A study of 12 healthy adults suggests that extended fasting does much more than simply force the body to burn fat.

Researchers tracked around 3,000 proteins in the blood of volunteers during a seven-day water-only fast.

They found the expected early change first.

Within two to three days, the body shifted from using glucose to relying more heavily on stored fat.

That part was not surprising.

What caught the researchers’ attention was what happened after that.

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The largest and most coordinated molecular changes appeared after around three days without calories.

More than a third of the proteins measured changed significantly over the course of the fast.

Some of the strongest shifts involved proteins linked to tissue structure, inflammation, metabolism and even support systems in the brain.

That suggests prolonged fasting pushes the body into a distinct biological state rather than simply extending the first day or two of calorie deprivation.

The pattern was also fairly consistent between participants, which makes the result more convincing.

Still, there are obvious caveats.

This was a very small study in healthy people.

It does not prove that fasting for seven days is good for the general population, and it certainly does not prove that it is safe for everyone.

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In fact, the researchers themselves highlight possible downsides, including inflammatory stress responses and changes in clotting-related pathways in later analyses.

That matters because prolonged fasting can also bring dehydration, electrolyte imbalance, dizziness and loss of lean tissue.

So the findings are best seen as a map of what fasting does biologically, not as a blanket recommendation to try it.

The science is fascinating.

The lifestyle advice is much less straightforward.

A new study suggests diets high in ultra-processed foods may be linked to a much higher risk of asthma in children.

Researchers followed 691 Spanish children who were aged four or five at the start of the study.

Parents reported the children’s diets using a detailed questionnaire, and the researchers classified foods using the NOVA system, which groups foods by processing rather than by nutrients alone.

The children were then followed for an average of 3.4 years.

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During that time, higher intake of ultra-processed foods was associated with a sharply increased risk of asthma.

Children getting more than 30% of their daily energy from ultra-processed foods had nearly four times the risk of asthma compared with those with the lowest intake.

The researchers also found a dose-response pattern.

As the proportion of ultra-processed food rose, so did the apparent asthma risk.

Interestingly, the same pattern was not seen for other allergic conditions.

That suggests the effect may not be acting through classic allergy pathways.

Instead, the authors think ultra-processed foods may be contributing to a different type of inflammation that affects the airways.

This is still an observational study, so caution is needed.

Families whose children eat more ultra-processed food may differ in other ways too, even when researchers adjust for things like weight and screen time.

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But the study fits a wider pattern.

Ultra-processed foods are increasingly being linked to poor health outcomes across multiple systems, and childhood is unlikely to be an exception.

The practical message is not complicated.

A child’s diet does not need to be perfect, but when packaged snacks, fizzy drinks and sweetened cereals start becoming a large share of daily calories, it may be doing more harm than just crowding out healthier food.

Researchers in Minnesota have been looking at how bacteria in the mouth talk to each other.

That may sound abstract, but it could matter a lot for gum disease.

Dental plaque is not just a random mass of microbes.

It develops in stages, and different bacteria use chemical signals to coordinate who grows and when.

Some of those signals are called AHLs.

The new study suggests that if you interrupt those signals, you may be able to steer plaque towards a healthier state.

In the lab, removing AHL signals with specialised enzymes increased populations of bacteria associated with good oral health.

At the same time, bacteria linked to gum disease were reduced.

That is potentially important because most traditional approaches focus on killing bacteria as broadly as possible.

The problem with that strategy is obvious.

Not all bacteria in the mouth are harmful, and wiping them out indiscriminately can create its own problems.

A more selective approach would be to change microbial behaviour rather than simply trying to destroy everything.

The study also found that oxygen levels changed the way this signalling worked.

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Above the gumline and below it, the same signals appeared to have different effects.

That means the ecology of the mouth is even more complex than it looks.

This is still very early work and far from a new dental treatment.

But the principle is interesting.

If gum disease can be influenced by disrupting bacterial communication, future treatment may become more about balance than brute force.

A new national study has identified five broad dietary patterns among older adults in the United States.

At first glance, that might sound descriptive rather than useful.

But the patterns reveal some fairly stark divides in diet quality, health and food security.

The largest group relied heavily on smoothies, juices, soups and grain drinks.

This pattern had moderate overall diet quality, but also the lowest protein and energy intake.

That raises concerns about undernutrition and muscle loss, especially in older adults who may already be vulnerable.

A second pattern, built around yoghurt and cooked cereals, had the highest diet quality score and was linked to better overall health.

There was also a vegetable-and-seafood pattern that resembled a Mediterranean-style diet and had among the lowest rates of food insecurity.

By contrast, processed-food-heavy patterns based on cured meats, pastries, sandwiches, quick breads, alcohol and meat had the poorest diet quality.

These groups were more likely to include people with obesity, smoking history and other health risks.

The study also found that food insecurity was not spread evenly.

Some of the softer-food patterns seemed to reflect a mix of financial pressure, physical limitations and poorer health rather than simple preference.

That is the important point.

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Older adults do not just eat the way they do because of taste.

Income, mobility, dentition, cooking ability and access to food all shape the result.

So if policymakers want to improve nutrition in later life, telling people to eat better is not enough.

The barriers are often practical, physical and economic.

Bariatric surgery can be highly effective for obesity and type 2 diabetes, but not everyone gets the same result.

A new study suggests part of that difference may come down to what happens to the gut microbiome afterwards.

Researchers followed changes in gut bacteria after gastric bypass and sleeve gastrectomy.

They found that patients with better glycaemic improvement tended to show greater bacterial gene richness and more microbial activity linked to fermentation, including butyric acid production.

That matters because butyrate and related compounds are thought to influence metabolism, inflammation and insulin sensitivity.

In other words, the microbiome may not just be along for the ride.

It may be helping shape the outcome.

The study also found some differences between procedures.

Gastric bypass tended to produce more consistent microbiome changes, while sleeve gastrectomy led to a more individual response.

That fits with the idea that different procedures alter the gut environment in different ways.

The most important point is that the metabolic benefit of surgery may not be explained by weight loss alone.

Changes in gut bacteria and their function also seem to matter.

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That opens up interesting possibilities.

If researchers can work out which microbial changes are most helpful, they may be able to boost those changes with diet, probiotics or other targeted treatments.

That is still speculative.

But this study adds to a growing picture that bariatric surgery is not just a mechanical or hormonal intervention.

It is also a major ecological event inside the gut.

One of the biggest problems in cell-based treatments for type 1 diabetes is keeping transplanted insulin-producing cells alive.

Many die early because they do not get an adequate blood supply quickly enough.

Researchers at McGill say they may have found a way round that problem.

They have developed an implant with a pre-formed network of artificial blood vessels.

The idea is to connect insulin-producing cells to the circulation from the start, while also placing them behind a protective barrier that helps reduce immune rejection.

That could make a big difference.

Traditional islet transplantation can work, but donor tissue is scarce and lifelong immunosuppression is often needed.

This new device is designed to use lab-grown cells instead.

That would make supply less dependent on deceased donors.

It also offers a more structured, engineered system rather than simply injecting cells and hoping they settle in.

The researchers describe it as starting to look like a true artificial organ.

That may sound grand, but the concept is straightforward.

Insulin-producing cells need oxygen, nutrients and rapid access to the blood if they are going to function well.

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A device that solves those problems while blocking the immune system would address some of the biggest obstacles in the field.

For now, though, this is preclinical work.

It is promising engineering, not a cure that is about to arrive in clinic.

Still, it is one of the more practical attempts to deal with the blood supply problem that has held back cell therapy for type 1 diabetes for years.

Metformin has been used for decades, but scientists have never completely agreed on how it works.

The usual explanation has been that it mainly acts on the liver to reduce glucose production.

A new study suggests the gut may be the more important target.

Researchers found that metformin seems to block part of the mitochondria’s energy machinery in intestinal cells.

That forces the gut to use more glucose itself.

In simple terms, the intestine starts acting like a sponge, pulling more glucose out of the bloodstream.

The team tested this in mice engineered so that their gut cells were resistant to this mitochondrial effect.

In those mice, metformin lost much of its glucose-lowering power.

That strongly suggests the gut is not just involved, but central to the drug’s action.

The finding also helps explain a few long-standing clinical observations.

People on metformin often have lower blood sugar after meals.

They also tend to have lower citrulline levels and higher GDF15, both of which make more sense if the drug is stressing intestinal metabolism.

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The study also found parallels with berberine, a popular supplement sometimes marketed online as a natural alternative to diabetes drugs.

The researchers say berberine may be acting through the same pathway, although metformin has the far stronger evidence base.

This is a mouse study, so caution is needed.

But it is a serious piece of work and it adds to a growing shift in how metformin is understood.

The drug may still be old, but it clearly still has surprises left in it.

A large new study suggests exposure to PFAS is now so widespread that it is close to universal.

Researchers tested 10,566 blood samples and found at least one PFAS in 98.8% of them.

More strikingly, 98.5% of people were carrying multiple PFAS at the same time.

PFAS are often called forever chemicals because they do not break down easily and can build up in the environment and in the body.

They are used in a huge range of products, from non-stick cookware and stain-resistant fabrics to electronics and firefighting foam.

That is why the findings are worrying, but not exactly surprising.

The more useful part of the study is that it looked at combinations, not just single compounds.

That matters because people are rarely exposed to one PFAS in isolation.

They are usually exposed to mixtures, and those mixtures may behave differently from any one chemical on its own.

The most common pattern in this study involved five PFAS together.

Researchers say this should push risk assessment towards mixture-based thinking rather than treating each compound as a separate issue.

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There are limits.

The study does not tell us where the exposures came from or what health effects these specific combinations are causing.

It also cannot capture every PFAS that may have been present.

But it does underline the scale of the issue.

For many people, PFAS exposure is no longer a rare environmental problem. It is part of everyday background biology.

A new study suggests you may not need to stand up to do useful balance work.

Researchers in Japan tested a short, low-intensity exercise routine performed entirely while lying on the back.

The idea was to train the core and legs to work together more effectively.

That matters because balance depends on the trunk and lower body coordinating well, not just on leg strength alone.

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The exercises were simple.

They included tightening the abdominal muscles, making small pelvic lifts, sliding the heels along the floor and controlled ankle and toe movements.

Participants did the routine once a day for two weeks.

Afterwards, they showed less body sway when standing still and were quicker in a side-step agility test.

That suggests the routine may have improved coordination and postural control.

There were no major gains in muscle strength or explosive power.

So this does not appear to be a strength-building programme.

It looks more like a coordination and control programme.

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That may still be useful, especially for older adults or people who want a low-risk way to work on balance.

The study is small, and most of the early testing was done in healthy adults rather than people at high risk of falls.

So the findings should be kept in proportion.

Still, the basic message is sensible.

Simple, safe movements done consistently may improve balance more than people assume.

A new study suggests egg intake may be linked to a lower risk of Alzheimer’s disease in older adults.

Researchers followed around 40,000 people aged 65 and over and linked dietary data with Medicare records over an average of more than 15 years.

They found that people who ate eggs regularly were less likely to be diagnosed with Alzheimer’s disease.

The strongest association was seen in those eating eggs at least five times a week.

That group had up to a 27% lower risk compared with people who never ate eggs.

Even smaller amounts were linked to lower risk, which makes the result a bit more plausible than a simple all-or-nothing effect.

Why might eggs matter?

They contain several nutrients relevant to brain health, including choline, lutein, zeaxanthin, omega-3 fats and phospholipids.

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Choline is especially important because it helps make acetylcholine, a neurotransmitter involved in memory and communication between nerve cells.

All that said, this is not proof that eggs protect the brain.

People who eat eggs regularly may differ in other ways too, including their overall diet and lifestyle.

The researchers themselves stress that eggs should be seen as part of a broader healthy eating pattern, not as a magic food.

That is the right note to end on.

This is a useful and interesting association, but it is not a reason to oversell eggs as a stand-alone dementia prevention strategy.

A new study suggests smoking during pregnancy may leave offspring more vulnerable to metabolic disease later in life, especially if they also adopt a poor diet as adults.

Researchers used a mouse model to test what happened when prenatal smoke exposure was followed by a high-fat, high-sugar diet in early adulthood.

The idea was to look at a double-hit effect.

First, the body is exposed to cigarette smoke before birth. Later, it is exposed to the kind of Western diet already linked to obesity and metabolic disease.

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The results suggest that combination may be worse than either factor on its own.

Male mice exposed to smoke in the womb and then given the unhealthy diet had more body fat and a worse lipid profile than mice in any other group.

Mice with no smoke exposure and a low-fat diet had the healthiest profile.

Those exposed to only one of the two factors tended to sit somewhere in the middle.

That pattern matters because it suggests the prenatal exposure may prime the body for later harm rather than causing the whole problem by itself.

The researchers think changes in the liver and fat tissue may help explain this.

In other words, cigarette exposure before birth may alter the way the body handles energy and fat long before obvious disease appears.

There are some important limits.

This was a mouse study, not a human one.

It also ran for a relatively short period once the offspring reached adulthood, and the strongest effects were seen in male mice.

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So this is not proof that the exact same pattern happens in people.

Still, the message is hard to ignore.

Pregnancy exposures can have long tails, and later lifestyle may either worsen or soften the damage.

For people who know they were exposed to smoking in the womb, the study is another reminder that diet and metabolic health may deserve especially close attention.

Some days everything feels straightforward.

Other days even simple tasks feel strangely hard.

A new study suggests that difference is not just in your imagination.

Researchers followed university students over 12 weeks and tracked how daily changes in mental sharpness affected what they planned and what they actually completed.

On sharper days, students set more ambitious goals and were more likely to follow through.

On foggier days, even routine tasks became harder.

The researchers estimate that being above or below your usual level of mental sharpness can shift productivity by about 30 to 40 minutes in a single day.

Across the gap between your best and worst days, that can add up to around 80 minutes.

That is a meaningful difference.

Importantly, these day-to-day swings were not explained away by personality.

Traits such as grit or self-control mattered overall, but they did not protect people from having bad days.

The study also looked at what seemed to influence mental sharpness.

More sleep than usual helped.

Earlier times of day helped too, while performance tended to decline later on.

Depressive mood was linked to worse sharpness.

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Workload showed a more mixed pattern.

A short burst of intense effort could sharpen performance in the moment, but sustained overwork eventually pushed things in the other direction.

That fits with what most people already suspect.

You can push hard for a while, but not indefinitely.

The practical lesson is sensible rather than revolutionary.

Sleep matters, burnout matters and there is no point pretending every day is equal.

Sometimes the reason you got less done is not laziness. Sometimes your brain was simply not firing as well as usual.

First it was Ozempic butt, but now, over in America, Hershey says one unexpected group is helping drive sales of gum and mints: people taking GLP-1 weight loss drugs.

On a recent earnings call, chief executive Kirk Tanner said appetite suppressants are changing the way some consumers snack.

People may be eating less overall, but they may also be buying more products such as mints and chewing gum.

He said Hershey had seen strong demand for its gum and mint range, with Ice Breakers sales up 8% over the quarter.

The company believes part of that growth is linked to GLP-1 use.

That claim is not as odd as it first sounds.

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Doctors have noted that some people taking drugs such as Ozempic and Wegovy report bad breath, unpleasant burping or a fishy smell on the breath.

The phrase ‘Ozempic breath’ has started doing the rounds online, although it is not a formal medical diagnosis.

Drug makers do not list bad breath itself as an official side effect.

But they do list related problems that could help explain it.

Burping, nausea and vomiting are all recognised side effects of GLP-1 drugs, and any of those could make breath smell worse for some users.

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There are other possible explanations too.

Eating less, changes in digestion, slower stomach emptying and dehydration could all potentially affect breath quality.

That means the gum and mint trend is plausible, but still not fully pinned down.

It is also a reminder that the real-world effects of GLP-1 drugs are often broader than the trial headlines suggest.

Some change appetite, some change food choices and some may simply leave people reaching for a mint.

A large study from the University of Sydney offers a fairly encouraging message for people who spend much of the day sitting.

More daily steps were linked to lower risks of death and cardiovascular disease, regardless of how sedentary people were.

The researchers analysed data from more than 72,000 adults in the UK Biobank.

Participants wore accelerometers that measured both steps and sedentary time.

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Over an average follow-up of nearly seven years, those who walked more had lower risks.

The strongest reduction in risk was seen at around 9,000 to 10,000 steps a day.

At that level, mortality risk was around 39% lower and cardiovascular disease risk was around 21% lower.

But one of the most useful findings is that the benefits did not suddenly appear at 10,000 steps.

About half of the total risk reduction was already seen at roughly 4,000 to 4,500 steps a day.

That matters because it makes the message more realistic.

Not everyone is going to hit 10,000 steps, but many people could still do meaningfully better than they are doing now.

The authors are careful not to present this as a free pass for sitting all day.

Long sedentary time is still not ideal.

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But the study suggests that if sitting is hard to avoid because of work or other circumstances, increasing daily movement can still make a noticeable difference.

This was an observational study, so it cannot prove that the extra steps directly caused the lower risk.

Even so, the overall message is both plausible and useful.

Walking more is one of the simplest health interventions most people can actually do, and this study suggests it is worth doing even if the rest of the day is spent behind a desk.

Fitness trackers and health apps are often sold as useful tools for self-improvement.

For many people, they are.

But new research suggests they can also backfire.

Researchers from UCL and Loughborough University analysed tens of thousands of posts on X about popular fitness apps.

They focused on posts with negative sentiment and found repeated patterns.

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Users described feeling ashamed when they logged unhealthy food, irritated by app notifications and disappointed when they failed to hit goals.

Some also described becoming demotivated and giving up altogether.

That is the opposite of what these apps are supposed to do.

The problem, according to the researchers, is that many of these platforms use rigid targets that do not reflect real life.

Calories, steps and exercise goals can be treated as if they are the whole story, even when people are tired, stressed, unwell or simply having an off day.

In some cases, users reported targets that seemed absurd or unhealthy.

That highlights a wider issue.

An algorithm may be good at setting numerical goals, but not at understanding a person’s actual life.

The study does not say fitness apps are harmful across the board.

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The researchers themselves note that they only looked at negative posts, not the overall balance of benefits and harms.

Still, the warning is a fair one.

If these tools are going to support long-term behaviour change, they need to do more than punish people for falling short.

Health is not just about hitting numbers – as people with diabetes know all too well.

A new analysis suggests people in the UK are now spending fewer years in good health than they were a decade ago.

Healthy life expectancy has dropped to just under 61 for both men and women.

That is different from overall life expectancy, which has remained broadly stable.

In simple terms, people are not necessarily dying much earlier, but they are spending more of their lives in poor health.

That is a serious shift.

According to the report, the UK is one of only a handful of wealthy countries to see healthy life expectancy go backwards, and the fall has been one of the steepest.

The regional picture is even worse.

People in the wealthiest areas can expect around 20 more years in good health than those in the poorest.

In Richmond, healthy life expectancy is around 69 to 70 years.

In places such as Blackpool and Hartlepool, it is closer to 51.

That is not a small gap.

It is a profound inequality in the basic experience of life.

The report points to poverty, poor housing, obesity and the lasting effects of the Covid pandemic as part of the explanation.

Mental ill health, especially among younger people, is also a growing concern.

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The economic implications are obvious.

If more people fall into poor health before pension age, more people struggle to stay in work and more pressure falls on public services.

This is why the findings matter beyond public health circles.

They suggest the UK is drifting into a situation where longer life is no longer matched by better life.

For some people with chronic limb-threatening ischaemia, there are simply no good revascularisation options left.

Their arteries are too damaged, the procedural risks are too high, or previous attempts have failed.

That is why this group is often described as having no-option disease.

An emerging procedure called transcatheter arterialization of the deep veins aims to create a new route for blood to reach the foot.

Instead of trying to reopen blocked arteries, it redirects blood through a healthier vein.

The latest PROMISE III data suggest this may improve not just limb outcomes, but everyday quality of life too.

Six months after the procedure, fewer patients said they were worried about poor circulation in their legs.

Concerns about taking part in social activities also fell.

Sleep problems dropped sharply, and the day-to-day burden of foot wounds was much lower.

That matters because these patients are often dealing with pain, tissue loss, poor mobility and a serious risk of major amputation.

Even modest improvements in sleep, function and confidence can be meaningful.

The earlier headline result from PROMISE III was that the study met its main endpoint for amputation-free survival.

These new findings add patient-reported outcomes to the picture.

Still, caution is needed.

This was a single-arm study, which means there was no direct comparison group.

And these quality-of-life results were presented at a scientific meeting, not yet published as a full paper.

So the data are promising, but not definitive.

Even so, for patients with no other realistic options, a procedure that may improve both limb salvage and day-to-day life is worth paying attention to.

Heart failure with preserved ejection fraction, or HFpEF, has long been seen mainly as a problem of stiffness.

The heart appears to pump normally on standard measures, but it relaxes poorly and does not fill properly.

A new study suggests that in people with severe obesity, that is not the whole story.

Researchers examined heart muscle cells from people with HFpEF and found that those with the highest BMI had weaker contraction at cell level.

That is striking because preserved ejection fraction can give the impression that pumping function is intact.

The researchers found that heart muscle cells from the most obese HFpEF group behaved more like cells from patients with classic heart failure and reduced ejection fraction.

They also identified a chemical change in a muscle protein called troponin I.

This change was more prominent in patients with severe obesity and seemed to weaken contraction.

That makes troponin I a possible treatment target in this subgroup.

The study also included a smaller group of patients who underwent weight loss treatment, mostly with GLP-1 drugs.

Those who lost the most weight showed improved contraction of heart muscle cells.

In people who lost at least 10% of body weight, peak force came close to normal.

That does not prove weight loss is a cure.

But it does suggest that some of the cellular damage linked to severe obesity in HFpEF may be reversible.

The broader message is important.

HFpEF is not one single disease.

In people with severe obesity, it may involve weaker muscle, not just stiffer muscle, and that may call for a different treatment approach.

One of the biggest problems with GLP-1 weight loss drugs is what happens after people stop taking them.

Many regain a large share of the weight they lost.

A new study suggests an outpatient procedure targeting the upper small intestine may help reduce that rebound.

The treatment is called duodenal mucosal resurfacing.

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It works by using controlled heat to remove the top layer of the duodenal lining, allowing healthier tissue to grow back.

Researchers think that may help reset some of the metabolic signals involved in weight regulation.

In the REMAIN-1 trial, all participants had previously lost at least 15% of body weight on tirzepatide before stopping the drug.

The early six-month results compared 29 people who had the real procedure with 16 who had a sham version.

Those in the sham group regained more weight.

People who had more extensive resurfacing appeared to do particularly well, regaining less and keeping more than 80% of their earlier weight loss.

That is encouraging.

So is the safety profile reported so far, with no serious complications linked to the procedure and a quick recovery time.

But the limits need spelling out.

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This is still an investigational treatment.

The data are early, the sample is small and the longer-term picture is not yet known.

There is also a risk of getting carried away by the phrase “gut reset”, which sounds more settled than the evidence really is.

Still, the idea is important.

If some people cannot stay on GLP-1 drugs because of cost, side effects or preference, a treatment that helps preserve the benefit after stopping would fill a real gap.

Diabetic foot ulcers are one of the hardest wounds to treat.

Poor circulation, chronic inflammation, weak blood vessel growth and an overactive immune response can all slow or block healing.

That is why these wounds can become so serious.

Current biological dressings can help, but they come with drawbacks.

Some are made from pig tissue, which can trigger immune reactions or raise concerns about pathogen transfer.

Others come from donated human tissue, which is limited in supply and can vary from one donor to another.

Researchers at Texas A&M are trying a different approach.

Instead of using donor skin directly, they grow human cells in the lab and guide them to build the kind of extracellular structure found in normal skin.

That structure is the important bit.

It acts like a scaffold that helps organise repair.

Once the scaffold has been built, the researchers remove the cells that made it.

So the final material is biological, but cell-free.

That matters because living donor cells can create storage, transport and compatibility problems.

Removing them may reduce the risk of immune reaction while leaving behind a framework that helps the patient’s own cells repair the wound.

The researchers describe this as an interwoven extracellular matrix.

In simple terms, it is a tissue-like mesh built by cells under controlled conditions.

The hope is that, once placed in a wound, it will guide the body’s own healing response and then gradually be replaced by native tissue.

That is a sensible idea.

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A good wound dressing should not just cover the ulcer. It should help create the right environment for healing without provoking more damage.

The team also says this approach could be scaled up using bioreactors rather than relying on small lab dishes.

If that works, it may make production faster and more consistent, which is important if the material is ever going to be used widely.

For now, though, this is still early research.

It is an interesting biomaterials study, not a ready-made clinical breakthrough.

But in an area where treatment options are limited and outcomes can be grim, a better wound scaffold would be worth having.