologist at Mount Sinai, said the authors questioned whether PM2.5’s neurotoxic effects and obesity were “part of the same processes”.

“Our study shows that greater early exposure to PM2.5 in the first year of life is associated with alterations in inhibitory control function in childhood,” the study’s authors wrote. “The effect is likely due to altered eating behaviors related to inhibitory control that are programmed early in life.”

The findings suggest that air pollution exposure early in life may affect brain pathways involved in self-regulation, which could then influence eating behaviours and weight gain later in childhood.

Study limitations and wider context

The study acknowledges several limitations, including its small population size and limited covariates.

However, Cecilia Moura, a clean transportation scientist with the Union of Concerned Scientists, who was not involved in the research, said the study was sound and that the novel findings “indicate there is sufficient evidence supporting the correlation to motivate policies and regulations that mitigate exposure to PM2.5”.

The research comes against the backdrop of high levels of obesity in the United States. In 2018, about 42% of American adults were estimated to have obesity.

Steps families can take to reduce exposure

The researchers said people can take some steps to help protect themselves and their children from PM2.5 exposure.

Home HEPA air filtration systems are effective at removing PM2.5. Furnace filters rated MERV 13 or higher can also capture much of the pollutant. DIY filtration systems made with a box fan, cardboard, tape, and pleated air filters have also been shown to reduce particulate matter.

The authors advised parents to avoid high congestion areas as much as possible and to stay indoors when wildfire smoke is heavy.

Researchers call for policy action

Despite these individual measures, researchers stressed that people cannot fully protect themselves from air pollution exposure on their own. They said the findings underline the need for wider policy solutions and greater public awareness.

“There is not going to be change if people are not aware and lobbying for it, but policy change takes a long time and there are things we can do to protect ourselves,” Wright said.

CCH insights:

This study provides more evidence of the complex array of factors that can contribute to obesity, and may be one reason (of many) that people from lower socioeconomic backgrounds have a higher risk of developing obesity. When we use the term ‘obesogenic environment’ most of us think of the plethora of fast-food outlets, the abundance of UPFs in food shops and our reliance on motorised transport – but we need to think even more widely than that, to include the quality of air we are breathing.

Building that wider, evidence-based picture of what actually drives obesity – across the biological, behavioural, social and environmental – is the foundation of good obesity care, and it’s what our CPD short course Obesity Essentials is designed to give any healthcare professional. Those wanting to go further can explore our PGCert in Obesity Care, which examines the full range of contributing factors in depth.

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Intermittent Fasting Maintains Long-Term Weight Loss Irrespective of Meal Timing, Study Shows

Key Takeaways: 

• Adults living with overweight or obesity who followed a 16:8 fasting pattern for 12 weeks kept off significantly more weight a full year after the intervention ended.
  
• The benefit held whether the eight-hour eating window fell early or late in the day, giving people the freedom to fit fasting around their own routines.
  
• One in three participants chose to carry on fasting unprompted during the follow-up year, pointing to a habit that is relatively easy to sustain.
  
  
  

A twelve-week habit with lasting results

New research has shown that confining daily food intake to an eight-hour window helps people living with overweight or obesity maintain their weight loss 12 months after a structured intervention comes to an end. The work was carried out by scientists from the University of Granada (UGR), the Granada Institute for Biomedical Research (ibs.GRANADA), the Public University of Navarra and the Biomedical Research Networking Center (CIBER), and was recently published in the journal Clinical Nutrition.

The trial followed 99 adults, half of them women, all of whom were living with overweight or obesity. It focused on intermittent fasting, and specifically the approach widely known as 16:8, in which people fast for 16 hours and eat only during the remaining eight. The findings indicate that this pattern is an effective way to hold on to weight loss over the medium term.

Crucially, the researchers found that the benefits endured a year later regardless of when the eating window fell. Whether participants ate early in the day, between 9 a.m. and 5 p.m. (early fasting), or later on, between 1 p.m. and 9 p.m. (late fasting), they fared better than people who kept to their usual routine of eating across a window of 12 hours or more. Both the early- and late-fasting groups sustained significantly greater weight loss at 12 months, and the early-fasting group also held on to a greater reduction in fat mass. According to the team, this suggests that the approach is not only feasible and effective in the short term but also produces effects that last.

Body composition assessed one year later

For the first 12 weeks, participants were split into four groups, each of which took part in a Mediterranean diet education programme. A control group kept its usual eating window of 12 hours or longer. An early-fasting group used an eight-hour window that began before 10 a.m., while a late-fasting group used an eight-hour window that started after 1 p.m. A fourth, self-selected group chose its own eight-hour window.

Weight, fat mass and fat-free mass were measured before and after the 12-week intervention, and again a year after the study finished. The work forms part of a larger project whose principal results appeared in the journal Nature Medicine. That analysis found that people who practised time-restricted eating (TRE), whatever their eating schedule, lost an average of 3–4 kilograms (6.6–8.8 pounds) more than those given nutritional advice alone.

Dr Alba Camacho Cardeñosa, a researcher at the University Joint Institute for Sport and Health (iMUDS) at the University of Granada and a postdoctoral fellow at ibs.GRANADA in the Endocrinology and Nutrition Department at San Cecilio University Clinical Hospital, is the study’s first author. She explains that “to date, although we knew that intermittent fasting promotes modest weight loss in the short term, it was unclear whether its effects were sustained over time. By evaluating the participants 12 months after the intervention ended, we demonstrated that the changes in body weight persist.”

The researchers also point to the strength of ongoing adherence, noting that “a very positive finding is that one in three people decided to continue practicing intermittent fasting on their own during that year of follow-up, suggesting that it is a relatively easy habit to integrate into daily life.”

A flexible strategy against obesity

The study was led by researchers from ibs.GRANADA belonging to the PROFITH CTS-977 research group at the University of Granada, headed by Professor Jonatan Ruiz Ruiz. It was conducted in collaboration with the San Cecilio University Clinical Hospital and the Virgen de las Nieves University Hospital in Granada, the Public University of Navarra, the CIBER on Obesity (CIBEROBN) and the CIBER on Frailty and Healthy Aging (CIBERFES).

The team emphasises that as little as 12 weeks of intermittent fasting may serve as an effective medium-term strategy for weight management in adults living with overweight or obesity. Because both early- and late-day regimens proved effective, the findings give people the flexibility to choose the schedule that best fits their lifestyle, which may in turn improve adherence and support more successful obesity treatment.

CCH insights:

These are very encouraging results for the use of time-restricted eating (TRE) as a strategy for weight loss maintenance. It would be good to now see research into the use of TRE as a tool to prevent weight regain after cessation of GLP-1 therapy. If TRE is adopted during GLP-1RA treatment, and continued after stopping the medication, could it help maintain weight loss and cardiometabolic gains?

Helping patients hold on to their gains — during treatment and in the months after it ends — is exactly the terrain of our two-hour CPD course GLP-1RAs in Practice: Supporting Patients During Treatment, which covers nutrition, monitoring and preparing patients for life after treatment for any clinician managing the full arc of GLP-1RA care.

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Maternal Obesity Before Pregnancy Tied to 64% Higher Childhood Obesity Risk

Key Takeaways:

• Children whose mothers had obesity before pregnancy were 64% more likely to be affected by overweight or obesity by age 3.
  
• Gaining excess weight during pregnancy – common among about 41% of mothers studied – was linked to a 39% higher risk.
  
• Maternal weight factors mattered at different stages, and the links varied between Hispanic and non-Hispanic families.
  
  
  

The roots of childhood obesity may begin in the womb

New research led by the George Mason University College of Public Health has found that children whose mothers began pregnancy with obesity were 64% more likely to be affected by overweight or obesity by age 3. Excessive weight gain during pregnancy was associated with a 39% increase in that risk.

“Our findings suggest that childhood obesity risk may not develop in a single, uniform way, but maternal health before and during pregnancy may play a larger role than many people realize,” said study lead author Hua Min, associate professor in the Department of Health Administration and Policy.

Timing appears to matter

Different pregnancy-related weight factors appeared to matter at different stages. Excess weight gain during pregnancy was more closely linked to infant weight, while maternal obesity was more strongly associated with weight later in toddlerhood. Researchers also found that excess weight gain during pregnancy was common, affecting about four in 10 mothers in the study.

A large, ethnically diverse US study

Published in the International Journal of Obesity, the research is among the largest and most ethnically diverse longitudinal studies in the United States to examine how maternal weight may influence obesity risk in early childhood. Researchers tracked nearly 3,000 mother-child pairs, drawing on data from a Northern Virginia birth cohort taking part in the National Institutes of Health’s Environmental influences on Child Health Outcomes (ECHO) Program.

The George Mason research team included Michael S. Bloom of the Department of Global and Community Health, along with Grace Lawrence, Alma Fuller and Kathi C. Huddleston of the School of Nursing.

Why this matters

Childhood obesity remains one of the most pressing health challenges in the United States. The study notes that nearly 90% of children with obesity at age 3 will continue to be affected by overweight or obesity into early adulthood. Those early patterns can carry long-term consequences, increasing the risk of diabetes, cardiovascular disease and other chronic health problems.

Researchers say the findings reinforce the importance of maternal health before and during pregnancy – not just for pregnancy outcomes, but also for a child’s long-term health trajectory. The findings also suggest that obesity risk may develop differently across populations, with patterns varying among demographic groups.

Study details

The findings were based on the First Thousand Days of Life Study, a Northern Virginia birth cohort taking part in the ECHO Program, which examines how early-life experiences affect child health. George Mason was selected as an ECHO research site in 2019.

Researchers enrolled 2,899 mother-child pairs in Northern Virginia between 2012 and 2019, following families from pregnancy through to age 3.

Key findings

The strongest signal came from maternal weight before conception. Children whose mothers had obesity before pregnancy were 64% more likely to be affected by overweight or obesity by age 3, and the risk rose incrementally with weight: for every one-point increase in maternal pre-pregnancy body mass index (BMI), the likelihood of childhood overweight or obesity climbed by about 4%.

Weight gain during pregnancy carried its own, separate risk. Children whose mothers gained excessive weight while pregnant were about 39% more likely to be affected by overweight or obesity by age 3, and roughly 41% of mothers in the study gained more than national guidelines recommend. Notably, the two factors seemed to act at different points in early life: excess weight gain during pregnancy showed stronger links to higher weight in infancy, whereas maternal weight before pregnancy became more strongly associated with higher child weight later in early childhood. The associations also differed between Hispanic and non-Hispanic families, suggesting that obesity risk may develop differently across populations.

Looking ahead

Taken together, the findings point to the period before and during pregnancy as a meaningful window for a child’s long-term health, rather than a single moment or cause. Because the maternal weight factors appeared to matter at different stages, and because the associations varied between demographic groups, the researchers suggest that efforts to understand and address childhood obesity may need to account for how risk builds over time and how it differs across populations.

Source: George Mason University

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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.

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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.

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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. 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.

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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.”

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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!

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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

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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.

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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.

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