A new study suggests the same habits that protect the heart may also help reduce type 2 diabetes risk after menopause.

Researchers used data from the Women’s Health Initiative, a long-running study of postmenopausal women aged 50 and over.

They looked at how closely women followed the American Heart Association’s Life’s Essential 8.

These include diet, physical activity, not smoking, sleep, body weight, cholesterol, blood sugar and blood pressure.

The researchers gave women a score from 0 to 100, with higher scores meaning better cardiovascular health.

They then followed participants for an average of 16 years to see who developed type 2 diabetes.

Among women assessed using all eight measures, 20% developed type 2 diabetes.

Those in the highest Life’s Essential 8 category had a 57% lower risk than those in the lowest category.

The researchers also looked at a simpler five-factor version covering diet, exercise, smoking, sleep and body mass index.

In that larger group, women with the highest scores had a 40% lower risk of diabetes.

Body mass index had the strongest link with diabetes risk among the lifestyle factors.

Blood sugar was also one of the strongest individual markers in the full eight-factor score.

The findings do not mean diabetes prevention is only about willpower.

Ageing, hormones, genetics, deprivation and access to healthy food all play a part.

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But they do show that modifiable factors still matter later in life.

The takeaway is practical.

Improving heart health is not just about preventing heart attacks or strokes.

For postmenopausal women, the same package of habits may also reduce the risk of type 2 diabetes.

Metformin is one of the most widely used medicines in the world.

It has been used for decades to treat type 2 diabetes, but scientists are still uncovering exactly how it works.

A new study from the University of Montreal suggests metformin directly targets a protein called ATP5I.

ATP5I is part of the mitochondrial machinery involved in producing ATP, the cell’s main energy currency.

The researchers found that cells lacking ATP5I became resistant to metformin.

When ATP5I was restored, the cells became sensitive to the drug again.

That points to ATP5I as an important part of metformin’s action.

This matters because metformin has long been linked with effects beyond glucose control.

Some studies have associated it with lower cancer risk and possible effects on lifespan in animals.

Those findings have always raised a difficult question.

How can one old diabetes drug appear to affect so many biological processes?

The answer may lie in the fact that metformin touches a central part of cellular energy handling.

Mitochondria are not a minor target.

They influence metabolism, cell growth, stress responses and survival.

That makes ATP5I an interesting new research focus.

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It may help scientists understand how metformin affects diabetes biology, cancer cell growth and ageing-related pathways.

But this is still mechanistic laboratory research.

It does not prove that metformin prevents cancer or extends life in humans.

Nor does it justify people taking the drug without a medical reason.

What it does show is that metformin still has secrets left, even after decades of use.

Spices are often treated as flavour, not nutrition.

But a new review suggests common kitchen spices may have wider effects on health than many people realise.

Researchers looked at evidence on spices including cinnamon, turmeric, red pepper, black pepper, ginger, rosemary and oregano.

They focused on human studies and lab work, including research from the UCLA Center for Human Nutrition.

Cinnamon has been studied for its effects on blood sugar and insulin.

Some trials suggest it may help reduce post-meal insulin and glucagon levels, and may influence the gut microbiome.

Turmeric’s main active compound, curcumin, has been linked with anti-inflammatory and antioxidant effects.

Some studies have explored its possible role in memory, mood, osteoarthritis pain and cholesterol levels.

Red pepper compounds may influence thermogenesis, which is the body’s heat production and energy use.

However, the results are mixed, and higher doses of pungent capsaicin can cause gut side effects.

Spice mixes may also affect gut bacteria.

Some studies suggest polyphenol-rich spices can encourage beneficial bacteria such as Lactobacillus and Bifidobacterium while reducing certain less helpful bacteria.

Spices may also help reduce salt intake.

That matters because using herbs and spices instead of salt can make food taste better without increasing sodium.

Still, the evidence needs keeping in proportion.

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Many lab studies use doses far beyond what people normally eat.

Cooking methods, digestion and food combinations can also change how much of a spice compound is actually absorbed.

So this is not a case for treating spices as medicine.

The better message is simpler.

Using more herbs and spices can make healthier food more enjoyable and may add small biological benefits along the way.

CBD is being studied for a range of possible effects, including on brain inflammation.

A new mouse study suggests it may influence inflammatory pathways involved in Alzheimer’s disease.

Alzheimer’s research has traditionally focused on amyloid plaques and tau tangles.

Those are still central features of the disease.

But chronic inflammation in the brain is increasingly seen as another important driver of damage.

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In this study, researchers used a mouse model of Alzheimer’s disease and delivered CBD through inhalation.

They then examined immune activity and inflammatory signalling in the brain and spinal cord.

CBD reduced the activity of several regulators linked to neuroinflammation.

It was also associated with lower levels of pro-inflammatory molecules.

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That suggests CBD may calm some of the immune overactivation seen in Alzheimer’s models.

The researchers say this could matter because Alzheimer’s is not driven by one pathway alone.

A treatment that affects several processes at once may eventually be more useful than one focused on a single target.

That is the optimistic view.

But the evidence still needs to be kept firmly in context.

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This was not a human trial.

It does not show that CBD slows Alzheimer’s in patients, improves memory or prevents dementia.

It also does not mean over-the-counter CBD products should be treated as medicine.

The study is useful because it adds to the biological case for targeting brain inflammation.

CBD may be one way to explore that pathway, but there is a long distance between promising mouse data and a safe, effective treatment for people.

A new systematic review has looked at whether yoga and meditation can affect the gut microbiome.

The answer is possibly, but the evidence is still very limited.

Researchers screened 247 titles and abstracts, but only four studies met the criteria for inclusion.

One study looked at yoga and three looked at Buddhist meditation.

Together, they included 440 healthy adults from China and the United States.

Across the studies, yoga and meditation were associated with changes in gut bacteria that looked broadly favourable.

These included increases in bacteria such as Bacteroides, Faecalibacterium, Roseburia and Lactobacillus.

Some studies also found changes in metabolites, including short-chain fatty acids.

That is interesting because the gut microbiome is linked with metabolism, immunity, inflammation and the gut-brain axis.

Stress and mental health can also affect gut biology.

So it is plausible that mind-body practices could have some effect.

But there is a major problem.

Many participants in these studies also followed vegan or vegetarian diets.

Diet is one of the strongest influences on the gut microbiome.

That makes it difficult to separate the effect of meditation or yoga from the effect of food.

The review also found a lack of high-quality randomised controlled trials.

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That means we cannot say with confidence that yoga or meditation directly caused the microbiome changes.

Still, the idea is worth studying properly.

Yoga and meditation are low-risk for most people and already have evidence for stress reduction and wellbeing.

If future trials show they also affect gut health, that would be useful.

For now, though, the microbiome claim remains promising rather than proven.

Cannabis and male fertility have been debated for years.

Some studies have suggested cannabis may reduce sperm count, concentration or motility.

But evidence on testosterone has been inconsistent.

A new study from the University of Geneva looked at the question in more detail by measuring hundreds of steroid hormones in blood samples from young Swiss men.

The study included 47 confirmed cannabis users and 47 non-users aged 18 to 23.

The researchers found that cannabis users had about 23% higher testosterone.

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By looking across a wider set of androgens, they traced the increase to the testes rather than the adrenal glands.

That suggests cannabis may be affecting Leydig cells, which produce testosterone.

The team also identified two progesterone-derived metabolites that were much higher in cannabis users.

These were hydroxyprogesterone and dihydroprogesterone.

The researchers suggest these may become useful biomarkers for tracking endocrine disruption linked to regular cannabis exposure.

But the fertility question is still unresolved.

Higher testosterone does not automatically mean better sperm quality or improved fertility.

The relationship between hormones and reproductive function is more complicated than that.

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It is also possible that the increase reflects a compensatory response, or that men with naturally higher testosterone are more likely to use cannabis because of risk-taking behaviour.

So this study challenges the simple claim that cannabis lowers testosterone.

But it does not show cannabis is harmless for male reproductive health.

The honest conclusion is that cannabis appears to alter steroid metabolism in young men, but what that means clinically still needs more work.

Weight training may do more than build muscle.

New research suggests regular resistance training could help people live longer and reduce their risk of dying from major conditions such as heart disease, stroke and neurological disease.

Researchers analysed data from three long-running studies involving 147,374 men and women over 30 years.

They found that people who consistently did between 90 minutes and two hours of weight training each week had a 13% lower risk of premature death from any cause.

The risk of death from cardiovascular disease, including heart attack and stroke, was 19% lower.

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The reduction was even greater for neurological disease, with the risk of death falling by 27%.

The findings add to growing evidence that strength training should not be seen as optional or only for people who want to build muscle.

It may be an important part of healthy ageing.

Aerobic exercise such as walking, running, cycling and swimming is already known to improve heart health, reduce type 2 diabetes risk and support mental wellbeing.

But this study suggests weight training brings its own benefits too.

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The lowest risks were seen in people who combined strength training with high levels of aerobic activity.

Among the most active people, the risk of early death from any cause was up to 58% lower.

That does not mean people need to spend hours in the gym every day.

The study found that doing more than two hours of strength training a week did not seem to bring much extra benefit.

That is a useful message.

A couple of well-planned strength sessions each week may be enough to make a meaningful difference.

Resistance training can include lifting weights, using resistance bands, bodyweight exercises or gym machines.

For older adults, it can help preserve muscle, protect bones, support balance and maintain independence.

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That matters because losing strength with age is one of the main reasons people become frailer, less mobile and more dependent on care.

It may also help with blood sugar control, joint pain, energy levels and confidence.

The practical takeaway is simple.

Cardio still matters, but strength training deserves a regular place in the week too.

For many people, the goal is not just to live longer.

It is to stay strong enough to enjoy those later years properly.

Most people know caffeine can make them feel more alert after a bad night.

A new study suggests it may also help restore a specific type of memory affected by sleep loss, at least in mice.

Researchers focused on social memory, the ability to recognise familiar individuals.

This depends partly on a region of the hippocampus called CA2.

In the study, mice were exposed to five hours of sleep deprivation.

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Afterwards, researchers found that synaptic plasticity in the CA2 region was disrupted.

In plain English, the connections between nerve cells were less able to strengthen properly.

The mice also showed problems with social recognition memory.

Caffeine appeared to reverse those effects.

It restored communication between neurons in the affected pathway and improved social memory performance.

The researchers say the effect was fairly targeted.

Caffeine did not simply overstimulate the whole brain in animals that had not been sleep-deprived.

Instead, it seemed to help restore the pathway that had been disrupted by lack of sleep.

That is useful biology.

It helps explain why sleep loss affects memory and why caffeine may partially rescue some cognitive functions.

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But it does not make caffeine a substitute for sleep.

The study was done in male mice, not humans.

And even if similar mechanisms apply in people, sleep does far more than support one memory circuit.

So the practical message is limited.

Caffeine may help you function after poor sleep, but it does not erase the biological cost of missing it.

Bastian was best known as the founder of #dedoc, a global community created to bring people living with diabetes into the heart of diabetes conversations, conferences, research and policy discussions.

Through #dedoc, he helped open doors for people with lived experience of diabetes to take part in professional and scientific spaces that had too often spoken about diabetes without including the people living with it.

His work was closely associated with the principles of “Nothing about us without us” and “pay it forward”, both of which reflected his belief that people with diabetes should not only be represented, but actively involved in shaping the future of diabetes care.

Bastian’s contribution to diabetes advocacy spanned more than a decade. In 2016, he received the IDF Europe Social Media Award in recognition of his ability to connect people, amplify lived experience and encourage meaningful discussion across the diabetes community.

He later served two terms on the IDF Europe Board, where he was recognised not only for his strategic input and commitment, but also for the warmth and positivity he brought to his work.

One of Bastian’s major achievements was the development of a global scholarship programme that enabled hundreds of diabetes advocates to attend major scientific events, including the IDF World Diabetes Congress. This helped ensure that the voices of people living with diabetes were present in discussions that influence care, research and policy.

Bastian was also an IDF Blue Circle Voice and a strong supporter of World Diabetes Day, using the campaign to help unite people across the international diabetes community and strengthen advocacy and awareness.

His work helped change how lived experience is recognised in diabetes. He encouraged people to contribute in their own language, through their own platforms and within their own cultural contexts, making diabetes advocacy more inclusive and more representative.

Tributes from across the diabetes community have described Bastian as someone who understood the importance of connection, inclusion and community. He helped people feel heard, valued and supported, and his work inspired a generation of diabetes advocates.

The International Diabetes Federation has extended its condolences to Bastian’s family, friends, colleagues and the #dedoc community.

His legacy will continue through the many people and communities he helped bring together.

A tomato-soy juice rich in plant compounds reduced several markers of inflammation in adults with obesity after four weeks.

The study tested a specially formulated drink containing high levels of lycopene and soy isoflavones.

Lycopene is the red pigment found in tomatoes.

Soy isoflavones are plant compounds that can have weak oestrogen-like effects in the body.

The trial included 12 healthy adults with obesity.

Participants drank two cans of tomato-soy juice each day for four weeks, then later drank a control tomato juice with lower levels of the key compounds.

Blood tests showed that only the tomato-soy juice significantly reduced three inflammatory proteins.

These were IL-5, IL-12p70 and GM-CSF.

There was also a fall in TNF-alpha, although that result was not statistically significant.

The researchers also studied urine metabolites and found changes suggesting the drink was having measurable effects on human biology.

Some changes appeared after both tomato drinks, which suggests tomatoes themselves may have biological activity.

But the soy-related metabolite changes were more specific to the tomato-soy juice.

This matters because obesity is often linked with chronic low-grade inflammation.

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Reducing that inflammation could be relevant for long-term health.

Still, this was a small study and should not be overplayed.

It does not prove that tomato-soy juice prevents disease or treats obesity-related inflammation in routine care.

But it does support further research into food-based approaches that may help calm inflammation.

The same drink is now being studied in people with pancreatitis, where inflammation is a major problem.

Persistent tiredness is often blamed on stress, poor sleep or overwork.

Those factors matter, but a new study suggests vitamin status may also play a role.

Researchers in Japan looked at around 600 healthy adults and measured levels of homocysteine, vitamin B12 and folate.

Homocysteine tends to rise when B12 or folate levels are low.

Participants also completed questionnaires assessing fatigue and motivation.

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The researchers found that people with higher homocysteine generally had lower B12 and folate levels.

They then looked at fatigue outcomes in men and women separately.

In men, higher homocysteine was linked with greater physical fatigue.

In women, it was linked with lower motivation.

The analysis accounted for several factors that could affect fatigue, including age, sleep duration, workload and eating habits.

That makes the findings more useful, although they are still observational.

The study does not prove that low B12 or folate directly caused the symptoms.

But it does suggest these nutrients should not be ignored.

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B12 and folate are involved in nerve function, red blood cell production and metabolism.

If levels are low, it is not surprising that energy and motivation may suffer.

The practical message is sensible.

If someone feels constantly tired, diet should be part of the picture, especially if they follow a restricted diet or have risk factors for deficiency.

It is not the only explanation, but it is one worth checking.

Beetroot juice may help lower blood pressure in older adults, partly by changing bacteria in the mouth.

That sounds odd, but the biology makes sense.

Beetroot is rich in nitrate, a compound also found in vegetables such as spinach, rocket, celery, fennel and kale.

Certain bacteria in the mouth help convert nitrate into compounds that support nitric oxide production.

Nitric oxide helps blood vessels relax.

That is important for healthy blood pressure control.

In the study, older and younger adults drank nitrate-rich beetroot juice twice a day for two weeks.

They also completed a separate phase with a placebo beetroot drink that had the nitrate removed.

Both age groups showed changes in their oral microbiome, but the blood pressure effect was seen in older adults.

In this group, nitrate-rich beetroot juice was linked with a fall in blood pressure.

The researchers also saw a reduction in Prevotella and an increase in bacteria such as Neisseria, which are thought to support nitrate processing.

This may help explain why older adults responded differently.

As people age, nitric oxide availability tends to decline and blood pressure often rises.

Supporting the nitrate to nitric oxide pathway may therefore matter more later in life.

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The study also raises a useful warning about antibacterial mouthwash.

If mouth bacteria are part of the nitrate pathway, wiping them out too aggressively may interfere with some of the benefits of nitrate-rich foods.

This does not mean beetroot juice is a treatment for hypertension.

People on blood pressure medication should not stop it because of a juice study.

But it does suggest nitrate-rich vegetables may be a useful part of a heart-healthy diet.

And it shows, once again, that oral health and wider health are more connected than they look.

A banana and berry smoothie looks like an obvious health win.

But a UC Davis study suggests that combination may reduce how much of one group of beneficial plant compounds the body absorbs.

The compounds are flavanols.

They are found in foods such as berries, apples, grapes, cocoa and tea, and have been linked with heart and brain health.

The issue is not that bananas are unhealthy.

The problem is an enzyme called polyphenol oxidase, or PPO.

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This enzyme is involved in the browning you see when fruit is cut or bruised.

Bananas have high PPO activity, while berries have much lower activity.

In the study, participants drank a banana-based smoothie, a mixed berry smoothie and a flavanol capsule as a control.

Blood and urine tests showed that the banana smoothie led to 84% lower flavanol levels compared with the control.

The berry smoothie produced flavanol levels much closer to the capsule.

That suggests the banana was interfering with flavanol availability.

The researchers also tested a setup where flavanols and the high-PPO banana drink did not contact each other before being consumed.

Flavanol levels were still reduced, suggesting PPO activity may continue to matter after swallowing.

This does not mean bananas should be avoided.

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They provide fibre, potassium and other useful nutrients.

But if the point of a smoothie is to maximise flavanols from berries, cocoa or grapes, banana may not be the best ingredient.

Better options may include mango, pineapple, orange or yoghurt.

The wider point is useful too.

A smoothie is not just a list of ingredients blended together.

Food combinations can change what the body actually absorbs.

A large study from Weill Cornell suggests that pregnancy does not become riskier simply because someone is older.

Instead, the evidence points to a different explanation – pregnancy acts like a stress test that magnifies whatever cardiovascular risk is already there.

Researchers analysed hospitalisation data from more than 2.7 million people with a first pregnancy across 11 US states.

Each patient served as their own control, with cardiovascular events during pregnancy and the postpartum period compared against an equivalent time one year later.

Overall, pregnancy and the postpartum period were associated with about seven times the risk of major adverse cardiovascular events compared with the control period.

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That fits with earlier research.

But the key point is what happened when the team looked at age.

The relative increase in risk compared with baseline did not vary with maternal age.

Older patients did have more cardiovascular events overall.

But the researchers say that reflects higher baseline cardiovascular risk, not an age-specific effect of pregnancy itself.

The most common complications were venous thromboembolism, cardiomyopathy and heart failure.

Stroke and brain haemorrhage were less common, but when they happened they were often devastating.

The study also found racial inequality.

Black patients were more likely to experience cardiovascular events than white patients, but again the age pattern did not explain this.

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That points towards other factors such as access to care, social determinants of health and differences in how risk factors are identified and managed.

The practical implication is fairly blunt.

Doctors should not assume that youth is protective and age is the only thing worth worrying about.

A healthy 40-year-old may carry less pregnancy-related cardiovascular risk than a 25-year-old with poorly controlled blood pressure, high cholesterol or other underlying issues.

That shifts the focus towards prevention.

Researchers at CU Anschutz have added another piece to the type 1 diabetes puzzle by targeting molecules called hybrid insulin peptides, or HIPs. These peptides are thought to help trigger the immune attack that destroys insulin-producing beta cells.

Type 1 diabetes develops when the immune system wrongly identifies part of the pancreas as foreign and starts attacking it.

For years, researchers assumed normal insulin proteins were the main target.

But the field changed when Thomas Delong and colleagues showed that the immune system was reacting to hybrid insulin peptides instead.

These are unusual peptide fragments formed by linking part of an insulin sequence to part of another protein.

Because that combined sequence is not directly encoded in the genome, the immune system may see it as foreign.

The new study looked at whether stopping these HIPs from forming could delay disease.

The researchers focused on an enzyme called cathepsin D, which appears to be involved in generating the peptides.

By modifying one of the two insulin genes in non-obese diabetic mice so cathepsin D could no longer act in the usual way, they were able to reduce HIP levels in beta cells.

That had a clear effect.

The mice showed less immune reactivity against insulin and diabetes developed more slowly.

After one year, 43% of the modified mice were still diabetes-free, compared with only 10% of normal mice.

The team is now modifying both insulin genes and says preliminary data suggest this cuts HIP formation by 80% to 100%.

That is a serious result, even if it is still confined to a mouse model.

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It does not mean a cure is around the corner.

Mouse findings do not always translate cleanly to people, and type 1 diabetes in humans is more complicated than any lab model.

But the logic is strong.

If HIPs are helping to switch the autoimmune attack on, then reducing their formation could become a genuine prevention strategy.

At the very least, this work moves the field from simply describing the immune attack to interfering with one of the triggers behind it.

A team in Geneva has developed an experimental gel designed to help insulin-producing cells survive after transplantation for type 1 diabetes.

The goal is to solve one of the biggest problems in this field – getting the transplanted cells to stay alive and work properly once inside the body.

In type 1 diabetes, the immune system destroys the beta cells in the pancreas that make insulin.

Replacing those cells can restore blood sugar control, at least for a time.

But standard islet transplantation has major drawbacks.

Donor tissue is scarce, rejection is a risk and the cells often struggle after being infused into the liver, where poor blood supply and inflammation can damage them.

The new gel, called Amniogel, is made from human amniotic membrane taken from the placenta after birth.

Researchers say it provides a more natural environment for pancreatic islets and helps recreate some of the support they lose during isolation.

The key feature is that the gel is combined with vessel-forming cells before transplantation.

These cells build a microvascular network around the islets before the graft is implanted.

Once inside the body, that network can connect to the host’s own circulation.

That matters because blood supply is one of the main reasons transplanted cells fail.

In diabetic mice, the grafts kept blood sugar levels normal for at least 100 days, which was the full follow-up period.

They performed better than islets transplanted on their own and better than constructs without engineered blood vessels.

The gel also appeared to slow the movement of cytotoxic immune cells in lab testing.

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That suggests it may offer some early protection from immune attack, although it is not being pitched as a full solution to rejection.

This is still preclinical work, so there is a long way to go before anything like this reaches patients.

The researchers say the next challenge is scaling it up so that larger or multiple grafts could meet human insulin needs.

Even so, this looks like one of the more practical attempts to build a true bioartificial pancreas rather than just transplant cells and hope for the best.

A new study from the University of Sydney suggests dietary changes may influence biological ageing markers surprisingly quickly.

Researchers followed 104 adults aged 65 to 75 who were randomly assigned to one of four diets for four weeks.

The diets differed in two main ways.

Some were more plant-based in their protein mix, while others contained more animal protein.

Some were higher in fat and lower in carbohydrate, while others were lower in fat and higher in carbohydrate.

The researchers then looked at 20 blood-based biomarkers linked to biological age.

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These included measures such as cholesterol, insulin and C-reactive protein.

The diet that showed the clearest effect was the lower-fat, higher-carbohydrate omnivorous diet.

Three of the four groups showed reductions in biological age scores, while the group eating most similarly to their usual diet showed no significant change.

That sounds dramatic, but it needs translating into plain English.

The study does not show that ageing has literally been reversed.

It shows that short-term changes in biomarkers used to estimate biological age can shift within a month.

That is still interesting, because it suggests the body can respond quite quickly to changes in diet quality and composition.

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But it is not the same thing as proving longer life, lower disease risk or lasting rejuvenation.

The trial was short, modest in size and limited to a specific age group.

It also does not tell us whether the changes would persist once people returned to normal eating.

So the sensible conclusion is cautious rather than breathless.

Food clearly matters, and later-life dietary changes may improve health-related markers faster than expected.

A large study has found that taking a daily multivitamin may modestly slow biological ageing in older adults.

Researchers analysed data from the COSMOS trial, which included 958 healthy participants with an average age of 70.

They used five DNA-based epigenetic clocks to estimate biological ageing over time.

Compared with people taking placebo, those taking a multivitamin showed slower ageing across all five measures.

Two of the clocks showed statistically significant changes.

Overall, the researchers estimated the effect was roughly equal to four fewer months of biological ageing over two years.

That is not nothing, but nor is it dramatic.

The study also found that the people who seemed to benefit most were those whose biological age already looked older than their chronological age at the start.

That may matter if future work confirms it.

The more important point, though, is one of scale.

This is not evidence that multivitamins make people meaningfully younger in any obvious real-world sense.

The effect was modest, and it was based on biomarker clocks rather than visible health outcomes.

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Researchers now want to see whether these changes help explain previous findings around cognition, cancer or cataract risk.

That is a fair next step.

For now, the result is best seen as a small but potentially useful signal.

Multivitamins may have some value in certain older adults, especially where diet quality is not ideal.

But no one should mistake this for a shortcut around the basics of ageing well.

Diet, activity, sleep and not smoking still matter far more.

The NHS rollout of artificial pancreas technology in England and Wales appears to be doing something previous diabetes tech programmes often failed to do.

It is narrowing the gap in access between richer and poorer communities, and between white patients and those from minority ethnic backgrounds.

That matters because earlier waves of diabetes technology, including continuous glucose monitors, were marked by obvious inequality.

People from deprived backgrounds and some minority ethnic groups were often less likely to get access, even when the benefits were clear.

The new data suggest the picture is different with hybrid closed-loop systems.

These systems combine a continuous glucose monitor, an insulin pump and an algorithm that adjusts insulin delivery in response to glucose levels.

In practical terms, they take much of the relentless mental burden out of living with type 1 diabetes, especially overnight and around meals.

The first two years of the rollout in England and Wales have focused on children.

Around 32,000 have now been fitted with the device, representing 72.3% of those eligible.

According to the figures reported, the gap in uptake between the most and least deprived groups is only around 3%, with a similarly small difference between minority ethnic groups and white patients.

That does not mean access is now perfect.

It means this rollout has been more equitable than previous ones, which is an achievement worth noticing.

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It also matters because the technology can be genuinely life-changing.

For some people, it reduces admissions with diabetic ketoacidosis, improves sleep and allows day-to-day life to feel less dominated by constant calculations and corrections.

The next challenge is obvious.

The rollout has to keep going until all eligible children and adults who want the technology can access it, regardless of where they live or who they are.

The progress so far is encouraging.

A deep tooth infection may seem like a local problem, but researchers are increasingly looking at how it might affect the rest of the body.

The condition in question is apical periodontitis, an infection around the tip of the tooth root.

It often causes little or no pain, which means many people do not know they have it until it shows up on an X-ray.

That is part of the problem.

A silent infection can sit there for months or years while the immune system stays switched on in the background.

Researchers now think that low-grade inflammation from these infections may spill into the bloodstream and interfere with wider metabolic health.

In some studies, people who had root canal treatment for chronic tooth-root infections later showed lower blood sugar levels and reduced inflammatory markers.

The theory is straightforward.

If the body is constantly dealing with infection, insulin may work less effectively and tissue healing may be impaired.

That could be especially relevant in people with diabetes, who are already more likely to struggle with healing and inflammation.

The relationship appears to go both ways.

• Gum disease
• People with a sweet tooth are 31% more likely to have depression

Diabetes may make healing after root canal treatment more difficult, while untreated infection may add to the inflammatory burden.

That does not mean root canals are a treatment for diabetes.

The studies so far show association and possible metabolic benefit, but not proof of direct cause and effect.

Still, the broader lesson is useful.

Mouth health and general health are not separate worlds.

A hidden dental infection may be worth taking seriously not just to save the tooth, but because chronic inflammation rarely stays neatly contained.