A low-fat vegan diet that doesn’t limit calories or carbohydrates could help people with type 1 diabetes reduce insulin use and insulin costs, according to new research by the Physicians Committee for Responsible Medicine published in BMC Nutrition.
The new research, which is a secondary analysis of a 2024 Physicians Committee study, compared the effect of a low-fat vegan diet to a portion-controlled diet on insulin use and insulin costs in people with type 1 diabetes. The analysis found that the total dose of insulin decreased by 28%, or 12.1 units, per day in the vegan group, compared to no significant change in the portion-controlled group. The reductions in insulin use in the vegan group likely reflect improved insulin sensitivity, or how well the body responds to insulin. Total insulin costs decreased by 27%, or $1.08 per day, in the vegan group, compared to no significant change in the portion-controlled group.
The 2024 study found that a vegan diet also led to an average weight loss of 11 pounds, improved insulin sensitivity and glycaemic control, and improved cholesterol levels and kidney function in people with type 1 diabetes.
The new research comes as insulin prices in the United States continue to rise. Spending on insulin in the United States tripled in the past 10 years, reaching $22.3 billion in 2022, due to the increased usage and higher price of insulin, according to the American Diabetes Association. The inflation-adjusted cost of insulin increased by 24% from 2017 to 2022.
“As insulin prices continue to rise, people with type 1 diabetes should consider a low-fat vegan diet, which can help improve their insulin sensitivity and reduce the amount of insulin they need, potentially saving them hundreds of dollars a year,” says Hana Kahleova, MD, PhD, the lead author of the study and director of clinical research at the Physicians Committee for Responsible Medicine.
Mice who consumed high-fat diets, especially the ketogenic diet, experienced more weight gain, liver damage and other negative health effects than those who ate a high-carbohydrate diet
In recent years, many media reports and social media influencers have emphasised the dangers of eating too many carbohydrates. Though a carbohydrate-heavy diet can be harmful, consuming too many fats may cause more health problems, according to a study in mice led by researchers in the Penn State Department of Nutritional Sciences.
In a study published in the February issue of Journal of Nutrition, the researchers analysed how diets containing different ratios of fats and carbohydrates affected metabolic health and liver function in mice over time. They found, overall, higher-fat diets were more harmful than high-carbohydrate diets, but that fibre supplementation might be able to reduce harm in specific conditions.
Mice consumed one of four diets: high carbohydrate, high fat, ketogenic or a standard chow that was rich in whole grains and served as the experiment’s control group. In mice of normal weight, the keto diet led to weight gain, impaired the use of glucose, disrupted the balance of lipids in the body and increased inflammation and fat deposits in the liver. The high-fat diet also led to weight gain and other health problems not seen in mice who consumed the high-carbohydrate diet. Overall, mice who consumed the standard chow displayed the best markers of health.
“Human beings and mice have very different metabolisms, but there are relevant lessons in this study for people,” said Vishal Singh, associate professor of nutritional sciences and senior author of the study. “Most people are aware that a balanced diet is important, but some people are attracted to diets with very high fat content – like the keto diet – for weight loss. This research points to very real harm to the liver that can occur when these diets are not used appropriately.”
Fats versus carbohydrates
In each experimental diet in the study, the protein level of the food was always 18% of the total calories, so only the fat-to-carbohydrate ratios differed. The high-fat diet contained 42% carbohydrates and 40% fats, the high-carbohydrate diet contained 70% carbohydrates and 11% fat and the ketogenic diet contained 1% carbohydrates and 81% fats.
The fats in these diets were largely saturated fats, which are a group of fats that are typically solid at room temperature. The American Heart Association recommends that saturated fats make up 6% or less of the total calories in a person’s diet.
The carbohydrates in these diets were largely refined, which are processed foods including white flour and added sugars. Scientific research has frequently connected refined carbohydrates to metabolic dysfunction and other harmful physical and mental health outcomes.
These diets were compared to a whole-grain rich chow that is a standard diet for laboratory mice. It contained 29% proteins, 57.5% carbohydrates and 13.5% fats.
The researchers measured blood sugar and a broad array of markers of liver function and health at regular intervals during the 16-week study. Other measurements were gathered after the experimental diets concluded.
“We wanted to understand how altering the balance of carbohydrates and fats would affect health when the diet was maintained for 16 weeks,” said Umesh Goand, postdoctoral researcher in the Penn State Department of Nutritional Sciences and first author of the study.
Keto and high-fat diets harmed liver and increased weight
In the ketogenic or ‘keto’ diet carbohydrate consumption is nearly eliminated. This induces a metabolic state called ketosis, where the body burns fat for fuel instead of glucose, the typical source of energy.
Results from the study demonstrated that the high-fat and keto diets promoted obesity, with the weight of mice on these diets doubling over the 16 weeks of the study. Mice on the control diet increased weight by around 10% – a normal rate for mice of that age – despite all mice in the study consuming roughly the same number of calories. In addition, the high-fat and keto diets impaired glucose tolerance and compromised liver function. Liver damage and elevated levels of blood sugar were observed after only two weeks of both diets.
Mice on the keto diet also developed elevated levels of triglycerides and showed increased levels of systemic inflammation. Additionally, they developed fat deposits in the liver and expressed genes associated with inflammation and liver scarring.
“The keto diet was very damaging to the livers and overall health of mice with regular weights,” Singh said, explaining that the body can utilise fat for energy, but there are metabolic consequences associated with the increase in fat processing. “People who hear about the keto diet’s reputation for weight reduction may be tempted to try it themselves. What this research says is – don’t! This diet should only be considered when properly supervised by a physician and/or dietician.”
Whole grains and carbohydrates
In comparison, mice on the high-carbohydrate diet did not continuously gain weight nor experience liver damage like those on the high-fat diets. Singh emphasized that a highly processed, carbohydrate-heavy diet is not inherently healthy, but it did less damage to the liver than the high-fat diets.
Mice on the whole-grain rich chow diet gained the least weight and demonstrated the best health indicators.
“A whole-grain-based diet is always a win – for mice or people,” Singh said.
The potential of fibre
In a separate experiment in the study involving mice with obesity, the high-fat and keto diets also led to further weight gain. However, when the keto diet was supplemented with fibre – a condition not tested in mice with normal weights – mice with obesity maintained more stable weight and better health indicators in several areas compared to mice on the high-fat diet or the keto diet without extra fibre.
The researchers also found that fibre supplementation did not hinder ketogenesis in mice who ate the keto diet. This is important, Singh said, because the keto diet is used for managing specific medical conditions, like epilepsy.
“Incorporating dietary fibres into the keto diet may reduce gastrointestinal complications associated with very high-fat diets while maintaining the therapeutic benefits of ketogenesis for patients,” Singh said.
Dietary choices are complex, but that does not make them equivalent
The important thing to remember, Singh said, is that diet is complex, and there is no one-size-fits-all solution.
“Over time, researchers have learned a lot about what is healthy or unhealthy based on an individual’s health status, but there is no single dietary magic bullet for weight loss or any other metabolic health concern,” Singh said. “Anyone who experiences health problems or is concerned about their diet should talk to their physician or a registered dietician to develop a plan, based on research, that fits their specific needs and life circumstances.”
Intermittent fasting is unlikely to lead to greater weight loss in overweight or obese adults than traditional dietary advice or doing nothing, a new Cochrane review finds.
Obesity is a significant public health problem that has become a leading cause of death in high-income countries. Worldwide adult obesity has more than tripled since 1975, according to the WHO. In 2022, 2.5 billion adults were overweight. Of these, 890 million were living with obesity.
Intermittent fasting has surged in popularity in recent years, fuelled by social media, lifestyle influencers, and claims of rapid weight loss and metabolic benefits.
No meaningful difference in weight loss
Researchers analysed evidence from 22 randomised clinical trials involving 1995 adults across North America, Europe, China, Australia, and South America. Trials examined multiple forms of intermittent fasting, including alternate-day fasting, periodic fasting, and time-restricted feeding. Most studies followed participants for up to 12 months.
The review compared intermittent fasting with traditional dietary advice and with no intervention. Intermittent fasting did not appear to have a clinically meaningful effect on weight loss compared to standard dietary advice or doing nothing.
Reporting of side effects was inconsistent across trials, making it difficult to draw firm conclusions. The evidence base remains limited, with only 22 trials, many with small sample sizes and inconsistent reporting.
Hype outpaces the evidence
First author Luis Garegnani also cautioned against the hype surrounding fasting online.
Intermittent fasting just doesn’t seem to work for overweight or obese adults trying to lose weight. It may be a reasonable option for some people, but the current evidence doesn’t justify the enthusiasm we see on social media.
—Luis Garegnani, Universidad Hospital Italiano de Buenos Aires Cochrane Associate Centre.
Few trials have looked at the long-term results of intermittent fasting. The authors stressed that obesity is a chronic condition, and short-term trials make it difficult to guide long-term decision-making for patients and clinicians.
The majority of the included studies enrolled predominantly white populations in high-income countries. As obesity is a rapidly growing crisis in low- and middle-income countries, further research is needed in these populations.
The authors therefore warn that these results may provide clues, but cannot be extrapolated to the entire population, as they may vary depending on sex, age, ethnic origin, disease status, or underlying eating disorders or behaviours.
With the current evidence available, it’s hard to make a general recommendation. Doctors will need to take a case-by-case approach when advising an overweight adult on losing weight.
—Eva Madrid, Cochrane Evidence Synthesis Unit Iberoamerica.
Participants stopped meals three hours before bed, dimmed the lights and extended their overnight fast by two hours
Photo by Cottonbro on Pexels
A new Northwestern Medicine study has personalised overnight fasting by aligning it with individuals’ circadian sleep-wake rhythm, an important regulator of cardiovascular and metabolic function, all without changing their caloric intake.
The study found that among middle-age and older adults who are at higher risk for cardiometabolic disease, extending the participants’ overnight fast by about two hours, dimming the lights and not eating for three hours prior to bedtime improved measures of cardiovascular and metabolic health during sleep, as well as during the daytime. Nighttime blood pressure fell by 3.5mmHg while heart rate dipped by 5% compared to controls. while adherence was good – nearly 90%.
“Timing our fasting window to work with the body’s natural wake-sleep rhythms can improve the coordination between the heart, metabolism and sleep, all of which work together to protect cardiovascular health,” said first author Dr. Daniela Grimaldi, research associate professor of neurology in the division of sleep medicine at Northwestern University Feinberg School of Medicine.
“It’s not only how much and what you eat, but also when you eat relative to sleep that is important for the physiological benefits of time-restricted eating,” said corresponding author Dr Phyllis Zee, director of the Center for Circadian and Sleep Medicine and the chief of sleep medicine in the department of neurology at Feinberg.
Previous research has found only 6.8% of US adults had optimal cardiometabolic health in 2017 to 2018. Poor cardiometabolic health can lead to chronic illness, including type 2 diabetes, non-alcoholic fatty liver disease and cardiovascular diseases.
Time-restricted eating has continued to surge in popularity because research has shown it can improve cardiometabolic health and rival traditional calorie‑restricted diets, but most studies have focused on how long people fast, not how their fast lines up with their sleep schedule – a key factor in metabolic regulation.
Given the nearly 90% adherence rate in the study, the study’s novel approach of leveraging the sleep period as an anchor for the timing of time-restricted eating may be a more accessible non-pharmacological strategy for improving cardiometabolic health, particularly in middle-aged and older adults who are at higher risk for cardiometabolic disease, the study authors said.
The study authors said they plan refine the protocol from this study and take it to larger multi-centre trials.
Improved blood pressure, heart rate, blood-sugar control
In the 7.5‑week study, people who finished eating at least three hours before going to bed saw meaningful improvements compared with those who kept their usual eating routines. They experienced:
Improved nighttime patterns in blood pressure (dipping by 3.5%) and heart rate (dipping by 5%): Their bodies showed a more natural drop in both measures during sleep, which is an important sign of cardiovascular health. Notably, their hearts beat faster during the day when they were active and slowed at night when they were resting. A stronger day-night pattern is linked to better cardiovascular health.
Better daytime blood‑sugar control: Their pancreas responded more efficiently when challenged with glucose, suggesting it could release insulin more effectively and keep blood sugar steadier.
In the study, 39 overweight/obese participants (36 to 75 years old) completed either an extended overnight fasting intervention (13 to 16 hours of fasting) or a control condition (habitual fast of 11 to 13 hours). Both groups dimmed the lights three hours before bedtime. The intervention group consisted of 80% women.
A new prospective cohort study by investigators from Mass General Brigham and colleagues analysed 131 821 participants from the Nurses’ Health Study (NHS) and Health Professionals Follow-Up Study (HPFS), finding that moderate consumption of caffeinated coffee (2-3 cups a day) or tea (1-2 cups a day) reduced dementia risk, slowed cognitive decline, and preserved cognitive function. Their results are published in JAMA.
“When searching for possible dementia prevention tools, we thought something as prevalent as coffee may be a promising dietary intervention – and our unique access to high quality data through studies that has been going on for more than 40 years allowed us to follow through on that idea,” said senior author Daniel Wang, MD, ScD, associate scientist with the Channing Division of Network Medicine in the Mass General Brigham Department of Medicine and assistant professor at Harvard Medical School. Wang is also an assistant professor in the Department of Nutrition at Harvard Chan School and an associate member at the Broad Institute. “While our results are encouraging, it’s important to remember that the effect size is small and there are lots of important ways to protect cognitive function as we age. Our study suggests that caffeinated coffee or tea consumption can be one piece of that puzzle.”
Early prevention is especially crucial for dementia, since current treatments are limited and typically offer only modest benefit once symptoms appear. Focus on prevention has led researchers to investigate the influences of lifestyle factors like diet on dementia development.
Coffee and tea contain bioactive ingredients like polyphenols and caffeine, which have emerged as possible neuroprotective factors that reduce inflammation and cellular damage while protecting against cognitive decline. Though promising, findings about the relationship between coffee and dementia have been inconsistent, as studies have had limited follow-up and insufficient detail to capture long-term intake patterns, differences by beverage type, or the full continuum of outcomes—from early subjective cognitive decline to clinically diagnosed dementia.
Data from the NHS and HPFS help to overcome these challenges. Participants repeated assessments of diet, dementia, subjective cognitive decline, and objective cognitive function and were followed for up to 43 years. Researchers compared how caffeinated coffee, tea, and decaffeinated coffee influenced dementia risk and cognitive health of each participant.
Of the more than 130 000 participants, 11 033 developed dementia. Both male and female participants with the highest intake of caffeinated coffee had an 18% lower risk of dementia compared with those who reported little or no caffeinated coffee consumption. Caffeinated coffee drinkers also had lower prevalence of subjective cognitive decline (7.8% versus 9.5%). By some measurements, those who drank caffeinated coffee also showed better performance on objective tests of overall cognitive function.
Higher tea intake showed similar results, while decaffeinated coffee did not – suggesting that caffeine may be the active factor producing these neuroprotective results, though further research is needed to validate the responsible factors and mechanisms.
The cognitive benefits were most pronounced in participants who consumed 2–3 cups of caffeinated coffee or 1–2 cups of tea daily. Contrary to several previous studies, higher caffeine intake did not yield negative effects – instead, it provided similar neuroprotective benefits to the optimal dosage.
“We also compared people with different genetic predispositions to developing dementia and saw the same results – meaning coffee or caffeine is likely equally beneficial for people with high and low genetic risk of developing dementia,” said lead author Yu Zhang, MBBS, MS, PhD student at Harvard Chan School and a research trainee at Mass General Brigham.
Following a Mediterranean diet is associated with a lower risk of all types of stroke among women, according to a study published on February 4, 2026, in Neurology® Open Access, an official journal of the American Academy of Neurology. The study does not prove that the Mediterranean diet is the cause of the lower risk of stroke; it only shows an association.
The diet was associated with a lower risk of stroke overall, as well as ischaemic stroke and haemorrhagic stroke. The Mediterranean diet includes a high intake of vegetables, legumes, fruits, fish and healthy fats such as olive oil, and a low intake of dairy products, meats and saturated fatty acids.
“Our findings support the mounting evidence that a healthy diet is critical to stroke prevention,” said study author Sophia S. Wang, PhD, of City of Hope Comprehensive Cancer Center in Duarte, California. “We were especially interested to see that this finding applies to haemorrhagic stroke, as few large studies have looked at this type of stroke.”
The study involved 105 614 women with an average age of 53 at the start of the study who had no history of stroke. The participants filled out a questionnaire at the start of the study about their diet. Participants were given a score of zero to nine based on how closely they followed the Mediterranean diet. People received one point if they consumed above the overall average in the population in these categories: whole grain cereals, fruits, vegetables, legumes, olive oil and fish, plus drinking a moderate amount of alcohol.
They also received one point if they consumed a below-average amount of red meat and dairy products. A total of 30% of participants had scores of six to nine – the highest group. And 13% had scores of zero to two, the lowest group.
The participants were followed for an average of 21 years. During that time, 4083 strokes occurred, with 3358 ischaemic strokes and 725 haemorrhagic strokes. For ischaemic strokes, there were 1058 among the 31 638 people in the highest group compared to 395 cases among the 13 204 people in the lowest group.
For haemorrhagic stroke, there were 211 strokes among those in the highest group, compared to 91 among the lowest group. When researchers adjusted for other factors that could affect stroke risk, such as smoking, physical activity and high blood pressure, they found that those in the highest group were 18% less likely to have a stroke than those in the lowest group. They were 16% less likely to have an ischaemic stroke and 25% less likely to have a haemorrhagic stroke.
“Stroke is a leading cause of death and disability, so it’s exciting to think that improving our diets could lessen our risk for this devastating disease,” said Wang. “Further studies are needed to confirm these findings and to help us understand the mechanisms behind them so we could identify new ways to prevent stroke.”
A limitation of the study is that people reported their own diet information, so they may not have remembered correctly.
Higher intake of food preservatives, widely used in industrially processed foods and beverages to extend shelf-life, is associated with a modestly increased risk of cancer, finds a study from France published byThe BMJ.
While further research is needed to better understand these links, the researchers say these new data call for the re-evaluation of regulations governing the use of these additives by the food industry to improve consumer protection.
Preservatives are substances added to packaged foods to extend shelf life. Some experimental studies have shown that certain preservatives can damage cells and DNA, but firm evidence linking preservatives to cancer risk remains scarce.
To address this, researchers set out to examine the association between exposure to preservative food additives and risk of cancer in adults, using detailed dietary and health data from 2009 to 2023.
Their findings are based on 105,260 participants aged 15 years and older (average age 42 years; 79% women) enrolled in the NutriNet-Santé cohort study who were free of cancer and completed regular 24 hour brand-specific dietary records over an average 7.5 year period. Health questionnaires and official medical and death records were then used to track cancer cases up to 31 December 2023.
A total of 17 individual preservatives were analysed including citric acid, lecithins, total sulfites, ascorbic acid, sodium nitrite, potassium sorbate, sodium erythorbate, sodium ascorbate, potassium metabisulfite, and potassium nitrate.
Preservatives were grouped into non-antioxidants (which inhibit microbial growth or slow chemical changes that lead to spoilage) and antioxidants (which delay or prevent food deteriorating by removing or limiting oxygen levels in packaging).
During the follow-up period, 4,226 participants received a diagnosis of cancer, comprising 1,208 breast, 508 prostate, 352 colorectal, and 2,158 other cancers.
Of the 17 individually studied preservatives, 11 were not associated with cancer incidence, and no link was found between total preservatives and cancer incidence.
However, higher intakes of several preservatives (mostly non-antioxidants including potassium sorbate, potassium metabisulfite, sodium nitrite, potassium nitrate, and acetic acid) were associated with higher risk of cancers compared with non-consumers or lower consumers.
For example, total sorbates, specifically potassium sorbate, was associated with a 14% increased risk of overall cancer and a 26% increased risk of breast cancer, while total sulfites were associated with a 12% increased risk of overall cancer.
Sodium nitrite was associated with a 32% increased risk of prostate cancer, while potassium nitrate was associated with an increased risk of overall cancer (13%) and breast cancer (22%).
Total acetates were associated with an increased risk of overall cancer (15%) and breast cancer (25%), while acetic acid was associated with a 12% increased risk of overall cancer.
Among antioxidant preservatives, only total erythorbates and specific sodium erythorbate were found to be associated with higher incidence of cancer.
While more studies are needed to better understand these potential risks, the researchers note that several of these compounds can alter immune and inflammatory pathways, possibly triggering the development of cancer.
This is an observational study, so no firm conclusions can be drawn about cause and effect, and the researchers can’t rule out the possibility that other unmeasured factors may have influenced their results.
However, they say this was a large study based on detailed dietary records linked to food databases over 14 years and results are consistent with existing experimental data suggesting adverse cancer related effects of several of these compounds.
As such, they conclude: “This study brings new insights for the future re-evaluation of the safety of these food additives by health agencies, considering the balance between benefit and risk for food preservation and cancer.”
In the meantime, they call on manufacturers to limit the use of unnecessary preservatives, and support recommendations for consumers to favour freshly made, minimally processed foods.
From a policy perspective, preservatives offer clear benefits by extending shelf life and lowering food costs, which can be particularly important for populations with lower incomes, point out US researchers in a linked editorial.
However, they say the widespread and often insufficiently monitored use of these additives, with uncertainties of their long term health effects, call for a more balanced approach.
Findings from NutriNet-Santé may prompt regulatory agencies to revisit existing policies, such as setting stricter limits on use, requiring clearer labeling, and mandating disclosure of additive contents, while collaborative global monitoring initiatives, similar to those implemented for trans fatty acids and sodium, could also support evidence based risk assessments and guide reformulation by the food industry, they write.
“At the individual level, public health guidance is already more definitive about the reduction of processed meat and alcohol intake, offering actionable steps even as evidence on the carcinogenic effects of preservatives is evolving,” they conclude.
Salk Institute scientists uncover key role of kidneys in clearing inflammation from body, and show amino acid supplementation boosts this effect in mice
The latest findings from Salk scientist Janelle Ayres’s lab show that a deceptively simple dietary supplement could alter disease trajectory and make the difference between life and death for patients. Credit: Salk Institute
Disease trajectory is a unique journey from injury or infection, mediated by variable symptoms toward either recovery or death. It varies from person to person based on history, sex, age, and many other factors. Salk scientist Janelle Ayres, PhD, has spent decades unravelling the ways the body directs this journey – why some get sick and die while others go unscathed, and what sorts of methods could be used to shift trajectories of disease and death to ones of health and survival.
For many, inflammation is the ultimate cause of a downward trajectory toward death. Inflammation is a double-edged sword: a powerful weapon against intruders but an equally powerful generator of bodily damage if not properly regulated.
Since infections are some of the strongest drivers of inflammation-induced damage, the Salk team used a mouse model of infection to find that dietary supplementation of the amino acid methionine protected infected mice against inflammation-related wasting, blood-brain barrier dysfunction, and death. Methionine was accomplishing all this by boosting kidney filtration, revealing an underappreciated role the kidneys play in a successful journey from infection back to health.
The findings, published in Cell Metabolism on January 22, 2026, reveal the big impact that small dietary tweaks can have on disease trajectory, lighting the way to therapeutic strategies that steer patients from death to recovery. Methionine supplementation may be a useful tool for a variety of inflammatory conditions, as well as for patients with kidney disease or failure, or those undergoing dialysis.
“Our study indicates that small biological differences, including dietary factors, can have large effects on disease outcomes,” says senior author Ayres, professor and holder of the Salk Institute Legacy Chair at Salk, as well as a Hughes Medical Institute Investigator. “Our discovery of a kidney-driven mechanism that limits inflammation, together with the protective effects of methionine supplementation in mice, points toward the potential of nutrition as a mechanistically informed medical intervention that can direct and optimise the paths people take in response to insults that cause disease.”
Shifting the focus on inflammation
Research on the balance between too much and too little inflammation has been tricky, and mainly focused on how inflammatory responses are switched on and off. Ayres’s team is shifting the focus from these binary on/off mechanisms to studying how the body toggles the immune response higher or lower through the release and accumulation of pro-inflammatory cytokines.
“Pro-inflammatory cytokines are ultimately what leads to sickness and death in a lot of cases,” says first author Katia Troha, PhD, a postdoctoral researcher in Ayres’s lab. “The immune system has to balance inflammation to attack the invader without harming healthy cells in the body. Our job is to find the mechanisms it uses to do that, so that we can target them to improve patient outcomes.”
How can kidney function help reduce inflammation?
To understand how the body regulates its cytokine levels, the researchers used a mouse model of systemic inflammation induced by the pathogen Yersinia pseudotuberculosis. The first thing they noticed was that the infected mice were not eating as much – a sign of likely metabolic changes. To look at the nutritional status, the researchers looked at the levels of circulating amino acids, which are protein building blocks that support cellular health throughout the body.
Infected mice showed depressed methionine levels – an essential amino acid found in our everyday diets. Curious, Troha decided to feed a new batch of mice with methionine-supplemented chow, and surprisingly, these mice were protected against the infection.
Further experiments showed that methionine reduced circulating cytokine levels by partnering with a surprising ally: the kidneys. Methionine increased the kidneys’ filtration capacity, improving blood flow and helping the body excrete pro-inflammatory cytokines through the urine. Importantly, this methionine-kidney effect cleared excess cytokines without hindering other key aspects of the immune response.
Curious whether methionine’s effect was present in other conditions, the researchers also looked at sepsis and kidney injury models. They found that methionine was also protective for these mice, supporting that methionine may be a useful tool in other inflammatory disease settings.
Can dietary changes boost kidney performance?
By supplementing their diets with methionine, Salk scientists were able to give infected mice entirely different disease trajectories. The amino acid boosted the animals’ kidney function and protected them against wasting, blood-brain barrier dysfunction, and death without hindering their bodies’ ability to fight and kill Yersinia pseudotuberculosis.
And the sepsis and kidney injury models show these effects extend to other infections and inflammatory conditions, too, making methionine a potentially useful tool for the treatment of infectious diseases, particularly in cases of kidney disease or failure, or for patients undergoing dialysis.
“Our findings add to a growing body of evidence that common dietary elements can be used as medicine,” says Ayres. “By studying these basic protective mechanisms, we reveal surprising new ways to shift individuals that are fated to develop disease and die onto trajectories of health and survival. It may one day be possible for something as simple as a supplement with dinner to make the difference between life and death for a patient.”
While the results are promising, the researchers note that efficacy in humans is yet to be tested. Follow-up studies will explore the mechanisms by which methionine acts, whether other amino acids have similar or complementary effects, and how this may all translate to humans.
Martha Field, right, assistant professor in the Division of Nutritional Sciences, works with Chloe Purello in her Kinzelberg Hall lab. Jason Koski/Cornell University
Vitamin B12 is long understood as a vital nutrient required for red blood cell formation and nerve function, but a new Cornell University study suggests its role in human biology is far more intricate, with implications for aging, metabolism and disease prevention.
The research, published January 19 in the Journal of Nutrition, reports previously unrecognised pathways by which B12 influences cellular metabolism and uncovers biomarkers that may identify early nutritional stress far before classic deficiency symptoms appear.
“This is the first study that shows B12 deficiency affects skeletal muscle mitochondrial energy production,” said corresponding author Martha Field, PhD, associate professor in the Division of Nutritional Sciences and in the College of Human Ecology. “It’s highly relevant because muscles have high energy demands. More importantly, my co-author, Anna Thalacker-Mercer from the University of Alabama at Birmingham, wondered if B12 supplementation in aged mice would improve muscle mitochondrial function – and it did.”
Up until now, most research has focused on B12 deficiency and the resulting clinical syndromes – megaloblastic anemia, neuropathy and cognitive decline – rather than its deeper mechanistic roles.
At Cornell, a team including Field and two of her former lab members, first authors Luisa Castillo, PhD and Katarina Heyden, PhD, set out to probe those mechanisms, mapping how B12 interacts with lipid metabolism, organelle stress pathways and epigenetic regulation. What emerged was startling: The vitamin appears to act as a gatekeeper of multiple “hub” pathways, meaning that its insufficiency may ripple far beyond the classic symptoms.
“Another thing we observed in mice is that B12 deficiency seemed to inhibit growth or maintenance of muscle mass,” Field said. “It seems that low B12 status is associated with lower muscle mass and maybe muscle strength.”
B12 deficiency remains common worldwide, especially among older adults and in low-income settings where meat consumption (a major B12 source) is limited. According to one estimate, one in four older adults in developed countries may show suboptimal B12 status. This new insight underscores the urgency of screening and intervention.
This work also intersects with a growing body of evidence that micronutrient insufficiency – not complete deficiency – contributes significantly to chronic disease. Global public-health data indicate that while many developed countries see little outright B12 deficiency, suboptimal status remains widespread in older adults and among vegans, vegetarians or individuals with malabsorption. The study suggests that even “marginal” B12 status may compromise resilience to metabolic stress, immune challenge and accelerated aging.
From a clinical-science perspective, the authors propose that B12-based biomarkers could inform more personalised nutrition strategies. Instead of one-size-fits-all supplement guidelines, future nutrition guidance might tailor B12 intake to individual metabolic and lifestyle profiles – a shift toward precision nutrition. Such an approach aligns with the broader vision of integrating nutrient science with systems biology.
The findings are based on cell models and require confirmation in humans, Field said.
“We want to understand the whole causal pathway – understanding the molecules and mechanisms,” Field said. “This sets the stage for a future controlled human trial.”
When Americans begin taking appetite-suppressing drugs like semaglutide, the changes extend well beyond the bathroom scale. According to new research, the medications are associated with meaningful reductions in how much households spend on food, both at the grocery store and at restaurants.
The study, published December 18 in the Journal of Marketing Research, links survey data on GLP-1 receptor agonist use with detailed transaction records from tens of thousands of U.S. households. The result is one of the most comprehensive looks yet at how GLP-1 adoption is associated with changes in everyday food purchasing in the real world.
The headline finding is striking: Within six months of starting a GLP-1 medication, households reduce grocery spending by an average of 5.3%. Among higher-income households, the drop is even steeper, at more than 8%. Spending at fast-food restaurants, coffee shops and other limited-service eateries falls by about 8%.
Among households who continue using the medication, lower food spending persists at least a year, though the magnitude of the reduction becomes smaller over time, say co-authors, assistant professor Sylvia Hristakeva and professor Jura Liaukonyte, both in the Charles H. Dyson School of Applied Economics and Management in the Cornell SC Johnson College of Business.
“The data show clear changes in food spending following adoption,” Hristakeva said. “After discontinuation, the effects become smaller and harder to distinguish from pre-adoption spending patterns.”
Unlike previous studies that relied on self-reported eating habits, the new analysis draws on purchase data collected by Numerator, a market research firm that tracks grocery and restaurant transactions for a nationally representative panel of about 150 000 households. The researchers matched those records with repeated surveys asking whether household members were taking GLP-1 drugs, when they started and why.
That combination allowed the team to compare adopters with similar households that did not use the drugs, isolating changes that occurred after medication began.
The reductions were not evenly distributed across the grocery store.
Ultra-processed, calorie-dense foods – the kinds most closely associated with cravings – saw the sharpest declines. Spending on savory snacks dropped by about 10%, with similarly large decreases in sweets, baked goods and cookies. Even staples like bread, meat and eggs declined.
Only a handful of categories showed increases. Yogurt rose the most, followed by fresh fruit, nutrition bars and meat snacks.
“The main pattern is a reduction in overall food purchases. Only a small number of categories show increases, and those increases are modest relative to the overall decline,” Hristakeva said.
The effects extended beyond the supermarket. Spending at limited-service restaurants such as fast-food chains and coffee shops fell sharply as well.
The study also sheds light on who is taking GLP-1 medications. The share of U.S. households reporting at least one user rose from about 11% in late 2023 to more than 16% by mid-2024. Weight-loss users skew younger and wealthier, while those taking the drugs for diabetes are older and more evenly distributed across income groups.
Notably, about one-third of users stopped taking the medication during the study period. When they did, their food spending reverted to pre-adoption levels – and their grocery baskets became slightly less healthy than before they started, driven in part by increased spending on categories such as candy and chocolate.
That movement underscores an important limitation, the authors caution. The study cannot fully separate the biological effects of the drugs from other lifestyle changes users may make at the same time. However, evidence from clinical trials, combined with the observed reversion in spending after discontinuation, suggests appetite suppression is likely a key mechanism behind the spending changes.
The findings carry implications far beyond individual households.
For food manufacturers, restaurants and retailers, widespread GLP-1 adoption could mean long-term shifts in demand, particularly for snack foods and fast food. Package sizes, product formulations and marketing strategies may need to change. For policymakers and public-health experts, the results add context to ongoing debates about the role of medical treatments in shaping dietary behavior – and whether biologically driven appetite changes succeed where taxes and labels have struggled.
“At current adoption rates, even relatively modest changes at the household level can have meaningful aggregate effects,” Hristakeva said. “Understanding these demand shifts is therefore important for assessing food markets and consumer spending.”
