The findings from the current study suggest that magnesium also increases the gut synthesis of vitamin D, which does not go to the blood and takes effect locally.
Photo by Danilo Alvesd on Unsplash
Researchers from Vanderbilt University Medical Center have demonstrated in a precision-based clinical trial that a magnesium supplement increases gut bacteria in humans that have been shown to synthesise vitamin D and inhibit colorectal cancer carcinogenesis.
However, the effect was observed primarily in females – an outcome that the researchers surmised may be attributable to the role that oestrogen plays in shifting magnesium from circulation into cellular uptake.
Intestinal microbiome data and colonoscopy results were analysed from participants who were randomised by whether they had the TRPM7 genotype, which plays a crucial role in regulating magnesium and calcium uptake.
Previously, the investigators showed in the same randomised trial that magnesium enhances the synthesis of vitamin D and increases the blood levels of vitamin D. The findings from the current study suggest that magnesium also increases the gut synthesis of vitamin D, which does not go to the blood and takes effect locally.
“Our previous study showed magnesium supplementation increased blood levels of vitamin D when vitamin D levels were low,” said Qi Dai, MD, PhD, professor of Medicine. “The current study reveals that magnesium supplementation also increases the gut microbes which have been shown to synthesise vitamin D in the gut without sunlight and locally inhibit colorectal cancer development.”
The participants were divided into two arms, one that received the magnesium supplement and another that received a placebo. Their gut microbiome was analysed from stools, rectal swabs and rectal tissues. Among participants with adequate TRPM7 function, the magnesium supplement increased Carnobacterium maltaromaticum and Faecalibacterium prausnitzii, which were previously found to work synergistically to increase vitamin D and decrease colorectal carcinogenesis. Among those with inadequate TRPM7 function, the magnesium supplement reduced the abundance of F. prausnitzii in rectal mucosa.
Among 236 participants who all had a history of colorectal polyps, 124 underwent colonoscopies after completing the trial with a 3.5-year median follow-up time. A higher abundance of F. prausnitzii in rectal mucosa was associated with an almost threefold increase in developing additional polyps.
University students have limited spending money and their schedules are packed. Many are adapting to new lifestyles on campus. Eating a healthy diet is crucial: a poor diet leads to reduced concentration, lower grades and increased stress.
Campus cafés, especially at universities that are some distance from supermarkets, often sell mainly fast food such as white bread sandwiches, hot chips and doughnuts. It’s easy to eat on the go, but places nutritious choices out of reach.
I’m an urban geographer who researches the relationship between food, health and place. My work examines how urban agriculture, informal food systems and everyday urban infrastructures shape well-being, sustainability and spatial justice in African cities.
Research has already found that through pricing, menu design and information provision, campus cafés play a decisive role in shaping dietary behaviours among young adults. I wanted to find out how students at the University of the Western Cape in South Africa choose what to eat when they’re on campus, what they see as healthy food and what stands in the way of them buying nutritious meals.
The university is one that was underfunded during apartheid. Until 1994 it primarily taught students who were Black and people of Colour. Today, it serves about 23 000 students, many of whom are drawn from low-income backgrounds, and has few supermarkets within walking distance. The campus cafés are a key food supply area for students.
My research found that at the University of the Western Cape, only 32% of the food offered at the student café was healthy. It also cost more than the fast food. The students I surveyed knew healthy food was important. But only a small minority consistently chose nutritious meals. Nearly 40% of the group reported that the healthy options were too expensive.
When students face the twin challenges of financial hardship and inadequate access to affordable, nutritious food, this deepens inequality. It also undermines their efforts to succeed. Even worse, it can cause students to develop long term, unhealthy eating habits that damage their health.
Unless affordability, availability and awareness of healthy food choices are addressed together, students will struggle to eat well and to perform at their best.
Universities must implement targeted food subsidies, introduce clearer nutritional labelling, and expand healthy menu options to make nutritious eating more accessible and appealing to students.
Students speak out about their food choices
I conducted a survey that sampled 112 students in five campus cafés at the university. These cafés are mainly used by students in the 18-24 age group.
My survey revealed that 75.9% of students considered healthy offerings at least “somewhat important” when choosing where to eat. Yet only 6.3% always selected nutritious options; 28.6% rarely or never did so. Meanwhile, 38.4% of students described nutritious meals as “expensive” and another 8% found the healthy options “very expensive”.
My research also found that University of the Western Cape students ate very little fruit and vegetables. Just 41% of the students I surveyed ate two or more servings a day and 9.8% admitted they ate none.
I also did a detailed menu audit at one café to see what was on the menu. I found that only 32.6% of 46 distinct items met basic “healthy” criteria (they were low in saturated fats and made up of whole-grains or vegetables).
The majority of students (55.4%) had not noticed any campus healthy-eating campaigns, but agreed (57.1%) that balanced meals boosted academic performance and overall well-being:
I feel much more focused and energetic when I eat well, which helps me do better in my studies and feel healthier overall.
Only a small handful of the students said they could afford healthy campus café meals:
I choose cafés based on food quality. If the food is fresh and tasty, I’ll pay more, but it needs to be worth it.
What needs to happen next
High prices for nutritious items, narrow menu selections and barely visible information about nutrition are preventing students from eating healthy foods on campus.
Campus café offerings tend to mirror the broader inequities of national and global food systems. Food environments of big institutions like universities can prop up food inequality, even if these universities are committed to social justice.
Universities should adopt these steps to make healthy food available to students:
Subsidised meal plans and discounts: Introducing a tiered subsidy for students from low-income backgrounds would directly reduce costs. For example, meal vouchers could make salads, whole-grain sandwiches and fruit bowls as affordable as a pastry or soft drink.
A wider range of food on the menu and smaller portions: Partnerships between university caterers and local cooperatives or farmers could expand the range of fresh produce. Smaller portions or “light” meal options could be sold at lower prices to suit tighter budgets. Regularly rotating healthy specials and clearly labelling ingredients and calories would help students become accustomed to choosing healthy meals.
Visible nutrition campaigns: Digital and printed standout posters about healthy foods could be placed around campus. Universities could hold social-media challenges and pop-up tasting events. Integrating simple tips into lecture slides or student newsletters would also help by repeatedly exposing students to healthy food tips.
Peer-led workshops and cooking classes: These should be arranged to empower students to take ownership of their diets and learn about budgeting, meal planning and quick, nutritious cooking skills. Peer facilitators can demystify healthy eating and create a supportive healthy eating community.
Seeking feedback: To see if their healthy food campaigns are working, universities should survey students, and analyse sales data from the cafés to see what’s being eaten. They should get feedback from students through focus groups that identify emerging needs and ensure that campaigns and projects reflect the realities of students’ lives.
My research suggests that by tackling cost, choice and communication together, universities can transform their cafés from sites of compromise into engines of student well-being. Such interventions would unlock academic potential and set young people on healthier life paths. This is an outcome as enriching as any degree.
Ingredients of our daily diet – including caffeine – can influence the resistance of bacteria to antibiotics. This has been shown in a new study by a team of researchers at the Universities of Tübingen and Würzburg led by Professor Ana Rita Brochado. They discovered bacteria such as Escherichia coli (E. coli) orchestrate complex regulatory cascades to react to chemical stimuli from their direct environment which can influence the effectiveness of antimicrobial drugs such as ciprofloxacin.
In a systematic screening, Brochado’s team investigated how 94 different substances – including antibiotics, prescription drugs, and food ingredients – influence the expression of key gene regulators and transport proteins of the bacterium E. coli, a potential pathogen. Transport proteins function as pores and pumps in the bacterial envelope and control which substances enter or leave the cell. A finely tuned balance of these mechanisms is crucial for the survival of bacteria.
Researchers describe phenomenon as an ‘antagonistic interaction’
“Our data show that several substances can subtly but systematically influence gene regulation in bacteria,” says PhD student Christoph Binsfeld, first author of the study. The findings suggest even everyday substances without a direct antimicrobial effect – eg, caffeinated drinks – can impact certain gene regulators that control transport proteins, thereby changing what enters and leaves the bacterium. “Caffeine triggers a cascade of events starting with the gene regulator Rob and culminating in the change of several transport proteins in E. coli – which in turn leads to a reduced uptake of antibiotics such as ciprofloxacin,” explains Ana Rita Brochado. This results in caffeine weakening the effect of this antibiotic. The researchers describe this phenomenon as an ‘antagonistic interaction.’
“Caffeine triggers a cascade of events starting with the gene regulator Rob and culminating in the change of several transport proteins in E. coli – which in turn leads to a reduced uptake of antibiotics such as ciprofloxacin,” says Prof Brochado.
This weakening effect of certain antibiotics was not detectable in Salmonella enterica, a pathogen closely related to E. coli. This shows that even in similar bacterial species, the same environmental stimuli can lead to different reactions – possibly due to differences in transport pathways or their contribution to antibiotic uptake.
The study, which has been published in the scientific journal PLOS Biology, makes an important contribution to the understanding of what is called ‘low-level’ antibiotic resistance, which is not due to classic resistance genes, but to regulation and environmental adaptation. This could have implications for future therapeutic approaches, including what is taken during treatment and in what amount, and whether another drug or food ingredient – should be given greater consideration.
A new study tracked the acute muscle-building response in adults engaged in a weight-training exercise who were fed either high-fat or lean ground pork burgers with the same amount of protein in each. The findings surprised the scientists, adding to the evidence that muscle-protein synthesis in response to weight-training and a post-exercise meal is as complex as the high-protein foods people consume.
“What we’re finding is that not all high-quality animal protein foods are created equal,” said Nicholas Burd, a professor of health and kinesiology at the University of Illinois Urbana-Champaign, who led the research with graduate student Žan Zupančič.
A previous study from Burd’s lab found that consuming whole eggs after weight training was better for muscle-protein synthesis than eating only egg whites with equal amounts of protein. Another study from his lab revealed that eating salmon showed a more favourable rate of muscle-building after weight training than a processed mixture containing the same nutrients in the same proportions as the salmon.
These studies suggest that whole foods are better at stimulating post-workout protein synthesis than their processed counterparts, and that the fat content of whole foods may, in some circumstances, improve the rate of muscle-building, Burd said.
In the new study, the researchers used state-of-the-art methods to trace and calculate muscle-protein synthesis in 16 young, physically active adults. The team turned to the U. of I.’s Meat Science Laboratory for formulation of the pork patties.
“That took us a year because it was so hard to get those fat ratios correct,” Burd said. All the meat used in the study came from a single pig, and the researchers sent the patties off to another laboratory for analysis. Once the lean-to-fat ratios and other macros were confirmed, the pork burgers were frozen until needed in the feeding part of the study.
Before the weight-training and feeding intervention, all participants received an infusion of isotope-labeled amino acids. This allowed the researchers to track how quickly the labeled amino acids were incorporated into muscle. The team also took blood samples throughout the study to measure amino acid levels in participants’ blood.
Before and after the first two hours of the infusion, researchers took muscle biopsies of each participant to get a baseline measure of muscle-protein synthesis.
“And then we took them to the gym,” Burd said. “And they were wheeling that infusion pump and everything else with them.”
At the gym, the study subjects engaged in an acute bout of leg presses and leg extensions and then returned to the lab for a meal of either a high-fat pork burger, a lean pork burger or a carbohydrate drink. Five hours after the meal, another muscle biopsy was taken to measure protein synthesis in response to the weight-training and feeding intervention.
After a break of a few days, 14 of the 16 participants “crossed over, switching to a different feeding intervention to minimise the impact of individual differences in muscle-building responses,” Burd said.
The analysis revealed, as expected, that the amino acid content of the blood was significantly higher in those who ate pork than in those who consumed a carbohydrate drink. But the lean-pork group saw the greatest gains in amino acid levels in the blood. This was true for total and essential amino acids, the team found.
“When you see an increased concentration of amino acids in the blood after you eat, you get a pretty good idea that that is coming from the food that you just ate,” Burd said.
Those who consumed the lean pork burger after a bout of weight training also had a greater rate of muscle-protein synthesis than those who ate the high-fat pork burger. This was a surprise to Burd, as “the previous studies using fattier foods, such as whole eggs or salmon, generally showed enhanced post-exercise muscle-protein synthesis compared with lower fat food such as egg whites or nutritional supplements,” he said.
Although weight training boosted muscle-protein synthesis in the groups eating pork, the protein in the high-fat burger seemed to have no added benefit in the hours after participants consumed it, while the protein in the lean pork gave muscle-protein synthesis a boost.
“For some reason, the high-fat pork truly blunted the response,” Burd said. “In fact, the people who ate the high-fat pork only had slightly better muscle-building potential than those who drank a carbohydrate sports beverage after exercise.”
Interpreting the results of this study for people who want to optimise muscle gains from weight-training is tricky, Burd said. It could be that processing the ground pork patties, which involved grinding the meat and adding the fattier meat to the lean, affected the kinetics of digestion.
“There was a little larger rise in the amino acids available from eating lean pork, so it could have been a bigger trigger for muscle-protein synthesis,” Burd said. “But that seems to be specific to the ground pork. If you’re eating other foods, like eggs or salmon, the whole foods appear to be better despite not eliciting a large rise in blood amino acids.”
Burd stresses that exercise is the strongest stimulus for muscle-protein synthesis.
“Most of the muscle response is to weight-training, and we use nutrition to try to squeeze out the remaining potential,” he said. “When it comes to eating after weight-training, what we’re finding is that some foods, particularly whole, unprocessed foods seem to be a better stimulus.”
Could a keto diet affect males differently from females? A study from The University of Texas Health Science at San Antonio (UT Health San Antonio) suggests so, and oestrogen could promote different protections against adverse effects of the diet like the accumulation of cells expressing markers of age, or senescence.
The study, published Aug. 26 in the journal Cell Reports, found that male, but not female, mice on a ketogenic diet showed the accumulation of cells in organs expressing markers of cellular senescence. A keto diet is a popular low-carbohydrate, high-fat regimen that can help some Type 2 diabetes patients control blood sugar and those with epilepsy manage seizures. Cells expressing senescence markers can contribute to age-related declines in overall bodily function.
“These results suggest sex specificity alters the effects of a ketogenic diet, with important clinical implications,” said David Gius, MD, PhD, assistant dean of research and professor with the Department of Radiation Oncology at UT Health San Antonio, associate cancer director for translational research at the institution’s Mays Cancer Center and investigator for its Barshop Institute for Longevity and Aging Studies.
He is lead author of the study, titled, “Divergent sex-specific effects on a ketogenic diet: Male, but not female, mice exhibit oxidative stress and cellular senescence.”
Ketogenic diets induce ketogenesis, the generation of ketone bodies or water-soluble molecules from fat for use as fuel in place of glucose. They have shown benefits in controlling refractory epilepsy and are being investigated as potential therapies for other health conditions.
In the past decades, keto diets also have become popular in North America and Europe for weight loss.
While the diets can improve certain health parameters, evidence from mice and clinical studies suggest the effects may be dependent on multiple variables, including adherence, metabolism and, importantly, sex, suggesting that hormone status may impact response.
Gius says the role of gender in the response to keto diets has been understudied. One reason is that male mice have been used extensively for in vivo basic and translational research because it was assumed that females would give less consistent results due to variability from the oestrous cycle. Recent studies, however, suggest that largely is unfounded.
In the new study, Gius’ team observed a keto-diet-induced increase in cellular senescence only in male mice, except when they were given the female hormone oestrogen. Male mice on a keto diet also exhibited an increase in markers of oxidative stress, which is known to contribute to senescence in cells.
Notably, the researchers found, estrogen or estradiol treatment prevented increases in cell senescence and oxidated stress in male mice on a keto diet, as did several established antioxidants.
They also observed that when females were administered tamoxifen, a “selective oestrogen receptor inhibitor” that blocks the effects of oestrogen, they then exhibited an increase in oxidative stress and cells expressing senescence markers, the same as male mice. “These results strongly suggest that oestrogen is an important variable in the response to a ketogenic diet,” Gius said.
The researchers also found that a high-fat diet – comprising more carbohydrates than a keto diet – also induces cellular senescence in male, but not female, mice.
Epidemiological studies have revealed a strong correlation between red meat consumption and the development of inflammatory bowel disease. In a new study published in Molecular Nutrition and Food Research that was conducted in mice, red meat consumption caused an imbalance of bacteria in the intestinal microbiota.
Investigators fed mice various kinds of red meat, including pork, beef, and mutton, for two weeks, and then they induced colitis with 2.5% dextran sulfate sodium. Intake of these three red meat diets exacerbated colonic inflammation. Analyses revealed an overproduction of pro-inflammatory cytokines and infiltration of immune cells in the colon of mice fed red meat diets.
These diets led to a marked decrease in the relative abundance of Streptococcus, Akkermansia, Faecalibacterium, and Lactococcus bacterial strains, coupled with an increase in Clostridium and Mucispirillum.
“This study contributes to improving food innervation approaches for inflammatory bowel disease treatment and indicates a close crosstalk among diet, gut microbiota, and intestinal immunity,” said co–corresponding author Dan Tian, MD, PhD, of Capital Medical University, in China.
Analysis of lipid blood levels in women with Alzheimer’s disease has shown noticeable loss of unsaturated fats, such as those that contain omega fatty acids, compared to healthy women.
In men with Alzheimer’s, no significant difference was found in the same lipid molecule composition disease compared to healthy men, which suggests that those lipids have a different role in the disease according to sex. Fats perform important roles in maintaining a healthy brain, so this study could indicate why more women are diagnosed with the disease.
The study, published today in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association by scientists from King’s College London and Queen Mary University London, is the first to reveal the important role lipids could have in the risk for Alzheimer’s between the sexes.
Women are disproportionately impacted by Alzheimer’s Disease and are more often diagnosed with the disease than men after the age of 80. One of the most surprising things we saw when looking at the different sexes was that there was no difference in these lipids in healthy and cognitively impaired men, but for women this picture was completely different. The study reveals that Alzheimer’s lipid biology is different between the sexes, opening new avenues for research.
Dr Cristina Legido-Quigley, Reader in Systems Medicine
The scientists took plasma samples from 841 participants who had Alzheimer’s Disease, mild cognitive impairment and cognitively health controls and and were measured for brain inflammation and damage.
They used mass spectrometry to analyse the 700 individual lipids in the blood. Lipids are a group of many molecules. Saturated lipids are generally considered as ‘unhealthy’ or ‘bad’ lipids, while unsaturated lipid, which sometime contains omega fatty acids, are generally considered ‘healthy’.
Scientists saw a steep increase in lipids with saturation – the ‘unhealthy lipids’ – in women with Alzheimer’s compared to the healthy group. The lipids with attached omega fatty acids were the most decreased in the Alzheimer’s group.
Now, the scientists say there is a statistical indication that there is a causal link between Alzheimer’s Disease and fatty acids. But a clinical trial is necessary to confirm the link.
Dr Legido-Quigley added: “Our study suggests that women should make sure they are getting omega fatty acids in their diet – through fatty fish or via supplements. However, we need clinical trials to determine if shifting the lipid composition can influence the biological trajectory of Alzheimer’s Disease.”
Dr Asger Wretlind, first author of the study from the School of Cancer & Pharmaceutical Sciences, said: “Scientists have known for some time that more women than men are diagnosed with Alzheimer’s disease.
Although this still warrants further research, we were able to detect biological differences in lipids between the sexes in a large cohort, and show the importance of lipids containing omegas in the blood, which has not been done before. The results are very striking and now we are looking at how early in life this change occurs in women.
Dr Asger Wretlind, School of Cancer & Pharmaceutical Sciences
Eating animal-sourced protein foods is not linked to a higher risk of death and may even offer protective benefits against cancer-related mortality, new research finds.
The study, published in Applied Physiology, Nutrition, and Metabolism, analysed data from nearly 16 000 adults aged 19 and older using the National Health and Nutrition Examination Survey (NHAMES III).
Researchers examined how much animal and plant protein people typically consume and whether those patterns were associated with their risk of dying from heart disease, cancer or any cause.
They found no increased risk of death associated with higher intake of animal protein. In fact, the data showed a modest but significant reduction in cancer-related mortality among those who ate more animal protein.
“There’s a lot of confusion around protein – how much to eat, what kind and what it means for long-term health. This study adds clarity, which is important for anyone trying to make informed, evidence-based decisions about what they eat,” explains Stuart Phillips, Professor and Chair of the Department of Kinesiology at McMaster University, who supervised the research.
To ensure reliable results, the team employed advanced statistical methods, including the National Cancer Institute (NCI) method and multivariate Markov Chain Monte Carlo (MCMC) modelling, to estimate long-term dietary intake and minimize measurement error.
“It was imperative that our analysis used the most rigorous, gold standard methods to assess usual intake and mortality risk. These methods allowed us to account for fluctuations in daily protein intake and provide a more accurate picture of long-term eating habits,” says Phillips.
The researchers found no associations between total protein, animal protein or plant protein and risk of death from any cause, cardiovascular disease, or cancer. When both plant and animal protein were included in the analysis, the results remained consistent, suggesting that plant protein has a minimal impact on cancer mortality, while animal protein may offer a small protective effect.
Observational studies like this one cannot prove cause and effect; however, they are valuable for identifying patterns and associations in large populations. Combined with decades of clinical trial evidence, the findings support the inclusion of animal proteins as part of a healthy dietary pattern.
“When both observational data like this and clinical research are considered, it’s clear both animal and plant protein foods promote health and longevity,” says lead researcher Yanni Papanikolaou, MPH, president, Nutritional Strategies.
This research was funded by the National Cattlemen’s Beef Association (NCBA), a contractor to the Beef Checkoff. NCBA was not involved in the study design, data collection and analysis or publication of the findings.
Ultra-processed foods (UPFs) have become public enemy number one in nutrition debates. From dementia to obesity and an epidemic of “food addiction”, these factory-made products, including crisps, ready meals, fizzy drinks and packaged snacks, are blamed for a wide range of modern health problems. Some experts argue that they’re “specifically formulated and aggressively marketed to maximise consumption and corporate profits”, hijacking our brain’s reward systems to make us eat beyond our needs.
Policymakers have proposed bold interventions: warning labels, marketing restrictions, taxes, even outright bans near schools. But how much of this urgency is based on solid evidence?
My colleagues and I wanted to step back and ask: what actually makes people like a food? And what drives them to overeat – not just enjoy it, but keep eating after hunger has passed? We studied more than 3,000 UK adults and their responses to over 400 everyday foods. What we found challenges the simplistic UPF narrative and offers a more nuanced way forward.
Two ideas often get blurred in nutrition discourse: liking a food and hedonic overeating (eating for pleasure rather than hunger). Liking is about taste. Hedonic overeating is about continuing to eat because the food feels good. They’re related, but not identical. Many people like porridge but rarely binge on it. Chocolate, biscuits and ice cream, on the other hand, top both lists.
We conducted three large online studies where participants rated photos of unbranded food portions for how much they liked them and how likely they were to overeat them. The foods were recognisable items from a typical UK shopping basket: jacket potatoes, apples, noodles, cottage pie, custard creams – more than 400 in total.
We then compared these responses with three things: the foods’ nutritional content (fat, sugar, fibre, energy density), their classification as ultra-processed by the widely used Nova system – a food classification method that groups foods by the extent and purpose of their processing – and how people perceived them (sweet, fatty, processed, healthy and so on).
Perception power
Some findings were expected: people liked foods they ate often, and calorie-dense foods were more likely to lead to overeating.
But the more surprising insight came from the role of beliefs and perceptions. Nutrient content mattered – people rated high-fat, high-carb foods as more enjoyable, and low-fibre, high-calorie foods as more “bingeable”. But what people believed about the food also mattered, a lot.
Perceiving a food as sweet, fatty or highly processed increased the likelihood of overeating, regardless of its actual nutritional content. Foods believed to be bitter or high in fibre had the opposite effect.
In one survey, we could predict 78% of the variation in people’s likelihood of overeating by combining nutrient data (41%) with beliefs about the food and its sensory qualities (another 38%).
In short: how we think about food affects how we eat it, just as much as what’s actually in it.
This brings us to ultra-processed foods. Despite the intense scrutiny, classifying a food as “ultra-processed” added very little to our predictive models.
Once we accounted for nutrient content and food perceptions, the Nova classification explained less than 2% of the variation in liking and just 4% in overeating.
That’s not to say all UPFs are harmless. Many are high in calories, low in fibre and easy to overconsume. But the UPF label is a blunt instrument. It lumps together sugary soft drinks with fortified cereals, protein bars with vegan meat alternatives.
Some of these products may be less healthy, but others can be helpful – especially for older adults with low appetites, people on restricted diets or those seeking convenient nutrition.
The message that all UPFs are bad oversimplifies the issue. People don’t eat based on food labels alone. They eat based on how a food tastes, how it makes them feel and how it fits with their health, social or emotional goals.
Relying on UPF labels to shape policy could backfire. Warning labels might steer people away from foods that are actually beneficial, like wholegrain cereals, or create confusion about what’s genuinely unhealthy.
Instead, we recommend a more informed, personalised approach:
• Boost food literacy: help people understand what makes food satisfying, what drives cravings, and how to recognise their personal cues for overeating.
• Reformulate with intention: design food products that are enjoyable and filling, rather than relying on bland “diet” options or ultra-palatable snacks.
• Address eating motivations: people eat for many reasons beyond hunger – for comfort, connection and pleasure. Supporting alternative habits while maximising enjoyment could reduce dependence on low-quality foods.
It’s not just about processing
Some UPFs do deserve concern. They’re calorie dense, aggressively marketed and often sold in oversized portions. But they’re not a smoking gun.
Labelling entire categories of food as bad based purely on their processing misses the complexity of eating behaviour. What drives us to eat and overeat is complicated but not beyond understanding. We now have the dataand models to unpack those motivations and support people in building healthier, more satisfying diets.
Ultimately, the nutritional and sensory characteristics of food – and how we perceive them – matter more than whether something came out of a packet. If we want to encourage better eating habits, it’s time to stop demonising food groups and start focusing on the psychology behind our choices.
Weight-loss interventions, including gastric bypass surgery and drugs that prevent dietary fat absorption, can be invasive or have negative side effects. Now, researchers have developed edible microbeads made from green tea polyphenols, vitamin E and seaweed that, when consumed, bind to fats in the gastrointestinal tract. Preliminary results from tests with rats fed high-fat diets show that this approach to weight loss may be safer and more accessible than surgery or pharmaceuticals.
Yue Wu, a graduate student at Sichuan University, will present her team’s results at the ACS Fall 2025 Digital Meeting, a meeting of the American Chemical Society.
“Losing weight can help some people prevent long-term health issues like diabetes and heart disease,” says Wu. “Our microbeads work directly in the gut to block fat absorption in a noninvasive and gentle way.”
Weight gain is caused by genetic and lifestyle factors, including eating a high-fat diet. A high-fat diet is defined by the U.S. Department of Agriculture as one where 35% or more of a person’s daily calories come from fat, as opposed to protein or carbohydrates. Some pharmaceuticals, such as orlistat, inhibit certain gastric enzymes from breaking down dietary fats, leading to less fat being absorbed by the body. Orlistat is a U.S. Food and Drug Administration (FDA)-approved medication and is effective for weight loss. However, for some people it causes serious side effects, including liver and kidney damage.
So, Wu and her colleagues wanted to target the fat absorption process with their weight-loss intervention but do so without negative side effects. “We want to develop something that works with how people normally eat and live,” says Wu.
To get started, the team created tiny plant-based beads that spontaneously form through a series of chemical bonds between the green tea polyphenols and vitamin E. These structures can form chemical tethers to fat droplets and serve as the fat-binding core of the microbeads. The researchers then coated the spheres in a natural polymer derived from seaweed to protect them from the acidic environment of the stomach. Once ingested, the protective polymer coating expands in response to the acidic pH, and the green tea polyphenols and vitamin E compounds bind to and trap partially digested fats in the intestine.
The microbeads are nearly flavourless, and the researchers foresee them being easily integrated into people’s diets. For example, the microbeads could be made into small tapioca- or boba-sized balls and added to desserts and bubble teas.
The researchers assessed the microbeads as a weight-loss treatment in rats. They put the animals into three groups (eight rats per group), those which were fed a high-fat diet (60% fats) either with or without microbeads and those which were fed a normal diet (10% fats) for 30 days. Rats fed the high-fat diet and microbeads:
Lost 17% of their total body weight, while rats in the other groups didn’t lose weight.
Had reduced adipose tissue and less liver damage compared to rats fed the high-fat and normal diets without microbeads.
Excreted more fat in their feces compared to rats not given microbeads. The extra fat in the rats’ feces had no apparent ill effects on the animals’ health.
Additionally, the eight rats on high-fat diets that consumed microbeads showed similar intestinal fat excretion, but without the gastrointestinal side effects the researchers observed with a fourth group of rats they treated with orlistat.
Wu and her team have started working with a biotechnology company to manufacture the plant-based beads. “All the ingredients are food grade and FDA-approved, and their production can be easily scaled up,” says Yunxiang He, Sichuan University associate professor and co-author on Wu’s presentation.
They’ve also initiated a human clinical trial in collaboration with the West China Hospital of Sichuan University. “This represents a major step toward clinical translation of our polyphenol-based microbeads, following our foundational results,” says Wu. “We have officially enrolled 26 participants in our investigator-initiated trial, and we anticipate that preliminary data may become available within the next year.”
