
Novo Nordisk Launches Late-Stage Trial to Find the Lowest Effective Dose of Oral Wegovy
Key Takeaways:
- Novo Nordisk has begun OASIS-5, a 60-week late-stage trial testing lower maintenance doses of the oral Wegovy pill.
- The trial will enrol 450 adults with a BMI of 30 or above, or 27 with a weight-related health condition.
- Interest in lower dosing reflects real-world practice, where cost and side effects already drive some people to take reduced doses.
A trial built around dose flexibility
Danish drugmaker Novo Nordisk has started testing smaller doses of its Wegovy pill in a new late-stage study designed to identify the lowest dose that still supports weight loss, according to a listing on a US clinical trials database.
The study, known as OASIS-5, began on 12 August and is scheduled to run until 2028. It will examine lower strengths of the daily maintenance dose – the dose used to sustain weight loss once it has been achieved, rather than the escalating doses used at the start of treatment. At present, the approved long-term dose of the Wegovy pill is 25 milligrams.
“Having a broader range of maintenance doses could provide greater flexibility in treatment and optimising the patient experience,” Novo said in an emailed statement to Reuters.
Novo has not specified which new dose strengths are being tested. The Wegovy pill is also approved in doses of 1.5 mg, 4 mg and 9 mg.
What OASIS-5 will measure
The 60-week trial will recruit 450 adult participants who have previously struggled to lose weight, with a Body Mass Index of 30 or above, or 27 in combination with a weight-related health issue.
The primary objective is to establish whether lower doses of oral semaglutide – the active ingredient in Wegovy – produce greater weight loss than placebo over the 60-week period. Secondary objectives include changes in waist circumference, other health benefits and the side effect profile at these reduced strengths.
The study will exclude people living with diabetes, those who have experienced recent major weight changes, and anyone currently being treated with GLP-1 medications.
Seeking health benefits beyond weight loss
The trial arrives against a backdrop of dosing behaviour that is already happening outside clinical protocols. Some people taking GLP-1 medicines, including Wegovy and Lilly’s Zepbound injections, are microdosing or otherwise taking lower-than-approved doses. The practice has become popular largely because of the high cost of the medicines and the side effects associated with them.
“People are using low dosages of these products… they just decide on their own,” Novo CEO Mike Doustdar told Reuters in an interview last week, noting that patients often seek health benefits beyond weight loss.
That observation points to a broader question facing prescribers: what people hope to gain from GLP-1 therapy is not always confined to the number on the scales. Understanding the pharmacology behind dose escalation and maintenance, and being able to discuss the trade-offs between efficacy, tolerability and cost, is increasingly central to safe prescribing. It is a theme covered directly in the College of Contemporary Health’s CPD short course GLP-1RAs in Practice: Prescribing, which examines dose titration, monitoring and shared decision-making in day-to-day clinical settings.
Competitive pressure in a growing market
Novo is under pressure after losing ground to US rival Eli Lilly in an obesity drug market projected to exceed $100 billion by 2030. Investors are watching the Wegovy pill closely; it generated second-quarter sales of 3.22 billion Danish kroner ($499.89 million).
Doustdar expects market segmentation to prevent a winner-take-all contest with Lilly – a view consistent with a future in which different doses, formulations and treatment goals serve different groups of people rather than a single product dominating.
Lilly did not immediately respond to a Reuters request for comment on whether it plans to test smaller doses of its oral drug Foundayo, which has lowest approved doses of 0.8 mg and 2.5 mg.
What this could mean for practice
If OASIS-5 demonstrates that lower maintenance doses deliver meaningful weight loss, it would give clinicians a wider set of options for people who cannot tolerate higher strengths, who are managing the cost of long-term therapy, or who have reached a weight they wish to maintain rather than continue reducing. It would also bring an existing real-world practice within the evidence base, replacing self-directed dose reduction with an approved, monitored alternative.
Results are not expected until 2028, so any change to prescribing practice remains some way off. In the meantime, conversations about dosing, expectations and adherence will continue to sit with the healthcare professionals supporting people through treatment.
CCH insight
Dose selection, titration and tolerability are among the most common practical challenges in GLP-1 prescribing. The College of Contemporary Health’s CPD short course GLP-1RAs in Practice: Prescribing covers dose escalation and maintenance, managing side effects, patient selection and monitoring – equipping healthcare professionals to make confident, evidence-based decisions as the treatment landscape evolves.
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Source: Reuters
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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.
Explore Nutrition & Weight Management Essentials →
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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Weight Bias at Work: What New GLP-1 Research Reveals About Women’s Employment Prospects
Key Takeaways:
- Women who were unemployed when they started GLP-1 medications saw their employment rate rise by nearly 27 percentage points over 18 months, according to a 2026 NBER working paper.
- The gains appeared only among women entering the workforce – those already employed saw no rise in pay or promotion, pointing to perception rather than capability.
- The findings echo long-standing evidence on the financial cost of weight bias, from documented pay gaps to hiring professionals’ judgements based on photographs alone.
A new way to measure an old problem
For years, economists have documented what they call the “obesity penalty” – the social and financial disadvantages people can face because of their weight. It has been a difficult phenomenon to measure cleanly, because the factors that shape someone’s body weight also tend to shape their income, health and opportunities.
The rapid uptake of GLP-1 medications has given researchers something closer to a natural experiment. When large numbers of people begin treatment within a short window, and others who want the same treatment have not yet been able to start, it becomes possible to compare two otherwise similar groups and observe what changes.
That is the approach taken in a 2026 working paper published by the National Bureau of Economic Research, in which Harvard economist Rebecca Diamond examined what happened to women’s employment after they began taking GLP-1 medications.
What the researchers did
Diamond looked at survey data from around 15,000 people. She compared women who had started taking GLP-1 medications with similar women who wanted to take them but had not yet started. The two groups were matched on factors including income, race, body mass index and overall health, so that the comparison was not simply between people in very different circumstances to begin with.
The design matters. Because the comparison group consisted of women who also wanted the medications, the study is less vulnerable to the criticism that people who seek treatment are systematically different in motivation from those who do not.
The result that stands out
Among women who were unemployed at the point they began treatment, the employment rate rose by nearly 27 percentage points over the following 18 months, compared with the matched group who had not yet started.
To put that figure in context, it is a larger gap than the difference in employment between American women with a high school diploma and those holding a university degree. In other words, an 18-month change in body weight was associated with a bigger shift in employment than several years of formal education.
The research does not suggest that losing weight made these women more intelligent, more capable or better qualified for work. Nothing about their skills, experience or credentials changed. What the study raises is a different and more uncomfortable question: whether a change in appearance alters how women are perceived by employers.
Changes beyond the workplace
The effects were not confined to employment. The study also found that single women taking GLP-1 medications were nearly 29 percentage points more likely to get married or move in with a partner than similar women who had not started treatment.
Taken together, the employment and partnership findings describe something broader than a labour market effect. They describe a shift in social response.
The financial cost of weight bias
GLP-1 medications have moved quickly into the mainstream. In 2026, 11% of US adults said they were currently taking one to lose weight, up from just 3% in 2024, according to Gallup.
But the question of how weight shapes women’s working lives long predates the current wave of prescribing. Research was already pointing in this direction well before GLP-1 medications entered the cultural conversation.
What hiring professionals saw
A report from Fairygodboss, an employer review site for women, offered a particularly troubling look at how appearance can shape hiring decisions. In one study, hiring professionals were shown images of women with different body types and asked to evaluate them.
The woman pictured at the highest body weight was judged far more harshly than the others. Twenty percent of respondents described her as “lazy”, a label applied less frequently to every other woman pictured. Just 18% said she appeared to have leadership potential, while 21% described her as “unprofessional”.
These are judgements made on the basis of a photograph alone, with no information about experience, qualifications or performance.
Earnings gaps documented long before GLP-1 medications arrived
The pay data tells a similar story. In 2011, the Federal Reserve Bank of St Louis cited research finding that white women living with overweight earned about 4.5% less than white women whose BMI fell within what researchers classified as the normal range. White women living with obesity earned nearly 12% less.
Two caveats are important here. Those figures were specific to white women and do not apply to everyone. They also say nothing about anyone’s value, ability or contribution. What they suggest is that weight-related bias was already showing up in some women’s pay long before GLP-1 medications became widely available.
When appearance pays
The argument that appearance carries an economic premium is not new, and it is sometimes made bluntly. Codie Sanchez, CEO and founder of Contrarian Thinking, has said that women who wear makeup to work earn about 30% more on average than women who do not.
“Pretty privilege is very real,” she said on an episode of The Burnouts Podcast. “And you can either say ‘That’s not fair, so I’m not doing it.’ or you can win.”
Sanchez acknowledged that the advantage is unfair, but argued that women should use it rather than ignore it. “If it’s going to make me more money to paint my face, clown me up,” she said.
Diamond’s findings suggest weight bias may operate along similar lines. The women who benefited most were those seeking to enter the workforce, where first impressions carry disproportionate weight and where an employer’s judgement is formed quickly and on limited information. For women already in a job, whose managers had direct evidence of their performance, the effect disappeared.
Why this matters in clinical practice
For healthcare professionals, findings like these complicate the consultation room. People starting GLP-1 medications may be motivated by clinical goals, social goals, economic goals, or some mixture of all three, and those motivations shape expectations, adherence and how someone responds if treatment is paused or stopped.
Understanding the pharmacology well enough to have that conversation credibly is increasingly part of everyday practice rather than a specialist concern. Building that grounding is the focus of professional training such as the College of Contemporary Health’s GLP-1RAs in Focus – Why Drugs Like Ozempic Work, a CPD-accredited online short course covering GLP-1 physiology and pharmacology for prescribers and non-prescribers alike.
An uncomfortable conclusion
Losing weight does not make a person more intelligent, more capable, harder working or better qualified for a job. But it may change how other people perceive them.
That is precisely what makes Diamond’s findings difficult to sit with. If some women gain access to more opportunities after losing weight while their underlying abilities remain exactly the same, then the economic benefit is not really a benefit at all. It is a measure of how heavily appearance still shapes the way women are perceived and treated – and of how much value has been withheld from them beforehand.
The medication changed the response. It did not change the woman.
CCH insight
Findings like these are a reminder that GLP-1 medications carry social and economic weight as well as clinical effect – and that patients arrive at the consultation with motivations shaped by far more than a treatment target. CCH’s GLP-1RAs in Focus – Why Drugs Like Ozempic Work CPD short course (2 CPD hours, fully online, CPD-accredited) builds the foundation in GLP-1 physiology and pharmacology that healthcare professionals need to explain the science clearly, set realistic expectations and contribute confidently to treatment discussions, whether or not they prescribe.
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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.
Explore Nutrition & Weight Management Essentials →
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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Sensing, Liking and Wanting: Why Food Feels Different on GLP-1RAs
Key Takeaways:
- A Frontiers in Nutrition review finds that altered eating experience on GLP-1 receptor agonists (GLP-1RAs) reflects changes in food reward rather than impaired taste function.
- The authors separate three processes: sensing food, liking it, and wanting it.
- The evidence is heterogeneous and largely observational, so the framework is a conceptual model, not proof of causality.
Why reports of “taste changes” may not be about taste at all
Some people taking GLP-1RAs report that their favourite foods become less enjoyable or tempting, without this necessarily reflecting impaired basic taste function. That distinction sits at the centre of a recent review published in the journal Frontiers in Nutrition, in which the authors conducted a structured narrative review of current evidence on how glucagon-like peptide-1 receptor agonists influence sensory perception, food enjoyment and food motivation, using a sensory-liking-wanting framework.
Obesity is a chronic, progressive metabolic disease with growing global prevalence, which increases the demand for effective long-term treatment options. GLP-1RAs are widely used in obesity treatment because they enhance satiety, delay gastric emptying, reduce energy intake and support meaningful weight loss. Alongside those effects, some people also report that food tastes different, feels less enjoyable, or no longer seems tempting. These experiences are often described as “taste changes”, but the review argues that they may reflect several biological processes rather than a single taste disorder. Further research is needed to understand these mechanisms and to improve nutritional care during treatment.
Looking beyond appetite suppression
GLP-1RAs have changed the way obesity is managed by reducing energy intake and supporting meaningful weight loss. Growing clinical experience, however, shows that their effects extend beyond a simple reduction in hunger.
Some people describe food tasting different, reduced pleasure in eating, or lower cravings for high-calorie foods. The review suggests that these experiences should not be treated as simple taste disturbances, but as a combination of three components related to eating behaviour: sensory perception, liking and wanting.
The three components of eating behaviour
Eating begins with sensory perception, which includes detecting taste, smell and food texture. This stage determines how food is initially recognised.
The second component is liking, defined as the subjective pleasure or hedonic value associated with eating. It is influenced by flavour, prior experience, context, cognitive factors and physiological state.
The third component, wanting, describes the motivation or craving to seek out and consume food. Separating these components helps explain why reports of “taste changes” may in fact reflect different biological processes.
How GLP-1RAs may influence food reward and the eating experience
The review sets out how GLP-1RAs may influence eating behaviour through interconnected biological pathways rather than by directly changing taste. Preclinical studies indicate that endogenous glucagon-like peptide-1 (GLP-1) is produced by some mammalian taste bud cells and may modulate taste signalling. Those findings do not establish that GLP-1RA treatment directly alters taste in humans, and the limited human studies available have produced inconsistent results.
Taste signals are integrated in the nucleus of the solitary tract (NTS) before reaching brain regions involved in appetite and reward. Human studies have associated GLP-1RA treatment with reduced craving and weaker neural responses to calorie-dense food cues in some participants. Those findings are more consistent with altered food valuation and motivation than with impaired basic taste.
Gastrointestinal effects, including nausea and early satiety, may also reduce the pleasure of eating, which makes it difficult to distinguish altered food reward from genuine changes in taste perception.
What the clinical evidence does and does not show
Randomised controlled trials usually focus on body weight and metabolic outcomes. Eating-related experiences are rarely included as prespecified measures and are more often captured sporadically as adverse events.
Patient-reported outcome questionnaires may provide a more sensitive window into changes in food enjoyment and preference, but assessment methods vary considerably between studies. Real-world evidence presents additional challenges, as reports of “taste alterations” may encompass several distinct sensations, including olfactory changes, dry mouth, gastrointestinal discomfort and other symptoms that are difficult to distinguish clinically.
Spontaneous reporting databases can identify safety signals but cannot establish incidence or risk. Cohort studies, by contrast, provide better-defined populations and follow-up, yet remain vulnerable to subjective reporting and confounding.
Because this was a narrative review rather than a systematic review or meta-analysis, the authors did not conduct a formal risk-of-bias assessment.
A framework for understanding what people report
According to the review, alterations in the eating experience during GLP-1RA treatment should not be regarded solely as a biological phenomenon, but understood as the interaction between different processes.
Peripheral taste pathways, brainstem integration, central reward networks, interoceptive state and learned behaviour may all contribute. Their relative importance may differ between individuals and across treatment stages. A person’s report of a “taste change” may therefore not correspond to a clinically defined gustatory disorder.
The authors also note that alternative explanations should be considered when interpreting eating-related changes, including nausea, delayed gastric emptying, altered satiety, behavioural adaptation and medication adherence.
The framework additionally accommodates limited treatment response, persistent appetite, weight regain after treatment withdrawal or interruption, and rare atypical or paradoxical responses.
Clinical relevance and a possible stage-dependent pattern
The review highlights that reported changes in eating experience should not automatically be classified as taste abnormalities. Healthcare professionals may find it useful to establish whether a person is describing altered taste perception, reduced satisfaction from eating, or diminished interest in food, as these experiences can reflect distinct processes. Distinguishing between them well depends on the quality of the conversation in the consultation, and supporting people through the eating-related changes that accompany GLP-1RA treatment is the focus of professional training such as the College of Contemporary Health’s GLP-1RAs in Practice: Supporting Patients During Treatment, a CPD-accredited online short course.
The authors present these points as translational implications rather than formal clinical recommendations. They also propose a stage-dependent pattern in which these experiences may change over time.
Early in treatment, gastrointestinal discomfort and enhanced satiety may reduce the appeal of food, whereas later stages may involve a more persistent reduction in motivation towards highly rewarding foods in some individuals.
Why this matters for nutrition and obesity management
The proposed sensory-liking-wanting framework has practical implications for obesity treatment and nutritional counselling. Understanding whether someone is experiencing altered sensory perception, reduced enjoyment of food, or lower motivation towards food may support more individualised dietary guidance and improve communication between people receiving treatment and the professionals caring for them.
The review also highlights that the existing body of evidence is heterogeneous, owing to differences in endpoint definitions, measurement methods, populations, drugs, doses and follow-up periods. Much of the human evidence is observational, secondary or exploratory, and many studies were not designed to separate sensory function from liking and wanting. Current findings are therefore better interpreted as a conceptual framework for organising available evidence than as proof of a single causal pathway.
Future studies using standardised, multimodal assessments and longer follow-up may help clarify how these eating-related changes influence food preferences, dietary behaviour, long-term weight management and treatment adherence.
Conclusion
The review concludes that altered eating experiences during GLP-1RA therapy are more consistent with changes in food reward, hedonic evaluation and motivational drive than with a uniform impairment of taste function, although modulation of peripheral taste pathways may contribute in some cases.
Current evidence supports interpreting reported “taste changes” within a sensory-liking-wanting framework that distinguishes sensory perception from food enjoyment and craving. Because responses vary between individuals and the available evidence remains heterogeneous, the proposed framework should be considered a conceptual model rather than definitive proof of causality.
Longitudinal, multimodal human studies measuring sensory function, hedonic response, motivational drive and state-related symptoms in parallel are needed to clarify these effects and their implications for nutrition, dietary behaviour, treatment adherence and long-term obesity management.
CCH insight:
When someone says food no longer tastes right on a GLP-1RA, the clinically useful question is which part of eating has changed: the sensing, the liking or the wanting. Each points towards different advice, and each can shift as treatment progresses. CCH’s GLP-1RAs in Practice: Supporting Patients During Treatment CPD short course (2 CPD hours, fully online, CPD-accredited) equips healthcare professionals to have exactly those conversations – recognising what people are really describing, adapting dietary and nutritional support through the course of treatment, and monitoring for the changes that matter.
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GLP-1 Therapies Linked to Lower Fragility Fracture Risk in Adults Living With Type 2 Diabetes
Key Takeaways:
- Adults aged 50 and over living with type 2 diabetes who started a GLP-1 receptor agonist had a 21% lower three-year risk of fragility fracture than those starting a DPP-4 inhibitor (HR 0.79).
- Reductions were strongest for vertebral (HR 0.68) and hip or femur fractures (HR 0.70), and appeared independent of changes in BMI and HbA1c – pointing to a possible direct skeletal effect.
- The findings do not extend to younger people using GLP-1 medications for weight management alone, or to those with osteoporosis; among adults without diabetes, fracture risk was higher (HR 1.13).
A large-scale look at bone health during GLP-1 treatment
Initiating a GLP-1 receptor agonist for type 2 diabetes was associated with a lower risk of fragility fractures in adults aged 50 and over, including fractures of the hip and spine, according to a large target trial emulation study published in JAMA Network Open.
Over three years of follow-up, adults who newly started a GLP-1 medication had a 21% lower risk of fragility fracture than those who newly started a DPP-4 inhibitor (HR 0.79, 95% CI 0.76–0.83), reported Christopher Hamad, MD, of the University of California Los Angeles, and colleagues.
The authors were careful to frame the size of the effect in context rather than overstate it.
“Although the absolute risk reduction at 3 years was modest (0.79%), this magnitude is clinically relevant given a baseline 3-year major osteoporotic fracture risk of approximately 3% to 4% in comparable populations and the substantial morbidity and mortality associated with hip and vertebral fractures,” the authors wrote.
Why a modest absolute reduction still matters
The clinical weight of these numbers rests on how serious the events being prevented are. Hip fractures, for example, are associated with one-year mortality rates of up to 25% in women and up to 36% in men.
Given the potential for such severe outcomes, Hamad’s group emphasised that even modest absolute reductions in fragility fractures – which stem from low-energy trauma, such as a fall from standing height – can prevent a meaningful number of events at population level.
The findings build on several smaller observational studies in people living with diabetes that have similarly linked the use of GLP-1 medications such as semaglutide (Ozempic, Wegovy) to a reduced fracture risk. Hamad’s team noted that their analysis drew on the largest dataset assembled on this question to date.
Which fractures showed the strongest signal
The protective association was most pronounced at precisely the sites that carry the highest morbidity and mortality:
- Vertebral fractures: HR 0.68, 95% CI 0.63–0.73
- Hip or femur fractures: HR 0.70, 95% CI 0.63–0.79
- Rib fractures: HR 0.83, 95% CI 0.77–0.91
No significant associations were identified for fractures of the distal radius or ulna, or of the proximal humerus.
Weight loss, glycaemic control and the question of a direct skeletal effect
One of the more striking elements of the analysis concerns the mechanism. Mediation analyses indicated that the associations were independent of changes in BMI and HbA1c, a pattern consistent with a potential direct skeletal effect of GLP-1 medications.
That matters because weight loss itself is associated with reduced bone mineral density and a higher fracture risk – a relationship reflected in the study’s own data, which found that cumulative BMI loss was tied to a 2% increase in fracture risk. In other words, the expected consequence of the weight reduction these medications produce would be a rise in fracture risk, not a fall.
“Yet, GLP-1 RA [receptor agonist] use was associated with lower fracture risk despite these changes, suggesting that potential direct skeletal effects may outweigh the adverse consequences of weight loss,” the authors wrote.
Reassessing the assumption of neutral skeletal effects
Current American Diabetes Association Standards of Care classify GLP-1 medications as having neutral effects on the skeleton. The researchers argued that their results suggest this assumption warrants reevaluation.
They also acknowledged the limits of what an observational design can establish, noting that the findings could still reflect unmeasured factors such as improved balance or greater physical activity among people taking these medications. Making sense of evidence like this – and of the mechanistic arguments used to interpret it – is the focus of professional training such as the College of Contemporary Health’s GLP-1RAs in Focus, a CPD-accredited online short course that grounds healthcare professionals in how these medications act on the body.
How the study was conducted
For this comparative effectiveness study, the researchers drew data from the TriNetX Research Network, analysing 66,803 matched pairs, or 133,606 people in total, aged between 50 and 90 years.
Mean age was approximately 63 years, roughly 53% of participants were male, 58% were White, and average baseline BMI was around 33.
All participants were living with type 2 diabetes and had newly initiated either a GLP-1 receptor agonist or a DPP-4 inhibitor between 2015 and 2022. Dulaglutide (Trulicity), semaglutide and liraglutide (Victoza) together accounted for 91% of index prescriptions in the GLP-1 group. Exclusion criteria included fractures resulting from high-energy trauma, as well as osteoporosis and osteopenia.
Where the protective association held – and where it did not
In subgroup analyses, the lower fracture risk was consistent across age groups, across sexes and across levels of frailty.
A separate matched cohort, however, evaluated participants according to diabetes status and produced a notably different picture. Among adults living with type 2 diabetes, GLP-1 use retained a protective association (three-year HR 0.91, 95% CI 0.88–0.95). Among adults without diabetes, it was associated with an increased fracture risk (HR 1.13, 95% CI 1.04–1.23, P<0.001 for interaction).
Consequently, the authors emphasised that the findings cannot be generalised to younger people using GLP-1 medications solely for weight management, nor to those with known osteoporosis or a previous fragility fracture, who were excluded from the study altogether.
What this means for practice
Overall, “the findings do not argue against GLP-1 RA use on the basis of fracture risk, though bone health monitoring remains prudent,” according to the researchers.
They called for prospective randomised trials to evaluate the associations observed, including among people with osteopenia or early osteoporosis, alongside preclinical work to understand the potential mechanisms involved.
CCH insight
For healthcare professionals, this study is a useful reminder that the skeletal consequences of GLP-1 treatment are not yet settled science – and that the answer appears to differ depending on who is being treated and why. Interpreting findings of this kind with confidence depends on a firm grasp of how these medications act in the first place, from gut hormones and appetite regulation through to their wider effects beyond glycaemic control. That is exactly what CCH’s GLP-1RAs in Focus – Why Drugs Like Ozempic Work CPD short course (2 CPD hours, fully online, CPD-accredited) is built to provide, giving clinicians a clear grounding in the mechanisms behind these therapies and the ability to appraise emerging evidence critically, whether or not they prescribe.
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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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Ozempic and Mounjaro Linked to Modest Rise in Hair Loss Risk, BMJ Study Finds
Key Takeaways:
- Adults living with type 2 diabetes taking GLP-1 receptor agonists developed alopecia more often than those taking SGLT-2 inhibitors (37% higher risk) or DPP-4 inhibitors (68% higher risk), a BMJ study reports.
- Absolute risk stayed low, at 6.91 cases per 1,000 person years for GLP-1 receptor agonists against 5.04 for SGLT-2 inhibitors and 3.89 for DPP-4 inhibitors.
- The association was confined to non-scarring alopecia, where the follicle stays intact and regrowth remains possible.
A modest signal, but one worth discussing in the consultation
Medications from the GLP-1 receptor agonist class, now widely used in the management of type 2 diabetes and obesity, may be associated with a modest increase in hair loss. The finding comes from a study published by The BMJ on 22 July 2026.
The class includes semaglutide, marketed under brand names such as Ozempic and Wegovy, and tirzepatide, marketed as Mounjaro and Zepbound. Researchers found that adults living with type 2 diabetes who were treated with GLP-1 receptor agonists went on to develop alopecia more frequently than people prescribed two other commonly used classes of diabetes medication.
Although the relative increase was significant, the researchers emphasised that the absolute risk of hair loss remained low. Even so, awareness of the possible adverse effect could help people and their clinicians reach better informed treatment decisions together.
Reports of hair loss with semaglutide and tirzepatide
Hair loss has been reported before as a possible adverse effect of GLP-1 receptor agonists, particularly with medications containing semaglutide or tirzepatide. What has been missing is research that directly compares the risk among people taking these medicines with the risk among people taking alternative diabetes treatments.
To address that gap, the research team analysed electronic health records from the University of Pennsylvania Health System (Penn Medicine). They compared rates of alopecia among adults living with type 2 diabetes who began treatment with GLP-1 receptor agonists, SGLT-2 inhibitors or DPP-4 inhibitors.
The analysis covered people treated between January 2019 and September 2024. One comparison included 12,004 people taking GLP-1 receptor agonists and 15,221 taking SGLT-2 inhibitors. A second, separate comparison included 11,964 people taking GLP-1 receptor agonists and 11,233 taking DPP-4 inhibitors.
Accounting for differences between the treatment groups
The groups differed in several important respects before the researchers adjusted their results.
Compared with people taking SGLT-2 inhibitors, those taking GLP-1 receptor agonists were younger (mean age 58 v 65), had a higher body mass index (36.2 v 32.3), and had lower rates of cardiovascular disease and chronic kidney disease.
A similar pattern was seen in the comparison with DPP-4 inhibitors. People taking GLP-1 receptor agonists were again younger (mean age 58 v 67) and had a higher body mass index (36.2 v 31.3).
To limit the influence of these imbalances, the researchers adjusted for factors that might otherwise have shaped the findings, including age, sex, ethnicity, pre-existing conditions, use of other medications, and body mass index.
Higher rates of alopecia after adjustment
Once those adjustments were made, use of a GLP-1 receptor agonist was associated with a 37% higher risk of alopecia than use of an SGLT-2 inhibitor (6.91 v 5.04 per 1,000 person years).
The difference was larger in the second comparison. Risk was 68% higher among people taking GLP-1 receptor agonists than among those taking DPP-4 inhibitors (6.53 v 3.89 per 1,000 person years).
Further analysis indicated that the association was limited to non-scarring alopecia, the form in which hair follicles remain intact and the potential for regrowth is preserved. For this type of hair loss, risk was 53% higher among people taking GLP-1 receptor agonists than among those taking SGLT-2 inhibitors, and 72% higher than among those taking DPP-4 inhibitors.
Why rapid weight loss might disturb the hair cycle
The study did not establish why GLP-1 medications might be connected to hair loss, but the authors set out several plausible explanations.
Rapid weight loss is a well established cause of increased hair shedding. It may also contribute to iron or zinc deficiency, either of which can interfere with the normal hair growth cycle. Hormonal changes related to weight loss or to treatment itself could play a part as well, although further research will be needed to identify the mechanisms at work.
Important questions that remain open
The researchers acknowledged a number of limitations. The available clinical records did not contain enough detail to determine the severity, extent or duration of the alopecia. Nor could the team assess whether hair grew back after people stopped taking the medication.
Because the study was observational, it cannot demonstrate that GLP-1 medications directly caused the hair loss. Other factors that were not measured may have influenced the results.
Set against that, the authors described their work as rigorous, drawing on high quality data from a large and representative group of patients. The findings also held up across additional analyses, which supports their reliability.
What the findings mean for practice
For clinicians, the practical value of a study like this lies less in the headline percentages than in what it adds to the conversation before and during treatment. Anticipating adverse effects, recognising them early and folding them into shared decision-making are core parts of the GLP-1 consultation – the ground covered by CPD courses such as the College of Contemporary Health’s GLP-1RAs in Practice: How to Safely Prescribe Ozempic, Wegovy & Mounjaro, which works through initiation, titration and the avoidance of adverse reactions.
The researchers concluded: “Our findings extend previous anecdotal safety signals and provide more systematic evidence to inform clinical awareness of this potential adverse effect.”
CCH insight
This may seem like an odd perspective, but this could be a good thing if it means that people considering taking GLP-1 medications for vanity reasons (to slim down to their perfect weight when they do not have obesity or type 2 diabetes) are put off, leaving better availability for those who genuinely need it. I am sure that for most people living with obesity or diabetes, a small increased risk of alopecia is worth taking when balanced against the huge health benefits that these drugs usually bring.
Hair loss is unlikely to change prescribing decisions on its own, but it is exactly the kind of adverse effect that patients notice, worry about and sometimes stop treatment over. Knowing how to raise it, put the absolute risk in context and respond if it appears is part of delivering GLP-1 therapy well. CCH’s GLP-1RAs in Practice: How to Safely Prescribe Ozempic, Wegovy & Mounjaro (Or Any Other Weight Loss Drug) is a two-hour, CPD-accredited online course covering every stage of the consultation, from patient selection and titration through to managing adverse reactions, grounded in current NICE guidance and the ADA 2026 Standards of Care.
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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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Study Identifies Which Patients With Obesity Respond Best to GLP-1-Based Treatment
Key Takeaways:
- A Mayo Clinic study has identified a distinct biological subtype of obesity – a form of the “hungry gut” phenotype – that responds especially well to tirzepatide.
- People in this subgroup lost an average of 21.5% of their body weight after six months on tirzepatide, roughly double the 11.7% seen in other subtypes.
- The lower appetite-hormone levels traced back to reduced hormone production in the intestine rather than differences in the gut microbiome.
A step towards precision medicine for obesity
Why do some people lose a substantial amount of weight on GLP-1-based medications while others see far more modest results? A new Mayo Clinic study offers a potential answer, identifying a distinct biological subtype of obesity that responds especially well to tirzepatide – a medication that mimics two naturally occurring hormones involved in appetite and blood sugar regulation. The finding moves the field a step closer to precision medicine for obesity, where treatment is matched to an individual’s underlying biology rather than applied uniformly.
The research, published in the journal Gastroenterology, points to a future in which clinicians could predict, rather than simply hope, that a given therapy will work for a given person.
What the researchers found
The team studied 483 adults living with obesity and identified three distinct biological types of the disease. About one in four participants produced lower levels of GLP-1 and other hormones that help people feel full after eating.
This subgroup saw markedly better results on treatment. Patients in this group lost an average of 21.5% of their body weight after six months of tirzepatide, compared with 11.7% for patients in the other groups – losing nearly twice as much weight over the same period.
“Obesity is a complex disease driven by different biological mechanisms,” says senior author Andres Acosta, M.D., Ph.D., a gastroenterologist and the Delaney Family Director of the Nutrition Obesity Research Program at Mayo Clinic in Minnesota. “Our findings suggest we can begin identifying which patients are most likely to respond to specific therapies rather than treating obesity as a single disease.”
Understanding the “hungry gut” subtype
The subgroup that responded so strongly to tirzepatide shares a recognisable biological signature: people in this group produce lower levels of natural appetite-regulating hormones, experience faster stomach emptying and report greater hunger after meals.
Researchers describe this as a form of the “hungry gut” obesity phenotype, which is characterised by an abnormal duration of fullness. Rather than eating unusually large amounts at any one sitting, people with hungry-gut obesity may eat normal portion sizes but find themselves snacking more frequently, because the sense of fullness does not last as long as it should.
Because tirzepatide acts on the same appetite pathways that are underactive in this group, it appears especially well suited to addressing the biology that drives their eating patterns.
Why the underlying biology matters
The study also sheds light on why hormone levels differ in this subgroup. The researchers found that the reduced hormone levels were associated with decreased hormone production in the intestine itself, rather than with differences in the gut microbiome. That distinction offers new insight into the biology underlying this subtype and helps explain where the difference in treatment response originates.
Identifying the right therapy sooner could carry significant long-term benefits. Because obesity increases the risk of diabetes, heart disease, certain cancers and many other serious chronic conditions, matching people to the treatment most likely to help them – rather than relying on a one-size-fits-all approach – could improve long-term health outcomes.
What this means for clinical practice
The findings support growing efforts to personalise obesity treatment based on an individual’s biology. For clinicians, interpreting studies like this one increasingly depends on a firm grasp of how GLP-1-based medications act on appetite hormones and gastric emptying in the first place – the kind of grounding offered by CPD courses such as the College of Contemporary Health’s GLP-1RAs in Focus, which examines why some people respond more strongly to these treatments than others. Still, the authors are careful to note the limits of the current work. They caution that prospective studies are needed before this approach can be incorporated into routine clinical practice.
Even so, the results represent an important step towards more precise, individualised treatment for obesity – and towards a future in which people are guided to the therapy most likely to work for them from the outset.
Studies like this one land almost weekly, and making sense of them starts with understanding how GLP-1 receptor agonists actually work – from gut hormones and appetite regulation to why some people respond far more strongly than others. CCH’s GLP-1RAs in Focus – Why Drugs Like Ozempic Work is a two-hour, CPD-accredited online course created by Prof. Mike Bewick and Nigel Hinchliffe that builds exactly this foundation, whether or not you prescribe. Explore the course and interpret the next headline with confidence.
Source: Mayo Clinic
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