Obesity Care

Immune Cells May Keep a Biological Memory of Obesity

Key Takeaways: 

• Mice lacking a protein called CWC22 in their fat tissue immune cells struggled to lose weight on a reduced-fat diet.
  
• Over half of the obesity-related genetic changes in these cells persisted after weight loss, suggesting a biological “memory” of obesity.
  
• Correcting one of those changes restored normal cell function and helped the mice shed fat again.
  
  
  

Why weight loss can become harder after obesity

According to the World Health Organization, one in eight people worldwide lives with obesity. Yet despite the volume of health education programmes, books, articles and treatments available, many people continue to find weight loss extremely difficult once obesity has developed. Precisely why the body resists losing weight, and why lost weight is so often regained, remains a complex puzzle for researchers.

A new study published in the journal Science Translational Medicine may offer part of the answer. The research points to changes in a particular type of immune cell known as an adipose tissue macrophage (ATM). In mice, these changes appeared to make weight loss harder, because the cells seem to carry a biological “memory” of obesity that outlasts the obesity itself.

What the researchers did

Researchers from several institutions across Japan set out to study ATMs directly. These immune cells help regulate fat tissue health in a number of ways, one of the most important being the safe removal of dying cells from the tissue.

The team fed laboratory mice a high-fat diet for 12 weeks until the animals developed obesity, then switched them to a low-fat diet for a further six weeks. When they compared the animals, they noticed a pattern: the mice that lost the least weight after the dietary switch had lower levels of a protein called CWC22 in the nucleus of their ATM cells. This suggested that CWC22 might play a role in helping the body shed weight.

To test that idea, the researchers genetically modified a group of mice so that they lacked the CWC22 gene in a group of immune cells that includes macrophages. Under normal circumstances, CWC22 helps cells splice messenger RNA, the editing process that RNA undergoes before it is used as a template to make proteins.

A clean-up failure in fat tissue

When the modified mice were placed on a weight-loss diet, they struggled to shed fat. Their ATMs could not clear away dead cells effectively, and as a result dead cells accumulated in the fat tissue.

Closer analysis of these immune cells revealed the mechanism. The absence of the Cwc22 gene caused a splicing error involving a gene called Scarb1. Because of that error, the macrophages destroyed their own clean-up receptors before those receptors could reach the cell surface, leaving the cells without the tools they needed to do their job.

The knock-on effect involved a chemical messenger. Because the macrophages were less able to clear dead cells, they released less inosine. Inosine normally acts as a signal instructing fat cells to break down their stored fat, so with less of it available, fat breakdown was impaired.

A memory that persists after weight loss

Perhaps the most striking finding concerned how long these changes lasted. The research team found that 51.9% of the genes showing obesity-induced RNA splicing changes in these immune cells remained altered even after the animals had lost weight.

In other words, the immune cells retained a biological record of the period of obesity, including alterations that continued to impair their normal clean-up duties long after the diet had changed.

“These findings reveal that aberrant alternative splicing in macrophages underlies resistance to postobesity weight loss,” commented the study authors in their paper.

Rewriting the memory

Encouragingly, at least one component of that memory appears to be reversible. When the scientists corrected the Scarb1 splicing error using a synthetic genetic patch, the clean-up receptors were restored. This in turn increased the amount of inosine available and helped the mice to lose fat once again.

“Our study suggests that specific alternative splicing events can shape macrophage phenotypes under defined environmental conditions.”

What this could mean for people living with obesity

The findings may eventually help inform treatments for people who struggle to lose weight after developing obesity. When the team analysed human tissue samples, they found abundant CWC22 in the nuclei of immune cells taken from people who were lean, but reduced levels in samples from people living with obesity. That parallel between the mouse and human findings is what makes the work potentially translatable.

It is worth keeping the limitations in view. The functional experiments were carried out in mice, and the human element of the study was limited to tissue analysis rather than any test of treatment. No synthetic genetic patch has been trialled in people, and there is a considerable distance between correcting a splicing error in a mouse model and offering a therapy in clinical practice.

Even so, the study adds to a growing body of evidence that weight regain is not simply a matter of behaviour or willpower. Biological adaptations in fat tissue, appetite regulation and now immune cell function all appear to work against sustained weight loss. Clinicians who want to explore these mechanisms and their practical implications in more depth may find it useful to look at structured CPD, such as the College of Contemporary Health’s Obesity Essentials short course, which covers the biological, clinical and behavioural drivers of obesity and weight management.

For people living with obesity, findings like these carry a useful message: the difficulty of maintaining weight loss has measurable biological underpinnings, and understanding them may in time lead to better-targeted support.

CCH insight

Understanding why the body resists weight loss is central to supporting people living with obesity well. Our Obesity Essentials CPD short course explores the physiology, clinical management and behavioural dimensions of obesity, giving healthcare professionals a grounded, evidence-informed basis for the conversations they have every day.

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Ketogenic Diet Cut Liver Fat by 67% in a Randomised Trial

Key Takeaways:

• People with obesity who followed a ketogenic diet reduced their liver fat by an average of 67%, compared with an average reduction of 45% in both the Mediterranean and low-fat plant-forward groups – even though all three groups lost a comparable amount of weight.
  
• Around half of the participants following the ketogenic diet no longer met the criteria for prediabetes by the end of the study, compared with 29% in the Mediterranean group and 7% in the plant-forward group.
  
• Despite obtaining 73% of their calories from fat, participants in the ketogenic group showed no increase in blood fat or cholesterol levels, alongside the largest rise in glucagon and the steepest fall in blood insulin of the three groups.
  
  
  

Carbohydrate restriction appeared to add benefits beyond weight loss

A very low-carbohydrate, high-fat diet may deliver stronger metabolic benefits for people with obesity than either a Mediterranean diet or a low-fat diet, according to a clinical trial published on 27 August in the Cell Press journal Cell Metabolism. After four to five months on a ketogenic (or “keto”) diet, about half of the participants with obesity and prediabetes no longer met the criteria for prediabetes.

“We know weight loss can improve metabolic health in people who are obese,” says Samuel Klein, the study’s corresponding author at Washington University School of Medicine in St. Louis, Missouri. “Our data suggest that if you have high liver fat content and prediabetes, reducing carbohydrate intake can have important therapeutic effects on metabolism beyond just weight loss alone.”

The distinction matters clinically. Weight loss itself is known to improve metabolic markers, so the open question has been whether the composition of a diet contributes anything further once the amount of weight lost is held constant. This trial was designed to test exactly that.

Comparing three widely used weight loss diets

An estimated 40% of adults in the United States have obesity. Doctors often recommend low-fat, low-carbohydrate or Mediterranean diets for weight loss, but researchers have not known whether one approach provides extra metabolic advantages beyond the effects of losing weight.

The three diets differ sharply in how much carbohydrate and fat they provide:

• A low-carbohydrate diet, also known as the Atkins or ketogenic diet, greatly restricts carbohydrates. A ketogenic diet can include foods rich in saturated fat, including animal products.
  
• A low-fat diet, by contrast, can obtain as much as 70% of its energy from carbohydrates.
  
• A Mediterranean diet emphasises plant-based foods such as vegetables, olive oil and nuts, along with moderate amounts of fish and dairy.
  
  
  

To compare their effects, Klein and his colleagues enrolled 42 people with obesity, prediabetes and fatty liver disease in a clinical trial. Participants were randomly assigned to follow a ketogenic diet, a Mediterranean diet, or a low-fat, plant-forward diet. The research team supplied all of their food, and participants met with a dietitian every week to help them stay on their assigned eating plan.

That level of support is worth noting. Providing every meal and offering weekly dietetic contact removes much of the adherence variability that undermines free-living diet studies, which strengthens confidence that the differences observed between groups reflect the diets themselves rather than differences in how closely people managed to follow them.

Matching weight loss across the three groups

The ketogenic diet supplied just 4% of calories from carbohydrates and 73% from fat. In the Mediterranean group, 50% of calories came from carbohydrates and 35% from fat. The plant-forward diet provided 70% of calories from carbohydrates and 15% from fat.

Researchers adjusted calorie intake for each person so that participants in all three groups would lose about 10% of their body weight. Reaching that target took roughly four to five months.

By the end of the study, participants in every diet group had significantly reduced their body fat. Insulin sensitivity also improved across all three groups, helping the body control blood sugar more effectively. In other words, all three approaches worked – the question was whether any of them worked better than the others once weight loss was equalised.

The ketogenic diet produced the largest fall in liver fat

Despite similar weight loss, the ketogenic diet produced the strongest changes across several measures of liver and metabolic health. Liver fat fell by an average of 67% among people following keto, compared with an average reduction of 45% in both the Mediterranean and plant-forward groups.

The researchers also tracked participants’ metabolism over a 24-hour period by repeatedly analysing their blood. People in the ketogenic group showed the largest rise in glucagon, a hormone that helps reduce fat stored in the liver. They also had the greatest decline in blood insulin levels, another change that can help lower liver fat, compared with participants following the other two diets.

Together, the hormonal findings offer a plausible mechanism for the liver fat result: lower circulating insulin and higher glucagon both shift the liver away from storing fat, and both are the expected consequence of sharply restricting carbohydrate intake.

Blood fats did not rise on the highest-fat diet

One of the more counter-intuitive results concerned the lipid profile of the ketogenic group, whose diet contained by far the most fat and could include saturated fat from animal products.

“The most surprising finding was that participants in the ketogenic diet group didn’t experience an increase in blood fat or cholesterol levels despite consuming the most fat,” says Max Petersen, the study’s first author at Washington University School of Medicine.

Prediabetes improved most in the ketogenic group

After the weight loss intervention, about 50% of participants following the ketogenic diet no longer met the criteria for prediabetes. That compared with 29% of those on the Mediterranean diet and 7% of those following the plant-forward diet.

The researchers were careful to position dietary composition alongside, rather than against, current pharmacological options for people living with obesity.

“GLP-1-based medications have revolutionized the therapy of obesity. We now have a very effective pharmacotherapy for achieving significant weight loss,” Petersen says. “But in addition, our study shows that the specific composition of the diet can give you added benefits.”

What the findings mean for everyday practice

For healthcare professionals supporting people with obesity, prediabetes or fatty liver disease, the practical implication is that the content of a weight loss plan may deserve as much consultation time as the calorie target attached to it. Two people can lose the same 10% of their body weight and still arrive at meaningfully different liver fat and glycaemic outcomes.

This is the kind of nuance that clinicians increasingly need to be able to explain confidently in a short appointment, and it is a core focus of continuing professional development in nutrition. The College of Contemporary Health’s Nutrition & Weight Management Essentials CPD short course is designed for practitioners who want to strengthen their grounding in evidence-based nutrition and weight management before applying it in conversations with patients.

It is also worth keeping the study’s limits in view. This was a small trial of 42 people, conducted under closely controlled feeding conditions with weekly dietetic support and all food provided. Whether the ketogenic advantage persists in free-living conditions, over longer periods, and across broader populations remains to be established.

The research was supported by the National Institutes of Health and the Foundation for Barnes-Jewish Hospital.

CCH insight

Findings like these are only useful at the point where a clinician can translate them into a realistic, personalised plan with a patient. Nutrition & Weight Management Essentials is a CPD-accredited short course from The College of Contemporary Health, developed for healthcare professionals who want a practical, evidence-informed foundation in nutrition and weight management.

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Higher Coffee Intake Linked to Lower Visceral Fat and Greater Muscle Mass

Key Takeaways: 

• Higher habitual coffee intake was associated with lower total and visceral fat and greater skeletal muscle mass, despite a similar BMI.
  
• Coffee intake was linked to lower branched-chain amino acids in both sexes, and to sex-specific differences in testosterone and SHBG.
  
• The study was observational, so it cannot show that drinking coffee caused any of the differences identified. 
  
  
  

A familiar drink with poorly understood biology

Coffee is consumed around the world every day, and earlier research has associated coffee drinking with a reduced risk of conditions including type 2 diabetes and cardiovascular disease. What has remained unclear is why. Scientists still do not fully understand the biological processes that might explain those connections, which has made it difficult to interpret the epidemiological signal.

New research from Finland now suggests that regular coffee consumption is associated with healthier body composition, favourable metabolic markers, and distinct patterns involving sex hormones in men and women.

What the researchers examined

Researchers at the University of Oulu analysed information from 2,264 people who were 46 years old and taking part in the Northern Finland Birth Cohort 1966. The team investigated how participants’ usual coffee intake related to circulating metabolites, indicators of cardiometabolic risk, and sex hormone levels.

Studying a single birth cohort at a single age has a particular advantage: it removes age itself as a source of variation, allowing differences between people with higher and lower coffee intake to stand out more clearly.

Lower body fat and greater muscle mass

People who consumed more coffee tended to have lower levels of both total body fat and visceral fat, along with greater skeletal muscle mass.

Notably, these differences appeared even though participants with higher and lower coffee intake had a similar body mass index (BMI). That detail matters clinically. BMI cannot distinguish fat mass from lean mass, or subcutaneous fat from the visceral fat that sits around the abdominal organs and carries the stronger association with cardiometabolic risk. Two people with an identical BMI may therefore have meaningfully different metabolic profiles, and in this cohort coffee intake tracked with that hidden difference rather than with weight itself.

A metabolic marker associated with diabetes risk

Higher coffee consumption was also associated with lower circulating concentrations of branched-chain amino acids in both men and women. When chronically elevated, these biomarkers have previously been associated with insulin resistance and a greater risk of developing type 2 diabetes.

This finding sits alongside the body composition results rather than separately from them, since visceral fat and insulin resistance are themselves closely linked.

Different hormonal patterns in men and women

Some of the clearest differences appeared among men. Greater coffee consumption was associated with a more favourable glucose-insulin profile, higher levels of total and bioavailable testosterone, and greater concentrations of sex hormone-binding globulin (SHBG). However, free testosterone and the free androgen index were modestly lower.

The hormonal associations were less extensive in women. Higher coffee consumption was mainly associated with increased SHBG and lower measures of free androgens.

The common thread across both groups was SHBG, the carrier protein that binds circulating sex hormones and influences how much is biologically available to tissues. Higher SHBG has itself been studied in relation to metabolic health, which makes it a plausible point of connection between the hormonal and cardiometabolic findings.

“Coffee is consumed by millions of people every day, yet we still know surprisingly little about how it relates to our metabolism and hormones. What stood out in our findings was a distinct hormonal signature that didn’t disappear even after we took into account BMI and lifestyle factors, with several of these associations differing between men and women,” says Luca Verroest, lead author of the study and Doctoral Researcher at the University of Oulu.

Why the hormonal findings could matter

The findings raise the possibility that hormonal pathways could help explain some of the previously observed relationship between coffee consumption and metabolic health.

Because the research was observational, however, it cannot establish that drinking coffee directly caused any of the biological differences identified in the study. People who drink more coffee may differ from those who drink less in ways the analysis could not fully capture, and the direction of any relationship cannot be determined from data collected at a single point in time.

For clinicians, the more immediately useful message concerns interpretation rather than advice. Findings of this kind reinforce how much a single anthropometric measure can conceal, and how dietary patterns, body composition, and endocrine markers interact when assessing cardiometabolic risk. Practitioners who want to strengthen that interpretive skill set often look to structured CPD such as the College of Contemporary Health’s Nutrition & Weight Management Essentials short course, which examines how dietary intake relates to body composition and metabolic health in everyday practice.

Finland as a study setting

The setting also makes the research especially relevant. Finland ranks among the world’s highest coffee-consuming countries, with average annual consumption of approximately 11.8 kilograms (26 pounds) per person. A population with high and widely varying intake offers greater statistical range than one in which most people drink little coffee at all.

What happens next

Researchers say the results offer a starting point for studies designed to determine whether coffee itself produces these biological changes and, if so, which compounds may be responsible. Scientists are currently investigating these questions using animal models, with the longer-term aim of moving towards human intervention studies.

Additional research will be necessary before the findings can be used to shape dietary recommendations. For now, the study contributes a mechanistic hypothesis rather than a change in practice.

The study, “Associations of habitual coffee intake with testosterone and cardiometabolic markers: the Northern Finland Birth Cohort 1966 study,” was published in the European Journal of Nutrition.

CCH insight

Body composition, dietary patterns, and metabolic markers rarely tell a complete story in isolation, and BMI alone can mask clinically important differences. The College of Contemporary Health’s Nutrition & Weight Management Essentials short course helps healthcare professionals interpret these measures together and apply nutritional evidence confidently in patient-facing practice.

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Source: University of Oulu, Finland

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Scientists Identify a Possible Biological Link Between Obesity and Alzheimer’s

Key Takeaways: 

• Researchers at Houston Methodist have identified phosphatidylethanolamines (PEs) – a class of fat molecule found in cell membranes – as a possible biological link between obesity and Alzheimer’s disease.
  
• Obesity appears to increase levels of these molecules in body tissue, after which they are packaged into tiny particles that travel to the brain, disrupting communication between brain cells, weakening immune protection and encouraging amyloid proteins to accumulate.
  
• Restoring a healthier balance of PEs reduced disruption in lipid regulation and improved brain function and cognitive performance in models of Alzheimer’s disease, pointing to a possible target for future treatments.
  
  
  

Why researchers are looking beyond the brain

Alzheimer’s disease has long been studied as a condition of the brain itself, defined by the amyloid plaques and tangles found in brain tissue. A growing body of research, however, suggests that the disease may be influenced by biological changes taking place far beyond the skull. Metabolic health – and obesity in particular – is now emerging as a possible contributor to the processes that worsen the disease.

New findings from Houston Methodist add weight to that idea. The study examined how changes in body fat associated with obesity may send damaging signals to the brain, where they appear to interfere with the brain’s immune system and contribute to the biological damage linked to Alzheimer’s disease.

The team behind the study

The research was co-led by Stephen Wong, Ph.D., the John S. Dunn Presidential Distinguished Chair in Biomedical Engineering, and Li Yang, Ph.D., a research associate in the Chao Center for BRAIN at Houston Methodist. The findings were published in the journal Molecular Neurodegeneration.

Fat molecules may connect obesity and Alzheimer’s disease

At the centre of the work is a class of lipid, or fat molecule, called phosphatidylethanolamines, abbreviated to PEs. These molecules are found in cell membranes throughout the body, where they form part of the basic structure of every cell.

According to the study, obesity raises the amount of these molecules in body tissue. The PEs are then loaded into tiny particles that are capable of travelling through the body and reaching the brain – effectively carrying a metabolic signal from fat tissue to the central nervous system.

What happens once these particles reach the brain

Once inside the brain, these particles appear to do three things at once. They can interfere with communication between brain cells, they can weaken immune protection, and they can encourage amyloid proteins to accumulate. Amyloid buildup is one of the major biological features associated with Alzheimer’s disease.

That combination matters, because it suggests obesity is not simply sitting alongside Alzheimer’s risk as a separate problem, but may be actively feeding into the mechanisms that drive the disease.

“Obesity can change how signals travel to the brain,” Wong said. “The good news is that this may be something we can treat. Instead of looking at Alzheimer’s risk tied to obesity as just a metabolic problem, this research suggests we may be able to target the process that connects those changes to the brain.”

Restoring lipid balance improved brain function

The findings also suggest a possible direction for future treatments. When the researchers restored a healthier balance of PEs, they observed less disruption in lipid regulation.

Correcting the imbalance also improved brain function and cognitive performance in models of Alzheimer’s disease. Cognitive performance refers to abilities such as learning, memory, attention and problem solving – the domains most visibly affected as Alzheimer’s progresses.

Taken together, these results suggest that targeting the fat molecules themselves, or the pathway that carries them to the brain, could potentially reduce some of the damage associated with obesity and Alzheimer’s disease.

A growing public health challenge

The stakes are considerable. According to the Centers for Disease Control and Prevention, more than 6.5 million Americans are living with Alzheimer’s disease. That total is expected to rise to nearly 14 million by 2060.

Yang emphasised that a good deal more research will be required before treatments aimed at PEs can be tested as prevention or therapy in people. Even so, the findings introduce a possible strategy for intervening earlier in individuals whose metabolic health may place them at greater risk of Alzheimer’s disease.

What this may mean for practice

For healthcare professionals, work of this kind reinforces a message that has been building across obesity research for some years: excess weight is bound up with a wide range of downstream conditions through complex biological pathways, rather than existing in isolation. Understanding those pathways – and being able to discuss them sensitively with patients – is increasingly part of everyday clinical conversation. CCH’s Obesity Essentials CPD short course is designed with exactly that in mind, introducing the many factors that cause and contribute to obesity alongside the practical skills needed to assess and support people living with overweight and obesity.

It is worth being clear about the limits of the current evidence. The results described here come from laboratory models rather than clinical trials in people, and no PE-targeted treatment is close to being available. What the study offers is a plausible mechanism and a candidate target – both of which are needed before prevention strategies aimed at metabolic risk can be tested properly.

Study collaborators and funding

Other collaborators on the study include Li Yang, Jianting Sheng, Shaohua Qi, Zheng Yin, Michael Chan, Yuliang Cao, Hong Zhao, Zhihao Wan, Bill Chan, Ju Ahn, Xiaohui Yu, Matthew Vasquez and Shan Xu from Houston Methodist; Xianlin Han from the University of Texas, San Antonio; Weiming Xia from Boston University; and Willa Hsueh from Ohio State University.

The study was funded by grants from the Cure Alzheimer’s Fund, the T.T. and W.F. Chao Foundation, and the John S. Dunn Research Foundation.

CCH insight

Research linking obesity to conditions well beyond metabolic health is reshaping how clinicians talk to patients about weight. CCH’s Obesity Essentials online CPD short course gives healthcare professionals the knowledge and confidence to assess and manage overweight and obesity effectively, and to hold those conversations with compassion and clarity. The course takes 8–10 hours, is completed entirely online at your own pace, and carries 10 CPD hours plus a certificate of completion.

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Daily Tomato Intake May Lower Liver Fat in People With MASLD, New Study Suggests

Key Takeaways: 

• In a six-week randomised study of 79 adults with metabolic dysfunction-associated liver disease (MASLD), people who ate 200 grams of raw tomatoes and 50 grams of tomato sauce each day showed a greater reduction in hepatic steatosis than people following a tomato-free control diet.
  
• Liver fat fell in both groups, and researchers found no meaningful differences between the groups in liver stiffness, liver enzymes, lipids or body mass index after the intervention period.
  
• Independent specialists described the findings as exploratory rather than practice-changing, noting the short duration, the narrow participant profile and the absence of improvement in clinically relevant markers.
  
  
  

What the research set out to examine

Metabolic dysfunction-associated liver disease (MASLD) covers a spectrum of liver problems, but its defining feature is hepatic steatosis – the accumulation of fat within the liver. A diagnosis also requires the presence of at least one cardiometabolic risk factor, such as obesity or high blood pressure.

Diet and lifestyle changes are a mainstay of support for people living with MASLD, and researchers are increasingly interested in whether particular foods offer measurable advantages over others. A study published in Nutrients set out to test one such food: the tomato, a staple of the Mediterranean diet.

The research team wanted to establish whether regular tomato consumption would influence liver steatosis in people who already had a MASLD diagnosis.

How the study was designed

The study enrolled 79 adults with MASLD. Researchers applied a number of exclusion criteria, ruling out people who consumed above a set threshold of alcohol and those with a body mass index above 30, the point at which obesity is classified.

Participants were divided into two groups. One group followed a tomato-free control diet. The other consumed 200 grams of raw tomatoes and 50 grams of tomato sauce daily. All tomato products were supplied by the same producer to keep the intervention consistent, and participants were asked to carry on with their usual lifestyle in every other respect.

The intervention ran for six weeks. Across that period, researchers tracked a range of health indicators, including body composition, hepatic steatosis, liver stiffness and cholesterol levels.

What the researchers found

Hepatic steatosis declined in both groups over the six weeks. The decrease was greater, however, among people in the tomato group.

Further analysis showed that hepatic steatosis had been broadly similar between the two groups at baseline, which strengthens the comparison. Other measures told a quieter story. Researchers identified no major changes in liver stiffness, and no significant differences between the groups in lipids, liver enzymes or body mass index at the end of the six-week period.

Summarising the result, the authors suggested that “tomato consumption may reduce hepatic fat accumulation independently of major changes in body weight, total and abdominal adiposity.”

Because liver fat shifted while weight and body composition did not, the study raises a familiar practical question for clinicians: how far can dietary composition alone move metabolic outcomes when overall energy intake stays broadly the same? It is the kind of question CCH explores in its CPD short course Nutrition & Weight Management Essentials, which examines the relationship between modern nutrition and weight, and how evidence-based dietary advice translates into everyday clinical conversations.

Study limitations and continued research

The six-week window is short, so the study cannot speak to whether any benefit persists over the longer term. The research also recruited only adults aged 65 and under, leaving it unclear how the findings might apply to older adults.

Most participants were men, so more balanced recruitment would strengthen future work. The decision to exclude people with a body mass index above 30 also narrows how widely the results can be applied.

Endocrinologist and obesity specialist Randa Abdelmasih MD, DipABOM, from the University of Texas Medical Branch (UTMB), who was not involved in this study, told Medical News Today:

“The study demonstrates a modest reduction in hepatic steatosis over only six weeks in a highly selected population of adults with MASLD and BMI [body mass index] of 30 kg/m² [kilograms per square meter] or more. Most patients we see in clinical practice have obesity (BMI over 30 kg/m²), type 2 diabetes, or more advanced metabolic disease, so the generalizability of these findings is limited.”

Jonathan Jennings, MS, MD, a board-certified internist with Medical Offices of Manhattan, who was likewise not involved in the research, raised a related concern about how participants were selected.

“The inclusion criteria required only one cardiometabolic risk factor, and it could be any risk factor. I am concerned that not all risks are equal, and people with multiple factors are at higher risk than those with a single risk factor,” Jennings said.

“Type 2 diabetes is more likely to lead to MASLD than high blood pressure but the study evaluates them as equal risk factors,” he pointed out.

The researchers themselves note that the reduction in liver fat may have been influenced by other factors, including the effect that taking part in a dietary intervention study can have on participants’ behaviour. The team was also reliant on dietary counselling and on participants’ own reports of how closely they followed the intervention.

Abdelmasih added that because the intervention combined raw tomatoes with tomato sauce, it is “difficult to determine which component or combination was responsible for the observed effect.”

A further gap is that researchers did not measure circulating levels of lycopene and carotenoids, the compounds most often proposed as the mechanism behind any effect tomatoes might have on liver health.

Limited clinical application at this stage

The authors describe their study as exploratory, intended primarily to inform future research. They call for confirmation through larger and longer studies, and encourage readers to treat the findings as hypothesis-generating rather than conclusive.

The clinical value is also uncertain because so much else stayed the same. As Abdelmasih put it:

“The study showed improvement in liver fat but no significant improvements in liver stiffness, fibrosis scores, liver enzymes, insulin resistance, inflammatory markers, lipid profile, or body composition. Therefore, while the imaging findings are interesting, we cannot conclude that tomato consumption meaningfully alters disease progression or improves clinically relevant outcomes.”

What this means for people living with MASLD

Within its limits, the study does point to a possible benefit of tomato consumption for people with MASLD, and to a low-cost dietary strategy that may help with fat accumulation in the liver.

Tomatoes may carry other advantages too, with existing research pointing towards cardiovascular benefits and potential anti-cancer properties.

Even so, the sensible route is for people to work with their doctor and wider healthcare team on a dietary plan that addresses their overall health, rather than concentrating on any single food.

Jennings underlined that point, and flagged two practical cautions:

“The study’s conclusions are hopeful but careful discussion with a healthcare provider is still needed before engaging in any radical dietary adjustments. Tomatoes and tomato-based products may be problematic for individuals with gastroesophageal reflux disease (GERD). Many tomato-based foods are also calorically dense and may worsen insulin resistance in certain individuals.”

The broader treatment context matters as well. According to Abdelmasih: “Dietary interventions should be viewed within the broader context of treating the underlying metabolic disease. For patients with obesity, sustained weight loss of approximately 10% or more remains the intervention with the strongest evidence for improving steatohepatitis and fibrosis.”

“While tomatoes can certainly be part of a healthy Mediterranean diet, they should not distract from therapies that have demonstrated meaningful improvements in liver and cardiometabolic outcomes,” she concluded.

CCH insight

Conversations about diet sit at the centre of metabolic and liver care, and single-food headlines can make those conversations harder rather than easier. CCH’s CPD short course Nutrition & Weight Management Essentials gives healthcare professionals a grounding in the fundamentals of nutrition, the factors driving weight gain, and what effective weight management looks like in practice – so you can place findings like these in proportion for the people you support.

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Expert commentary in this article was provided to Medical News Today. Read the original report here.

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Abdominal Obesity and Vitamin D Deficiency Together More Than Double the Risk of Death After 50

Key Takeaways:

• In people aged 50 and over, having both abdominal obesity and vitamin D deficiency was linked to a 123% higher risk of death.
• Alone, abdominal obesity raised that risk by 47% and vitamin D deficiency by up to 91% – together, the two amplify one another.
• Abdominal fat sequesters circulating vitamin D, and the resulting deficiency worsens the chronic inflammation driven by excess fat.
  
  
  

A six-year study of ageing in England

New research has put a figure on something clinicians have long suspected: that two common and often overlooked problems in later life are considerably more dangerous when they occur together than either is alone.

The study, in the journal Diabetes, Obesity and Metabolism, followed 5,520 people aged 50 and older over a six-year period. It found that people with both abdominal obesity and vitamin D deficiency had a 123% higher risk of death than people without these conditions.

The work was coordinated by Tiago Silva Alexandre, a professor in the Department of Gerontology at the Federal University of São Carlos (UFSCar) in Brazil, and carried out in collaboration with University College London (UCL) in the United Kingdom. Participants were drawn from the English Longitudinal Study of Ageing (ELSA), one of the world’s largest studies on ageing.

The central message is not that either condition is newly dangerous, but that their combination multiplies risk.

“Abdominal obesity is a well-known risk factor because it’s associated with inflammation and metabolic problems. Vitamin D, on the other hand, is a hormone that acts on various organs, and its deficiency impairs several bodily functions. When these two conditions occur together, one amplifies the effects of the other, further increasing the risk of death,” explains Alexandre. “For that reason, monitoring vitamin D levels and treating excess abdominal fat are essential measures to prevent premature death, especially after age 50,” he adds.

How the two conditions were defined

The researchers used established thresholds for both measures, which makes the findings straightforward to translate into everyday practice.

Vitamin D deficiency was defined as a level below 30 nmol/L. Abdominal obesity was defined by waist circumference – greater than 102 centimetres (40 inches) for men and greater than 88 centimetres (35 inches) for women.

Both are measures that can be captured in a routine consultation, one through a standard blood test and the other with a tape measure, without recourse to specialist equipment or imaging.

Each condition carries risk on its own

When the two conditions were examined separately, the data produced a result that may surprise some practitioners: vitamin D deficiency alone posed a greater risk than abdominal obesity alone.

Abdominal obesity on its own was associated with a 47% increase in the risk of death. Vitamin D deficiency on its own raised that risk by up to 91%. When both were present, the risk of death more than doubled.

That pattern is what makes the combination clinically significant. The elevated risk seen in people with both conditions is greater than would be expected from simply adding the two individual risks together, which points towards a biological interaction rather than two independent problems sitting side by side in the same person.

Why the two conditions amplify one another

According to Alexandre, abdominal obesity and vitamin D deficiency feed into each other, creating what he describes as a vicious cycle.

The first mechanism is storage. Abdominal fat “sequesters” circulating vitamin D and holds it within adipocytes, or fat cells, preventing the vitamin from reaching the bloodstream in useful quantities.

“This means that although the body may have the vitamin stored in fat, it isn’t freely available in the blood to perform vital functions in other organs and systems,” he says.

In other words, a blood test may show deficiency even where the body’s total stores are not depleted, because the vitamin is effectively locked away where it cannot be used.

The second mechanism concerns metabolism. People with obesity have lower expression of the enzymes needed to metabolise vitamin D, which further reduces the amount available to the body.

The consequences then loop back on themselves. “Abdominal obesity reduces circulating vitamin D, and that deficiency impairs the immune system, exacerbating the chronic inflammation caused by excess fat and drastically increasing the risk of mortality,” Alexandre explains to Agência FAPESP.

Ageing, inflammation and a loss of regulation

The picture is complicated further by the biology of ageing itself. Later life is naturally marked by a process known as inflammaging – a state of low-grade chronic inflammation that develops with age.

Vitamin D ordinarily acts as a brake on that process. Where levels fall and abdominal fat is present, that brake is weakened at precisely the point where it is most needed.

“Under normal conditions, vitamin D acts as a regulator of the immune system, preventing inflammation from getting out of control. When vitamin D levels are low and there’s excess abdominal fat, an unfavorable systemic environment develops that accelerates cardiovascular and metabolic diseases, as well as muscle loss,” he stresses.

Part of a wider cascade

This study is the most recent in a series by the same group investigating the role of vitamin D in ageing, and its findings sit alongside earlier work linking deficiency to functional decline.

“In previous studies, we identified a cascade effect. Vitamin D deficiency leads to a loss of strength, which results in reduced walking speed, causing a loss of independence and greater dependence in daily activities,” Alexandre explains.

A further study by the group found that vitamin D deficiency increases the risk of cognitive decline.

Taken together, these strands describe a hormone with a reach that extends well beyond bone health.

“Vitamin D is a hormone with various functions. It plays a role in regulating blood pressure, heart rate, the central nervous system, the immune system and the endocrine system. Therefore, when its levels are low, several essential bodily functions are compromised,” he says.

What this means for practice

For healthcare professionals working with people over 50, the practical implication is a case for looking at these two markers together rather than in isolation. A raised waist circumference and a low vitamin D level each warrant attention on their own terms, but the study suggests that the presence of one should prompt closer interest in the other.

It also reinforces the value of waist circumference as an assessment measure in its own right, given that it is central adiposity – rather than body weight alone – that drives the inflammatory and metabolic processes described here.

Building that broader assessment skill set, and the confidence to act on it as part of whole-person care, is the focus of professional training such as the College of Contemporary Health’s Obesity Essentials, a CPD-accredited online short course covering the assessment and management of overweight and obesity.

As Alexandre puts it, monitoring vitamin D levels and treating excess abdominal fat are essential measures to prevent premature death after the age of 50 – two simple assessments that, on this evidence, carry considerable weight together.

CCH insight

This is an interesting study. At CCH we have held a longstanding interest in the wide- ranging functions of vitamin D, especially its role in immune function. These results suggest that vitamin D status should be checked routinely in patients with abdominal obesity, and any deficiency should be treated immediately. This would be a simple and inexpensive protocol and could significantly reduce premature death in this group.

Findings like these are a reminder that excess abdominal fat rarely acts alone – its metabolic and inflammatory effects reach into hormone regulation, immune function and, ultimately, life expectancy. CCH’s Obesity Essentials CPD short course (10 CPD hours, fully online, CPD-accredited) helps healthcare professionals assess and manage patients living with overweight and obesity using a rounded, evidence-based approach that looks beyond a single number on the scale to the wider systemic picture.

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One Avocado a Day May Lower a Hidden Heart Disease Risk in Adults Living With Obesity

Key Takeaways:

• Adults living with obesity who ate one avocado a day for six months showed a fall of 49 nanomoles per litre in LDL particle concentration – equivalent to roughly a 4% reduction in heart disease risk.
  
• LDL particle number is a risk factor distinct from LDL cholesterol itself, and it tends to be higher in people with abdominal obesity, meaning two people with identical cholesterol readings can carry very different levels of risk.
  
• The benefit appeared consistently across sex, race, ethnicity, age and body mass index, suggesting that a single, sustainable dietary addition can shift a meaningful cardiometabolic marker without any wider change to diet or activity.
  
  
  

A single dietary change, made in the real world

Adding one avocado to the daily diet may reduce heart disease risk in adults living with obesity, according to research led by the Penn State Department of Nutritional Sciences and published in the Journal of Clinical Lipidology.

The team found that regular avocado consumption was associated with a lower concentration of low-density lipoprotein (LDL) particles – the protein particles that transport cholesterol around the body – in the blood. That reduction corresponded to an approximate 4% decrease in heart disease risk.

What distinguishes the finding is its modesty. Rather than testing a wholesale dietary overhaul, the researchers examined what happens when people make one addition and otherwise carry on as normal.

“If people want to improve the quality of their diet, making one small change might be a more feasible strategy than attempting to change their entire diet,” said Janhavi Damani, postdoctoral scholar at Penn State and first author of the study. “For people with obesity, including avocados in their daily diet might be a good starting place.”

Why particle number matters, not just cholesterol

LDL particles represent a risk factor for heart disease that is separate from LDL cholesterol – the so-called “bad cholesterol” that is itself a significant contributor to risk. The risk posed by LDL particles is typically higher in people with abdominal obesity, the researchers noted.

The distinction rests on a point of basic physiology that standard lipid panels do not capture. LDL cholesterol cannot travel through the body unaided; it must be carried by a protein particle. When a greater number of protein particles are involved in transporting the same quantity of cholesterol, heart disease risk rises – even though the measured cholesterol figure is unchanged.

Damani illustrated the point directly.

“Imagine two people with the same high levels of LDL cholesterol,” Damani said. “Person A carries their cholesterol in fewer, larger LDL particles, and Person B carries their cholesterol in more, smaller LDL particles. Person B’s heart disease risk would be higher because their overall particle count is higher even though a test of their LDL cholesterol would look identical.”

How smaller particles do more damage

Those smaller particles penetrate artery walls more easily and contribute to the accumulation known as plaque, Damani explained.

Plaque raises heart disease risk through two mechanisms working together. It narrows the space available for blood to pass through a vessel, and it reduces the vessel’s flexibility. The consequence becomes clearest under load: when a person’s heart is working hardest – through exertion, heat, stress or any other cause – their blood pressure rises more sharply than it otherwise would, because the vessel can no longer expand to accommodate the increased demand. That failure to compensate can be enough to trigger a cardiac event such as a heart attack.

This mechanistic detail matters clinically, because it explains why particle count can carry prognostic weight even when a patient’s cholesterol result looks reassuring. Practitioners working in weight management and cardiometabolic care increasingly need to interpret markers of this kind alongside anthropometric measures, and this is territory that CCH’s CPD short course provision in obesity care covers in some depth.

Inside the Habitual Diet and Avocado Trial

For this analysis, the researchers drew on data originally collected from 786 participants in the Habitual Diet and Avocado Trial, a six-month study of adults aged 25 years and older.

Eligibility was defined by waist circumference. Men qualified if their waist circumference exceeded 102 centimetres (40 inches); women qualified if theirs exceeded 89 centimetres (35 inches).

Participants were divided into two groups. Half were instructed to maintain their usual diet and activity levels. The other half were provided with one avocado to consume each day and were also instructed to maintain their usual diet and activity levels. No other dietary guidance or restriction was applied.

The original Habitual Diet and Avocado Trial had already established that adding avocado to the diets of people living with obesity did not alter weight or waist circumference, but could reduce levels of LDL cholesterol.

What the blood samples showed

In the current study, the researchers compared blood samples collected at the start and at the end of the six-month period.

Across the study, LDL particle levels in the avocado-per-day group fell by 49 nanomoles per litre. That change corresponded to an approximate 4% reduction in heart disease risk, according to the researchers.

The team was careful to set this figure in proportion.

“Four percent is a modest reduction compared with the 14% to 29% lower heart disease risk associated with improving the overall diet,” Damani said. “However, it is a step in the right direction.”

A consistent effect across the study population

One of the more notable findings concerned who benefited. Regardless of participants’ sex, race, ethnicity, age or body mass index, they were equally likely to experience improvements in LDL particle levels.

The researchers took this to indicate that anyone living with obesity could benefit from avocado consumption. They added a clear caveat, however: people should speak to a registered dietitian nutritionist or their physician for personalised, expert guidance on improving their diets.

From controlled conditions to unpredictable lives

The study’s most significant contribution may lie less in the size of the effect than in the setting in which it was demonstrated.

“Penn State researchers demonstrated several years ago that avocado consumption could reduce LDL cholesterol and levels of LDL particles,” said Kristina Petersen, associate professor of nutritional sciences and senior author of this study. “But in that study, the researchers controlled participants’ entire diets throughout the experiment. This study demonstrated benefits in the real world, where people’s diets are much less predictable. In the course of people’s normal lives, avocado consumption still contributes to a healthier diet.”

That shift – from a tightly controlled feeding study to free-living participants managing their own meals – is what makes the result relevant to everyday practice. A 4% reduction achieved under laboratory conditions tells clinicians relatively little about what patients will actually sustain. A comparable reduction achieved by people eating as they normally do, with one addition, is a different kind of evidence.

What this means for practice

For healthcare professionals supporting people living with obesity, the findings reinforce a familiar principle with fresh quantitative backing: incremental, achievable changes can move clinically meaningful markers. They also underline the value of looking beyond standard lipid measurements when assessing cardiovascular risk in patients with abdominal obesity, where LDL particle number may reveal risk that a conventional cholesterol result conceals.

None of this positions a single food as a substitute for comprehensive care. The researchers’ own framing is deliberately measured – a step in the right direction, not a solution. But in a field where adherence often determines outcomes more than the theoretical strength of an intervention, feasibility is itself a clinical variable worth taking seriously.

CCH insight

It is always re-assuring to hear about studies which show clear benefits of foods we associate with good health, so this is great news for people who eat avocados regularly and a nice reminder for others to maybe eat them more often. However, high cholesterol and other risk factors for cardiometabolic diseases are most common in populations of high deprivation, who are unable to buy avocados regularly due partly to access but mainly due to cost.

This study’s practical value lies in feasibility – one addition, sustained over six months, moving a real marker of cardiovascular risk. Translating that kind of evidence into advice patients will actually follow is the core skill of nutritional care in obesity management. CCH’s Nutrition & Weight Management Essentials (6 hours, fully online, CPD-accredited) gives healthcare professionals a solid grounding in fundamental nutrition concepts, the factors driving weight gain, and evidence-based approaches to both weight loss and long-term maintenance, with real-life case studies throughout.

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Belly Weight Predicts Heart Health Better Than BMI, Study Indicates

Key Takeaways: 

• Fat stored around the waist is a stronger predictor of heart disease than body mass index alone.
  
• People with preclinical obesity face a raised cardiovascular risk despite appearing healthy.
  
• Researchers estimate early intervention could prevent 45% of new cardiovascular disease cases.
  
  
  

Why waist size matters more than the scales

People living with overweight or obesity can carry a higher risk of heart disease even when they appear to be perfectly healthy, according to new research presented at the International Congress on Obesity in Mexico City (15–17 July). Combining waist-based measurements with body mass index (BMI) to detect this hidden risk and act early could, over the years ahead, prevent hundreds of thousands of people from dying from heart attacks, strokes and other cardiac problems, researchers from the University of Glasgow, Glasgow, UK, said.

“We know that excess weight, particularly around the waist, increases the risk of heart disease,” said lead researcher Estefania Fuentes Avalos. “In 2021, an estimated 1.9 million cardiovascular disease deaths – almost one in 10 heart-related deaths worldwide – were attributed to high body mass index.

“The link between central, or abdominal, obesity and heart disease is especially strong because fat stored around the waist, known as visceral fat, is metabolically active and releases inflammatory substances into the bloodstream. Over time, this chronic inflammatory state can damage blood vessels and accelerate the buildup of arterial plaque, significantly increasing the risk of heart attacks.”

The limits of BMI

BMI, a measure of weight compared with height, is routinely used to assess a person’s weight status, defining whether they have a normal weight, overweight or obesity. However, it does not take into account where fat is stored in the body.

To address this and other shortcomings of BMI, The Lancet Diabetes & Endocrinology Commission recently proposed a different way of assessing obesity status. The Lancet Commission framework uses BMI together with central adiposity markers – waist measurements – to determine whether a person has excess body fat. People with excess body fat are then categorised as having either preclinical obesity or clinical obesity, depending on whether they also have long-term obesity-related conditions such as high blood pressure, joint pain and sleep apnoea.

The new study set out to establish whether this method is better at identifying people at high risk of cardiovascular disease than BMI alone.

“Detecting cardiovascular risk at an early stage is essential, particularly at the preclinical stage of obesity, as it provides a window of opportunity to implement timely, targeted interventions before obesity-related complications such as high blood pressure arise,” Fuentes Avalos said.

“This underpins our focus on risk stratification in this group, with the aim of detecting high-risk individuals who may otherwise be overlooked.”

What the study looked at

Fuentes Avalos examined data on 382,769 adults of white ethnicity in the UK Biobank study (age range 40–69 years, average age 56 years, 53% women).

Under The Lancet Commission framework, 285,190 (74%) of the participants had excess body fat, based on BMI and central adiposity markers. Within this group, 102,237 (26.7%) were classified as having preclinical obesity – excess body fat without long-term obesity-related conditions – and 182,953 (47.8%) as having clinical obesity, meaning excess body fat alongside long-term obesity-related conditions. The remainder had neither excess body fat nor long-term obesity-related conditions; they were classified as not having obesity and served as the reference group.

None of the participants had cardiovascular disease at the start of the study. Hospital and death records provided information about diagnoses of, and deaths from, heart attacks, strokes and other forms of cardiovascular disease over the following 12 years. During this time, there were 41,742 new cases of, and 8,832 deaths from, cardiovascular disease. Studies of this scale underline how much practical assessment skill clinicians need when supporting patients with excess weight – a competency CCH’s Obesity Essentials short course is designed to build.

Clinical obesity carried the sharpest risk

Analysis of the data showed that people with clinical obesity were far more likely to develop, or die from, cardiovascular disease than those without obesity.

Women with clinical obesity developed cardiovascular disease at a rate 2.5-fold higher than women without obesity, and died from it at an almost threefold (2.8-fold) higher rate. Men with clinical obesity developed cardiovascular disease at an almost twofold higher rate (1.9-fold) and had a 2.6-fold higher rate of cardiovascular death than men without obesity.

The hidden risk in preclinical obesity

People with preclinical obesity were also at greater risk, despite having no obesity-related conditions and appearing to be in good health.

Women with preclinical obesity developed cardiovascular disease at a 38% higher rate and died from it at a 46% higher rate than women without obesity. For men, preclinical obesity was associated with an 18% higher rate of developing cardiovascular disease and a 52% higher rate of cardiovascular death.

All of the results were adjusted for socioeconomic status and lifestyle factors, including smoking and alcohol consumption.

More waist markers, more risk

Further analysis showed that the more high-risk central adiposity markers a person had, the more likely they were to develop heart disease. For example, a woman with one high-risk marker – waist circumference, waist-to-hip ratio or waist-to-height ratio – was 17% more likely to develop cardiovascular disease than a woman with no high-risk waist measurements. Having all three high-risk measurements increased the risk by 64%. The study also found that waist measurements were more accurate at predicting cardiovascular disease than BMI.

A window of opportunity

The researchers concluded that people with preclinical obesity are at higher risk of developing, and dying from, cardiovascular disease despite appearing to be healthy.

“Preclinical obesity is a critical window of opportunity to improve heart health. Routinely measuring waist circumference, waist-to-hip ratio and waist-to-height ratio along with BMI would identify high-risk individuals who might be overlooked by assessing BMI alone,” Fuentes Avalos said.

“They could then be offered intensive diet and exercise programs to improve their cardiac and overall health.

“We have calculated that early intervention could prevent 45% of new cases of cardiovascular disease and 41% of cardiovascular disease deaths in similar populations.

“Given that cardiovascular disease remains a leading cause of ill health and death globally, routinely taking waist measurements along with BMI could prevent hundreds of thousands of deaths over a decade alone.”

CCH insight

This is very important work on two levels. Firstly, it not only re-enforces the importance of waist circumference measures as superior indicators of disease risk compared to the traditional BMI measure, but also suggests that calculating three waist circumference markers gives a more accurate indication of CV risk than just one. And secondly, it feeds into the current debate around the terms ‘clinical’ and ‘pre-clinical’ obesity coined by The Lancet Diabetes & Endocrinology Commission. The results indicate that, while people with clinical obesity have a far higher risk of cardiovascular disease or death, those with pre-clinical obesity are still at risk and still therefore warrant intervention. Depending on your perspective, you could argue this supports the Commission’s findings or contradicts them!

Findings like these are only useful in practice if clinicians feel confident assessing excess weight and having sensitive, evidence-based conversations with patients about it. CCH’s Obesity Essentials – an online CPD short course offering 10 CPD hours – equips healthcare professionals with the practical skills to assess and manage patients living with overweight and obesity, from measurement through to compassionate communication.

Explore Obesity Essentials and strengthen your day-to-day weight-management practice.

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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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