Coffee is often discussed as if all cups are equal.

A new UK Biobank analysis suggests the type of coffee may matter.

Researchers looked at more than 49,000 participants and compared coffee habits with three biological ageing measures.

These included telomere length and two biological age acceleration scores based on clinical and biochemical markers.

Filtered coffee and instant coffee showed different patterns.

Filtered coffee was associated with lower biological age acceleration and generally longer telomere length.

That points towards a more favourable ageing profile.

Instant coffee showed the opposite pattern.

Higher instant coffee intake was linked with higher biological age acceleration and shorter telomere length.

The effects were not huge.

The authors noted that the instant coffee estimates were generally equivalent to only around 0.1 to 0.2 years of age acceleration, which is marginal for an individual.

Still, the direction of the findings is interesting.

The difference may relate to how coffee is processed, brewed and consumed, or to the different people who choose different types of coffee.

The researchers adjusted for many factors, including age, sex, education, deprivation, smoking, alcohol intake, BMI, physical activity, additives in coffee and several health conditions.

Even so, residual confounding is still possible.

This was also a cross-sectional study.

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That means it looked at coffee intake and ageing markers at one point in time.

It cannot prove filtered coffee slows ageing or instant coffee speeds it up.

The better conclusion is measured.

Filtered coffee was linked with a better biological ageing marker profile than instant coffee.

That is not enough to rewrite dietary guidelines, but it does challenge the assumption that coffee type is irrelevant.

For people who already drink coffee, switching from instant to filtered may be a small, low-effort choice.

But the bigger foundations of healthy ageing remain diet quality, movement, sleep, blood pressure, smoking and metabolic health.

No cup of coffee outweighs those.

Diabetes care often focuses on medicines, blood tests and appointments.

But for many people, the hardest part of managing type 2 diabetes happens at home, in the kitchen, with limited money, limited time and limited access to healthy food.

A new trial suggests that fixing that gap can make a measurable difference.

Researchers tested a “Food is Medicine” programme among 460 Medicaid-insured adults with type 2 diabetes in Southern California.

All participants had persistently elevated blood sugar.

They were randomly assigned to usual care or medically tailored grocery deliveries for six months.

The grocery deliveries were not generic food parcels.

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They included healthy foods scaled to household size, culturally tailored recipes and access to phone-based nutrition counselling.

Participants received either about $135 or $175 worth of groceries per month.

Both amounts appeared to deliver similar blood sugar improvements.

Compared with usual care, people receiving groceries had an additional 0.40 percentage point reduction in HbA1c over six months.

That may sound modest, but in diabetes care it is meaningful, especially when achieved through food support rather than another medication.

The programme also improved food security.

The odds of food security rose by nearly 215%.

Nutrition security rose by 365%.

That distinction matters.

Food security means having enough food.

Nutrition security means having enough of the right kind of food to support health.

For people living with diabetes and low income, both are central to treatment.

The study does not suggest groceries replace medicines.

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It suggests medicines work in a real world, and that real world includes affordability, access, household size, cooking habits and cultural preferences.

Telling someone to eat better is cheap.

Making healthy food available is harder, but it may be far more effective.

This trial makes a strong case that diabetes care should not stop at the clinic door.

Sometimes the intervention is not another prescription.

It is making sure the food a person needs is actually within reach.

A new daily pill could become a serious challenger in the GLP-1 market.

Orforglipron is an oral GLP-1 drug developed by Eli Lilly.

Unlike oral semaglutide, it is a small-molecule drug rather than a peptide.

That difference matters.

It means orforglipron can be absorbed more easily through the gut and is simpler to manufacture.

It also does not need refrigeration and does not require the strict empty-stomach dosing routine used for oral semaglutide.

In a 52-week phase 3 trial, researchers compared orforglipron with oral semaglutide in 1,698 adults with type 2 diabetes across six countries.

The main outcome was HbA1c, a measure of average blood sugar over around three months.

Participants started with an average HbA1c of 8.3%.

After 52 weeks, orforglipron reduced HbA1c by an average of 1.71 to 1.91 percentage points.

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Oral semaglutide reduced it by 1.47 points.

Weight loss was also greater with orforglipron.

Participants lost an average of 6.1kg to 8.2kg, compared with 5.3kg for oral semaglutide.

That makes the results clinically interesting.

But tolerability is the counterweight.

Around 59% of participants taking orforglipron reported gastrointestinal side effects, compared with 37% to 45% on semaglutide.

About 10% of people taking orforglipron stopped treatment because of adverse effects.

That compared with around 4% to 5% on oral semaglutide.

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So the trade-off is clear.

Orforglipron may be more effective and easier to take, but harder for some people to tolerate.

Its convenience could still be a major advantage, especially in places where injections, cold-chain storage and expensive peptide manufacturing limit access.

For now, the results are promising but not the full story.

Long-term adherence will matter as much as headline weight loss.

A drug only works if people can stay on it.

Pancreatic cancer has long been one of the most difficult cancers to treat.

One major reason is KRAS.

More than 90% of pancreatic tumours are driven by mutations in this gene.

KRAS acts like a growth switch.

When mutated, it can become stuck in the “on” position, telling cancer cells to keep multiplying.

For decades, KRAS was considered almost undruggable.

Its protein surface lacked the usual pockets that drugs need to bind effectively.

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That left advanced pancreatic cancer treatment heavily dependent on chemotherapy.

Chemotherapy can slow disease, but it is often blunt, toxic and limited by resistance.

Daraxonrasib takes a different route.

Instead of attaching directly to KRAS, it binds to a molecule called cyclophilin A.

This complex can then bind to active KRAS and shut down its cancer-driving signal.

In a phase 3 trial of 500 patients with metastatic pancreatic cancer who had already received treatment, daraxonrasib nearly doubled overall survival.

Median survival rose from 6.7 months with standard chemotherapy to 13.2 months with daraxonrasib.

The drug reduced the risk of death by 60%.

For this disease, that is not a marginal result.

It is the kind of change researchers have been chasing for years.

The drug is taken daily by mouth.

The most common side effect was skin rash, affecting more than 86% of patients.

Mouth sores, diarrhoea, nausea and vomiting were also common.

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Even so, patients taking daraxonrasib were less likely to stop treatment because of severe side effects than those receiving chemotherapy.

They also reported better quality of life and less pain.

The next step is regulatory review.

If approved, daraxonrasib could mark a shift towards more precise treatment for pancreatic cancer.

It will not make the disease easy to treat.

Resistance may still develop, and combinations with other therapies will probably be needed.

But it shows that one of pancreatic cancer’s most important targets is no longer out of reach.

Exercising in hot weather is not just the same workout with more sweat.

Heat changes the physiology of exercise.

When muscles work, they produce heat.

To cool down, the body diverts blood towards the skin and produces sweat.

But those same working muscles also need blood and oxygen.

In hot conditions, that creates a competition inside the body.

The skin is trying to dump heat.

The muscles are trying to keep moving.

The heart has to work harder to support both.

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That is why a run, cycle or football session can feel dramatically harder in heat than it does on a cool day.

The best adjustment is timing.

Exercise earlier in the morning or later in the evening when temperatures are lower.

Shade matters too.

The difference between direct sun and shade can be far greater than the official air temperature suggests.

Humidity is another key factor.

Sweat cools the body when it evaporates.

In humid air, evaporation is less effective, so the same temperature can feel much more dangerous.

On hot days, reduce intensity before your body forces you to.

Shorter sessions, more breaks and slower pacing are not weakness.

They are heat management.

Cooling methods help, but some work better than others.

Ice packs feel cold but only cool a small area.

Water over the skin can be more useful because evaporation does the job of sweating.

Cold wet towels over the arms, legs and torso can also help.

For longer activity, pre-cooling can buy time.

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Cold drinks, icy slushies or cooling the body before heading out can slightly lower starting body temperature.

That gives a bigger buffer before heat stress builds.

The body can adapt to heat, but not instantly.

After 7 to 14 days of regular heat exposure, people can sweat more efficiently, expand blood plasma volume and tolerate heat better.

But this adaptation fades if it is not maintained.

The most important skill is knowing when to stop.

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Warning signs include dizziness, nausea, headache, unusual fatigue, cramps, confusion, palpitations or feeling chilled despite the heat.

Elite athletes can be at risk because they are trained to override discomfort.

Most people should not try to tough this out.

Heat is not just uncomfortable.

It changes the demands on the body.

Training smart in hot weather means respecting that.

Exercise does not just make muscles stronger by forcing them to work.

It also changes what happens inside muscle cells.

A new study from Duke-NUS Medical School suggests one important player is a gene called DEAF1.

As muscles age, they become less efficient at clearing damaged proteins.

At the same time, a growth pathway called mTORC1 can become overactive.

That combination is not ideal.

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Muscle cells may keep pushing protein production while failing to clean up damage properly.

Over time, this contributes to weakness, poorer repair and loss of function.

The researchers found that DEAF1 levels rise in ageing muscle.

Higher DEAF1 appears to drive excessive mTORC1 activity and worsen the imbalance between building new proteins and clearing damaged ones.

Normally, DEAF1 is held in check by FOXO proteins.

But FOXO activity tends to decline with age, allowing DEAF1 to rise.

Exercise seemed to push the system back towards balance.

Physical activity activated proteins that lowered DEAF1 levels.

That helped normalise mTORC1 activity and allowed ageing muscles to clear damage more effectively.

In experiments using fruit flies and older mice, raising DEAF1 made muscles weaken faster.

Lowering DEAF1 restored healthier protein balance and improved muscle strength.

That suggests the mechanism is not just a random finding in one model.

There is an important caveat.

Some older muscles may have DEAF1 levels so high, or FOXO activity so low, that exercise alone is not enough to fully restore repair capacity.

That may help explain why people respond differently to training later in life.

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The study may eventually point towards therapies that mimic some of exercise’s molecular effects.

That could be useful for people recovering from illness, surgery or cancer, where exercise is difficult.

But for now, the practical message is familiar and still powerful.

Muscle ageing is not just about losing bulk.

It is about losing repair capacity.

Exercise remains one of the best ways to keep that repair machinery online.

Alcohol can feel like a shortcut out of stress.

The problem is that the brain may learn that shortcut too well.

A new mouse study from the University of Massachusetts Amherst suggests drinking in response to chronic stress during early adulthood can leave lasting changes in the brain.

The researchers studied how alcohol and stress together affected decision-making circuits over time.

The combination was more damaging than either factor alone.

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Mice exposed to both early-life stress and heavy alcohol use were more likely to return to drinking during stressful periods in middle age.

This happened even after long periods without alcohol.

The biggest cognitive problem was not basic learning.

It was flexibility.

The mice struggled more with adapting to changing situations and updating behaviour when circumstances shifted.

That matters because cognitive flexibility is one of the abilities that can deteriorate early in some forms of cognitive decline.

The researchers focused on the locus coeruleus, a small brainstem region involved in alertness, stress response and adaptive decision-making.

In a healthy brain, this region activates during stress and then settles back down.

In the mice exposed to both stress and alcohol, the system looked disrupted.

The locus coeruleus lost some of the molecular machinery needed to regulate itself.

Researchers also saw oxidative stress, a type of cellular damage associated with ageing and neurodegenerative disease.

The point is not that one difficult period or one episode of drinking permanently ruins the brain.

This was an animal study involving controlled exposure.

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But the biology supports a serious concern.

When alcohol becomes the way a person manages stress, it may gradually weaken the brain systems needed to cope without it.

That is why relapse is not simply a willpower failure.

If stress and alcohol have reshaped the circuitry, recovery needs more than moral pressure.

It needs support that helps the brain relearn other ways of regulating stress.

Plant-based eating can be good for health and the planet, but it still needs proper planning.

A Dutch dietary modelling study looked at what happens when commonly eaten animal-based foods are replaced with plant-based alternatives.

Researchers used national dietary data from 3,570 people aged 1 to 79.

They modelled two scenarios.

One used more nutritionally favourable plant-based replacements.

The other used more widely available plant-based substitutes with lower nutritional quality.

This was not a trial of people eating vegan or vegetarian diets in real life.

It was a simulation of partial replacement.

That distinction matters.

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In the original diets, protein intake was generally above standard recommendations for most age groups.

After the substitutions, protein intake fell.

In several adult groups, especially women, intake dropped below recommended levels.

Older adults were a particular concern because they often need more protein to preserve muscle.

Essential amino acid intake also declined.

Most amino acids remained above recommended levels, but methionine plus cysteine fell below recommended levels in older adults in both scenarios.

Several vitamins also dropped after substitution.

These included vitamins A, B1, B2, B3, B6 and B12.

Vitamin D was already low before the dietary shift and stayed inadequate afterwards.

Calcium fell further too, becoming below recommended levels across all groups.

Iron intake rose slightly because of more non-haem iron, but remained low for children and women of reproductive age.

Iodine, selenium and zinc also fell.

Zinc became inadequate across all age groups after substitution.

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That sounds negative, but the right interpretation is more nuanced.

A well-planned plant-based diet can be nutritionally strong.

But swapping meat, fish and dairy gram for gram with whatever plant-based substitute is on the shelf may not deliver the same nutrient profile.

Fortification matters.

So do legumes, nuts, seeds, whole grains, calcium-set tofu, fortified milks and B12 supplementation.

The study is a reminder that plant-based eating should not be treated as automatically healthy by default.

The quality of the replacement matters just as much as what is being removed.

Speaking more than one language may do more than help on holiday.

New research suggests multilingualism may be linked with slower brain ageing.

Researchers studied people from the Basque region of Spain who spoke between one and four languages.

These included Spanish, Basque, French and English.

The team first built a brain ageing clock using magnetoencephalography, a technique that measures brain activity through tiny magnetic fields produced by active nerve cells.

Artificial intelligence was then used to estimate a person’s brain age from patterns of brain connectivity.

When researchers compared brain age with real age, they found a clear pattern.

People who spoke two languages had brains that appeared around 6 years younger than those who spoke only one.

Those who spoke three languages had brains around 7 years younger.

Those who spoke four languages had brains around 13 years younger.

The effect was not only about the number of languages.

Higher fluency and learning another language earlier in life were also linked with younger-looking brains.

That suggests language experience may work as a gradient.

It is not simply bilingual versus not bilingual.

Depth, duration and proficiency may all matter.

The researchers adjusted for age, sex and education, but they are cautious about the findings.

Other factors could still be involved.

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People who speak several languages may also differ in lifestyle, social engagement, education or cultural background.

So this is not proof that learning French, Spanish or Basque will shave years off your brain.

But it is biologically plausible.

Using multiple languages requires attention, switching, memory and control.

That is exactly the kind of effortful mental activity that may help maintain brain networks over time.

The broader message is useful.

The brain appears to benefit from being challenged.

Language learning is one way to do that, and it comes with social and cultural benefits too.

Even later in life, it may be worth learning for more than just vocabulary.

Blood sugar is usually discussed in relation to diabetes, weight and heart health.

A new study suggests it may also be tied to how quickly the brain ages.

Researchers analysed MRI scans, blood metabolite data and genetic information from the UK Biobank.

They used artificial intelligence to build a “brain age” model from more than 1,000 imaging-derived brain features.

The model estimated how old a person’s brain appeared compared with their actual age.

This difference is called the brain age gap.

A higher brain age gap suggests the brain looks older than expected.

The researchers then looked at blood metabolites linked to this gap.

Nine stood out.

Glucose had the strongest association.

People with higher blood glucose tended to have brains that looked older on scans.

The researchers also found genetic evidence supporting a possible causal role for glucose in accelerated brain ageing.

Higher glucose was linked with smaller volumes across 80 brain regions, including cortical, subcortical and cerebellar areas.

It was also associated with higher risk of several brain-related conditions.

These included all-cause dementia, Alzheimer’s disease, vascular dementia, Parkinson’s disease, stroke, depression and anxiety.

Cognitive performance, movement function and mental health outcomes were also poorer where glucose levels were higher.

This does not mean a single blood sugar reading tells you your brain age.

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Nor does it mean glucose is the only thing that matters.

Brain ageing is shaped by many factors, including blood pressure, sleep, physical activity, smoking, inflammation and education.

But the study adds weight to a bigger idea.

Metabolic health and brain health are not separate systems.

Keeping blood glucose in a healthy range may be one of the ways to protect the brain across the lifespan.

That matters for people with diabetes, but also for anyone drifting into poor metabolic health long before diagnosis.

Intermittent fasting may help people lose weight without the constant mental load of counting calories every day.

A new trial from the University of Adelaide compared intermittent fasting with continuous calorie restriction and standard care.

More than 200 adults with obesity took part in the 18-month study.

The intermittent fasting group ate only 30% of their daily energy needs between 8am and midday on three non-consecutive days each week.

After that, they fasted for 20 hours.

On the other days, they ate their usual diet.

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The calorie restriction group took a more traditional approach, eating about 70% of their usual calories every day.

After six months, both dieting groups had lost around 7kg on average.

The standard care group lost around 2kg.

So the weight loss result was similar between fasting and calorie restriction.

The difference was how it felt.

People in the calorie restriction group reported needing to consciously control intake, avoid overeating and keep restricting themselves.

Researchers estimated that this sense of effort accounted for about 15% of their weight loss.

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The fasting group did not report the same level of constant food control.

That may be the useful part.

For some people, deciding when to eat may be easier than trying to micromanage every meal, snack and portion.

The study also found improvements in depression and wellbeing in both dieting groups, including on fasting days.

That does not mean fasting is automatically better, or suitable for everyone.

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Some people find fasting miserable, and people with diabetes, eating disorders, pregnancy or certain medical conditions should seek clinical advice first.

But the study makes a fair point.

The best weight loss plan is not just the one that works on paper.

It is the one people can actually live with.

A tablet version of Wegovy has launched privately in the UK, giving people another way to access semaglutide-based weight loss treatment.

The pill is taken once a day and is the first oral GLP-1 weight loss medicine approved in the UK. The Medicines and Healthcare products Regulatory Agency approved the new tablet form on 11 June 2026.

Like the Wegovy injection, the pill works by mimicking GLP-1, a hormone involved in appetite regulation. It can help people feel fuller, reduce hunger and lower cravings.

However, it is not a quick fix. Wegovy should be used alongside a reduced-calorie diet, increased physical activity and ongoing clinical support.

Who can use the Wegovy pill?

The Wegovy pill is intended for adults living with obesity or overweight who meet clinical eligibility criteria.

It may be prescribed privately to people with a BMI of 30 or above, or to people with a BMI between 27 and 30 if they also have at least one weight-related health condition, such as type 2 diabetes, high blood pressure or obstructive sleep apnoea.

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A consultation is required before treatment starts. This may be completed online or face-to-face, depending on the pharmacy or provider.

The medicine should not be used by people under 18, or by those who are pregnant or breastfeeding.

Anyone with existing medical conditions or taking other medication should speak to a healthcare professional before starting treatment.

How is the pill taken?

The tablet has strict instructions because food, drink and other medicines can affect how well it is absorbed.

It should be taken after fasting for at least eight hours, with a small sip of plain water. People are then advised to wait at least 30 minutes before eating, drinking anything else or taking other tablets.

That means it may suit people who already have a regular morning routine, but it may be less convenient for those who struggle with fasting or need to take other medicines early in the day.

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If a dose is missed, the usual advice is to skip that day’s tablet and take the next scheduled dose the following day.

Wegovy pill vs Wegovy injection

The main difference is how the medicine is taken.

The injection is taken once a week, while the pill is taken every day.

The injection also needs fridge storage, whereas the tablet may be more convenient for some people.

For people who dislike needles, the tablet may feel like a more acceptable option.

For others, a weekly injection may be easier than remembering a daily tablet with fasting instructions.

The best choice will depend on medical history, lifestyle, treatment goals and personal preference.

What dose do people start on?

Treatment usually starts at a low dose and increases gradually.

The tablet strengths approved in Europe are 1.5mg, 4mg, 9mg and 25mg.

The dose is increased over time to help the body adjust and reduce side effects.

People should not try to switch between Wegovy injections and tablets without clinical advice.

The dosing is not a simple like-for-like swap, so any change should be supervised by a healthcare professional.

How well does it work?

Clinical trial data suggest that oral semaglutide can support significant weight loss when used alongside diet and physical activity.

In a 64-week trial, people taking Wegovy tablets lost an average of 13.61% of their body weight, compared with 2.18% among people taking a placebo.

The results are promising, but they also underline an important point: the medication was tested as part of a wider treatment plan, not as a standalone solution.

Weight regain can also happen after stopping GLP-1 medication, which is why long-term lifestyle support remains important.

What are the side effects?

The most common side effects are gastrointestinal. These can include nausea, vomiting, constipation, diarrhoea and stomach pain.

Some people may also experience headaches or tiredness.

More serious side effects are less common but can include pancreatitis, severe allergic reactions and low blood sugar, particularly in people taking other medicines that affect blood glucose.

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Anyone taking Wegovy should read the patient information leaflet and report concerning symptoms to a healthcare professional.

Is the Wegovy pill available on the NHS?

Not currently.

Although the tablet has been approved by the MHRA, it has not yet been recommended for NHS use.

NICE would need to review the clinical and cost-effectiveness evidence before it could be made available through NHS pathways.

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NICE already has guidance for injectable semaglutide for weight management, but the tablet form will need to be considered separately if it is to be used on the NHS.

How much does it cost privately?

Private prices vary by pharmacy, dose and introductory offers.

Some providers are pricing lower starting doses at around £99 per month, while higher doses may cost closer to £199 per month.

Prices may change as supply, demand and competition develop.

Patients should be cautious about very cheap offers, social media sellers or websites that do not require a consultation.

What about counterfeit medicines?

The growing demand for GLP-1 treatments has increased concern about counterfeit products.

People should only buy Wegovy from regulated pharmacies and should avoid sellers offering the medicine without a prescription or clinical assessment.

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Fake weight loss medicines can contain incorrect doses, unknown ingredients or harmful substances. Anyone unsure about a product should check with a pharmacist or healthcare professional before taking it.

Is this a turning point for weight loss treatment?

The arrival of an oral GLP-1 option is a major development because it gives patients more choice.

For some people, a tablet may reduce the barrier to starting treatment.

For others, the daily fasting routine may make the weekly injection more practical.

Either way, the same rule applies: Wegovy is a medical treatment for obesity and weight-related health conditions, not a cosmetic shortcut.

Its safest and most effective use is as part of a structured plan that includes nutrition, movement, behaviour change and ongoing clinical oversight.

Ageing is often discussed as if decline is inevitable.

A Yale study suggests that is only part of the story.

Researchers analysed more than 11,000 older adults from the Health and Retirement Study, following participants for up to 12 years.

They measured cognitive function and walking speed.

Walking speed may sound simple, but in geriatric medicine it is a serious marker.

It is linked with disability, hospitalisation and mortality.

Over the follow-up period, 45% of participants improved in at least one of the two areas.

Around 32% improved cognitively.

Around 28% improved physically.

That is not a small fringe group.

It suggests that improvement in later life is common enough to be part of how we talk about ageing.

The study also found that averages can hide this.

If you only average everyone together, decline dominates the picture.

But individual trajectories show a more varied reality.

Some people decline, some stay stable and many improve.

The researchers also looked at beliefs about ageing.

People with more positive views of ageing at the start were more likely to improve in both cognition and walking speed.

This relationship remained even after adjusting for age, sex, education, chronic disease, depression and follow-up length.

That does not mean positive thinking cures ageing.

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It means beliefs may influence behaviour, stress, recovery, confidence and engagement with life.

Those things can matter biologically.

The findings also challenge the idea that gains only happen when people recover from illness.

Even people who started with normal cognitive and physical function sometimes improved.

This is an important corrective.

Ageing is not automatically a one-way slide.

There is room for resilience, adaptation and gain.

And if age beliefs are modifiable, then the way society talks about ageing may be part of the health environment too.

As temperatures rise across the UK, health professionals are warning that people taking GLP-1 medicines for weight loss or type 2 diabetes should be alert to the risk of dehydration.

GLP-1 based treatments can help people feel fuller, reduce hunger and support weight loss.

However, they can also cause side effects such as nausea, vomiting, constipation and diarrhoea, all of which can make dehydration more likely in hot weather.

The risk may be higher during a heatwave because people can lose more fluid through sweating, even when they are not exercising.

If someone is also eating less, drinking less or struggling to keep fluids down, symptoms can worsen quickly.

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Why heat can be a problem on GLP-1 medicines

GLP-1 medicines work by affecting appetite and digestion. For many people, this means they feel less hungry and eat smaller portions.

But when appetite is lower, people may also drink less than usual.

Some may not notice they are thirsty until they are already mildly dehydrated.

This can be more of an issue during hot weather, when the body needs more fluid to stay cool.

People taking GLP-1 medicines should not rely on thirst alone during a heatwave. Instead, it may help to drink regularly throughout the day, especially during the morning and early afternoon when dehydration can creep up unnoticed.

Signs of dehydration to watch for

Common signs of dehydration include:

• Dark yellow urine
• Dizziness
• Tiredness
• Headaches
• Dry mouth
• Light-headedness
• Feeling unusually weak

Some people may also feel nauseous, shaky or faint, particularly if they have been standing outside, travelling on hot public transport or spending time in direct sun.

Anyone who is vomiting, has diarrhoea or cannot keep fluids down should speak to a pharmacist, GP or NHS 111 for advice.

Urgent help is needed if someone becomes confused, collapses, stops sweating despite feeling very hot or develops symptoms of heatstroke.

How to stay safer during a heatwave

People taking GLP-1 medicines can reduce their risk by planning ahead.

Keep water nearby, sip fluids regularly and consider setting reminders if you often forget to drink. If you are sweating heavily, an oral rehydration drink or electrolyte drink may be helpful.

Water-rich foods can also support hydration. Good options include cucumber, tomatoes, watermelon, berries, oranges, soups, yoghurt and salads.

It is also important not to skip meals completely just because you feel less hungry. Smaller, lighter meals may be easier to manage during hot weather, but the body still needs energy, protein and fluid.

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Avoid the hottest part of the day

Try to avoid prolonged time outside during the hottest part of the day, usually between late morning and late afternoon.

If you need to go out, wear loose clothing, stay in the shade where possible and take water with you.

People travelling on buses, trains or the Tube should take extra care, as crowded transport can become very hot and uncomfortable.

Do not stop medication without advice

Anyone worried about side effects should not stop their GLP-1 medication without speaking to a healthcare professional first.

However, if vomiting, diarrhoea, dizziness or dehydration symptoms become significant, medical advice should be sought promptly.

This is particularly important for people taking GLP-1 medicines for type 2 diabetes, as dehydration and reduced food intake may affect blood glucose levels, especially if they are also taking insulin or other diabetes medication.

A heatwave reminder

GLP-1 medicines can be effective for weight management and diabetes care, but they are still prescription medicines that need proper monitoring.

During hot weather, the key advice is simple: drink regularly, eat enough, avoid overheating and get help early if symptoms worsen.

The heat can place extra strain on the body, and people taking GLP-1 medicines should take that risk seriously.

The placebo effect is usually treated as a nuisance in research.

This study suggests it may also be a tool worth understanding.

Researchers in Milan recruited 90 healthy older adults and divided them into three groups.

One group received no intervention.

A second group took placebo pills but was told they contained active ingredients.

A third group took the same inactive pills and was openly told they were placebos.

That last group is important.

It means the researchers were not relying only on deception.

Before and after the three-week study, participants completed questionnaires and objective tests of memory, attention and physical performance.

The results were surprising.

Both placebo groups improved on some cognitive and physical measures.

The open-label placebo group, who knew the pills were fake, showed particularly interesting results.

They had lower perceived stress than both the deceptive placebo group and the control group.

They also improved significantly in short-term memory compared with controls.

Physical performance increased by 7% in the deceptive placebo group and 9.2% in the open-label group.

Cognitive performance improved too, though the size of the effect depended on the test.

This does not mean fake pills magically reverse ageing.

The trial was small, short and involved healthy older adults.

The results need replication.

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But the study does suggest that expectation, meaning and self-perception can influence measurable function.

That is not mystical.

The brain shapes stress, attention, motivation, confidence and bodily effort.

Those factors can affect performance.

The most interesting part is that open-label placebo may be ethically usable.

You do not need to lie to people for the mind-body response to do something.

Still, it needs careful framing.

A placebo is not a replacement for medical treatment.

But this study is a reminder that how people think about ageing, recovery and capability may matter more than we usually admit.

Fish oil supplements are often sold as brain protection in a capsule.

A new clinical trial suggests that claim deserves a lot more scepticism.

Researchers studied 365 adults aged 55 to 80 who rarely ate fish and were considered at increased risk of Alzheimer’s disease.

Nearly half carried the APOE4 gene, the strongest known genetic risk factor for late-onset Alzheimer’s.

Participants were randomly assigned to take either high-dose DHA fish oil or placebo for two years.

DHA is an omega-3 fatty acid involved in brain cell function.

The first question was whether the supplement actually reached the brain.

It did.

After six months, DHA levels in cerebrospinal fluid had increased by an average of 17%.

That means poor delivery was not the problem.

The issue was what happened next.

Despite reaching the brain, DHA supplementation did not improve memory or thinking test scores compared with placebo.

It also did not slow shrinkage of the hippocampus.

That is important because the hippocampus is central to memory and is commonly affected in Alzheimer’s disease.

The results do not mean omega-3 fats are useless.

They are important nutrients and oily fish can be part of a healthy diet.

But this trial does not support high-dose fish oil supplements as a way to prevent Alzheimer’s or protect memory in older adults at risk.

The researchers suggest omega-3s may work differently when consumed as part of an overall Mediterranean-style eating pattern.

That makes sense.

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A diet is not just one nutrient.

It is a whole pattern of fats, fibre, plant foods, fish, minerals and metabolic effects.

The lesson is familiar but worth repeating.

Brain health is unlikely to be solved by a single supplement.

Sleep, exercise, blood pressure, glucose control, diet quality and overall vascular health probably matter far more than a fish oil capsule.

Pancreatic cancer remains one of the hardest cancers to treat.

One reason is KRAS.

Mutations in this gene are extremely common in pancreatic ductal adenocarcinoma and help drive tumour growth, spread and treatment resistance.

Researchers are now testing a new class of experimental compounds called PCAIs.

These were designed to interfere with abnormal signalling linked to cancer-driving G-proteins, including KRAS-related pathways.

In the new study, scientists tested PCAIs on pancreatic cancer cells carrying KRAS mutations.

Two compounds showed strong anticancer activity.

The researchers then focused on one leading compound called NSL-YHJ-2-27.

At a low concentration, it blocked more than 90% of cancer cell migration.

That matters because the ability to move and invade is central to how pancreatic cancer spreads.

The compound also disrupted the actin cytoskeleton, which gives cells their shape and helps them move.

Cancer cells became rounder and less mobile.

The most surprising finding was how the compounds affected major cancer signalling pathways.

Rather than simply switching down MAPK and PI3K/AKT signalling, they pushed these pathways into overactivation.

That may sound counterintuitive because these pathways usually help cancer cells grow.

But too much activation can destabilise the cell.

In this case, it appeared to trigger oxidative stress, caspase activity and apoptosis, which is programmed cell death.

The compounds also changed gene expression.

Some tumour-suppressing genes became more active, while genes linked to progression and metastasis became less active.

The results were also seen in 3D tumour spheroid models, which are more realistic than flat cell cultures.

That strengthens the case for further research.

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But the caveat is big.

This is still preclinical work.

It does not mean there is a new pancreatic cancer treatment available.

Many compounds look impressive in lab models and fail later in animals or humans.

Even so, the study is interesting because it attacks pancreatic cancer from a different angle.

Instead of delicately suppressing one pathway, it may overload the cancer cell’s own signalling machinery until it breaks.

Multiple sclerosis does not behave the same way in everyone.

Some people live with relatively mild symptoms for years, while others develop rapid disability.

A new study points to one possible reason: brain immune cells overloaded with fat.

Researchers examined brain tissue from people with MS and focused on microglia, the brain’s resident immune cells.

Normally, microglia help clear debris and support repair.

In MS, one of their jobs is to deal with damaged myelin, the fatty protective coating around nerve fibres.

But the study found that in more severe MS, some microglia become packed with fat droplets after taking up damaged myelin.

These are known as foamy microglia.

The researchers found that patients with large numbers of these cells more often had a severe disease course.

That suggests the cells may be more than a bystander.

The likely problem is overload.

The cells appear to be trying to clean up damage, but become overwhelmed by the volume of fatty myelin debris.

Once that happens, they may stop supporting repair and begin driving chronic inflammation instead.

The study also found that MS lesions containing foamy microglia had a different molecular profile.

They were enriched with certain fats linked to persistent inflammatory activity.

That makes the biology more interesting than a simple “inflammation is bad” story.

It suggests that failed repair and altered fat metabolism may be central to progression.

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The researchers also found signs that some of these fat-related molecules may be detectable in cerebrospinal fluid.

If future studies confirm that, they could become biomarkers.

That would help doctors identify people at higher risk of rapid decline and choose treatment more precisely.

This is still research, not a clinic-ready test.

But it adds an important piece to the MS puzzle.

The cells meant to clean up damage may, once overloaded, become part of the damage process themselves.

GLP-1 drugs have changed obesity and type 2 diabetes treatment, but they are also creating new risks.

A study in JAMA Psychiatry suggests people with eating disorders may be using and misusing these medicines at much higher rates than the general population.

Researchers surveyed 436 people in the United States with eating disorders, including anorexia nervosa, bulimia nervosa and binge eating disorder.

About 32% had used GLP-1 medicines at some point.

That is more than double the estimated level of use in the general adult population.

Around 22% were actively using them at the time of the study.

Nearly 10% reported misuse.

That included taking higher doses than prescribed, staying on treatment longer than advised or sharing drugs with friends or family.

Some also reported buying compounded products online.

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That is especially worrying because these products may sit outside normal medical and regulatory oversight.

The issue is not simply that people are using weight loss medicines.

It is that eating disorders are serious mental health conditions where food, weight and body shape can become overwhelming and dangerous.

For someone with an eating disorder, a drug that reduces appetite and food intake may reinforce harmful restriction.

It may also worsen the drive to control weight.

That is why this study lands at a difficult moment.

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Demand for GLP-1 drugs is surging, new oral versions are coming and online marketing is everywhere.

At the same time, eating disorders are often underdiagnosed and poorly supported.

The researchers point out that there is no approved medical use for GLP-1 medicines to treat eating disorders.

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That does not mean these drugs could never have a role in carefully selected patients with binge eating or metabolic disease.

But it does mean casual prescribing or online access is risky.

Screening matters.

Clinicians should ask about eating disorder history before prescribing appetite-suppressing drugs.

Patients should also be asked how they are using the medicine, not just whether they are losing weight.

Weight loss is not automatically a good outcome if it is being driven by misuse, obsession or psychological harm.

Eye appointments for people with diabetes may be doing more than protecting vision.

A new study suggests they could also be a useful place to detect dangerously high blood pressure.

Researchers at the University of Virginia measured blood pressure in 172 adults with type 1 or type 2 diabetes who were attending eye clinic appointments.

The results were blunt.

Only 8.1% had a normal blood pressure reading.

Roughly half had stage 2 hypertension, meaning their readings were at least 140/90 mmHg.

More concerningly, 10.5% had readings in the hypertensive crisis range.

That is a level where blood pressure can become a medical emergency, especially if symptoms are present.

The study also exposed a gap between what people believed and what the numbers showed.

Among patients with no previous hypertension diagnosis, 85.7% had above-normal readings.

More than a third were already in stage 2 hypertension.

Even among those who thought their blood pressure was controlled, 52% still had stage 2 hypertension.

Another 8% were in hypertensive crisis range.

This matters because diabetes, high blood pressure and eye disease are deeply connected.

High blood pressure can worsen diabetic retinopathy and contribute to macular oedema, where fluid builds up in the central retina.

It also raises the risk of heart attack, stroke and kidney disease.

Eye clinics already see many people with diabetes who carry these wider vascular risks.

So adding a simple blood pressure check is not a huge leap.

In this study, it also led to practical action.

Almost 60% were advised to contact their primary care provider.

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Around 12% needed follow-up within one to two days, and one patient was sent to emergency care.

Importantly, 93% of patients said blood pressure checks at the eye clinic were reasonable and acceptable.

That is the point that makes this feel workable.

People with diabetes already attend retinal screening and eye reviews because the eyes are vulnerable to vascular damage.

Using that visit to pick up uncontrolled blood pressure makes clinical sense.

The eye is often described as a window into blood vessel health.

This study shows that eye clinics may need to act like one.