Continuous glucose monitors could provide benefits beyond helping people manage their blood sugar, according to a large study published in JAMA Network Open.

Researchers from Kaiser Permanente examined whether sustained use of continuous glucose monitoring (CGM) was associated with better long-term glucose control and kidney health in adults with type 2 diabetes.

The study included 25,648 adults considered at higher risk because they had poorly controlled diabetes or a history of severe hypoglycaemia.

Of these, 2,771 started using real-time CGM, while 22,877 served as a comparison group.

Researchers followed outcomes for up to three years.

What happened to HbA1c?

The differences in glucose control appeared relatively quickly and persisted.

After one year, HbA1c was approximately 1.1 percentage points lower in the CGM group than in the comparison group.

After three years, the difference remained substantial.

Average HbA1c was 7.83% in the CGM group, compared with 8.58% among non-users.

That represents a difference of approximately 0.75 percentage points, equivalent to around 8 mmol/mol.

The findings suggest that people who continue using CGM may be better able to maintain improvements in glucose management rather than experiencing a gradual deterioration over time.

What about kidney health?

Researchers also examined two important markers of diabetic kidney disease.

The first was the urinary albumin-to-creatinine ratio, or UACR, which measures how much albumin is leaking into the urine.

The second was estimated glomerular filtration rate, or eGFR, which assesses how effectively the kidneys filter blood.

After three years, UACR was approximately 125mg/g lower among people who continued using CGM than among those in the comparison group.

However, there was no significant difference in eGFR.

That distinction matters.

Lower albuminuria may indicate an improvement in kidney health, but the study did not establish that CGM prevents kidney failure or permanently preserves kidney function.

Why might CGM help?

CGM provides frequent glucose measurements throughout the day and night.

Unlike intermittent finger-prick blood glucose testing, it can show patterns and trends that may otherwise be missed.

This can help people understand how meals, physical activity, medication and illness affect glucose.

It may also provide earlier warnings of hypoglycaemia.

Over time, better glucose management could help reduce exposure to persistently high blood sugar, an important contributor to long-term complications.

What are the limitations?

This was not a randomised clinical trial.

Researchers used healthcare records and statistical techniques to approximate a trial comparing sustained CGM use with non-use.

People who continued using CGM may have differed from non-users in other important ways.

There was also substantial loss of participants from the analysis over time, including people who stopped using their sensors.

These factors mean the results demonstrate an association rather than proving that CGM caused the improvements.

What does this mean for the UK?

CGM is already an important part of diabetes management, particularly for people with type 1 diabetes and some people with insulin-treated type 2 diabetes.

The findings strengthen the case for studying its longer-term benefits among adults with type 2 diabetes who have difficulty maintaining glucose control.

But NHS eligibility and prescribing arrangements have not changed because of this study.

People with diabetes should continue attending their annual diabetes health checks, including kidney assessments.

Managing high blood pressure also remains essential for protecting kidney and cardiovascular health.

The important finding is that sustained glucose monitoring was associated with benefits lasting several years, although whether those benefits ultimately prevent serious kidney complications requires further research.

Primary study: Continuous Glucose Monitoring and Long-Term Glycemic and Kidney Outcomes – JAMA Network Open

An experimental treatment combining tirzepatide with a second hormone-based medicine has produced greater weight loss and reductions in blood glucose than tirzepatide alone in people with type 2 diabetes.

The new treatment, called EloraTZP, combines tirzepatide with eloralintide, an experimental drug that mimics the effects of the hormone amylin.

Tirzepatide is already used in the UK under the brand name Mounjaro for type 2 diabetes and weight management.

EloraTZP adds another hormonal pathway.

While tirzepatide acts on the GIP and GLP-1 receptors, eloralintide targets amylin signalling.

Amylin is a hormone normally released alongside insulin after eating. It can slow stomach emptying, suppress glucagon and help people feel fuller.

Diabetes.co.uk has more information on amylin and amylin analogue medicines.

What did the trial find?

The Phase 2b trial involved 367 adults with overweight or obesity and type 2 diabetes in the US and Argentina.

Participants were assigned to different doses of EloraTZP, eloralintide alone, tirzepatide alone or placebo.

After 48 weeks, people receiving the highest tested EloraTZP dose had lost an average of 23.3% of their starting body weight.

That compared with 14.8% among people taking the highest 15mg dose of tirzepatide alone.

The difference is notable because this was a direct comparison within the same clinical trial rather than a comparison between separate studies.

People with type 2 diabetes also tend to lose somewhat less weight with incretin-based medicines than people without diabetes, making the scale of weight loss particularly noteworthy.

Research into GLP-1 and newer multi-hormone treatments has expanded rapidly in recent years as companies investigate whether targeting several metabolic pathways can produce stronger effects.

HbA1c also fell substantially

The treatment also improved blood glucose.

People receiving EloraTZP experienced reductions in HbA1c of up to 2.9 percentage points, compared with a reduction of around 2.4 percentage points among those receiving tirzepatide alone.

HbA1c reflects average blood glucose over roughly the previous two to three months and is one of the principal measures used to monitor diabetes.

For people with type 2 diabetes, lowering persistently high blood glucose can reduce the risk of complications over time.

However, the exact HbA1c target varies between individuals and treatment decisions should consider factors such as age, other medical conditions and the risk of hypoglycaemia.

Why add amylin to tirzepatide?

Tirzepatide already acts on two hormone receptors – GIP and GLP-1.

The addition of eloralintide introduces a third pathway by targeting amylin.

Amylin plays several roles after eating.

It can:

• reduce appetite
• slow the movement of food out of the stomach
• reduce glucagon release after meals
• contribute to feelings of fullness

Researchers hope that combining these effects with GIP and GLP-1 activity could produce stronger weight loss without needing increasingly high doses of one single drug.

The strategy reflects a broader move towards multi-target medicines.

GLP-1 medicines were initially developed primarily to improve blood glucose, but newer treatments increasingly combine effects on appetite, body weight and metabolic health.

The side effects are an important caveat

The headline weight-loss figure needs to be considered alongside tolerability.

Gastrointestinal side effects were the most common adverse events and were generally described as mild or moderate.

They occurred particularly during dose escalation.

However, depending on the dose used, between 10.8% and 27% of participants receiving EloraTZP stopped treatment because of adverse effects.

The discontinuation rate with tirzepatide alone was substantially lower, at 2.9% in the trial.

This is important because a medicine’s effectiveness in a clinical trial matters less if a significant proportion of patients cannot tolerate taking it long term.

Nausea, vomiting and diarrhoea are already recognised side effects of GLP-1-based treatments.

Diabetes.co.uk has previously examined the digestive side effects and wider safety profile of GLP-1 medicines.

Lilly said that escalating two medicines simultaneously may have contributed to the dropout rate and plans to modify dosing approaches in later trials.

That remains a hypothesis until the Phase 3 studies show whether tolerability actually improves.

Is EloraTZP better than Mounjaro?

The trial found greater average weight loss and HbA1c reduction with some EloraTZP doses than with tirzepatide alone over 48 weeks.

That is a legitimate head-to-head finding.

But it would be premature to conclude that EloraTZP is a better treatment overall.

This was a Phase 2b trial involving only 367 people.

Phase 3 studies will need to confirm the effect in much larger populations and establish whether the additional weight loss outweighs the increased side effects.

There are also no long-term cardiovascular or kidney outcome data for EloraTZP.

For people with type 2 diabetes, those outcomes matter because the condition is associated with increased risks of heart disease and kidney disease.

What about the 23% weight-loss figure?

The 23.3% result refers to the average weight reduction in the highest-dose EloraTZP group within this particular trial.

It does not mean everyone taking the drug lost 23% of their body weight.

Individual responses to weight-loss and diabetes medicines vary considerably.

The study also lasted 48 weeks, so it does not yet tell us what happens after several years of treatment or after the medicine is stopped.

Research with existing GLP-1 treatments suggests that some weight can return after treatment is discontinued.

Longer-term data will therefore be essential.

Is EloraTZP available in the UK?

No.

EloraTZP is an investigational treatment and has not been approved for routine prescribing in the UK.

Lilly says it plans to begin Phase 3 trials during the final quarter of 2026.

People currently prescribed tirzepatide should not change or combine their medication on the basis of these findings.

Eloralintide is also not an approved UK diabetes or weight-loss medicine.

Current treatment decisions for type 2 diabetes should continue to be based on licensed medicines and advice from the person’s diabetes team.

The trial nevertheless provides an important indication of where obesity and diabetes treatment may be heading.

Rather than relying on one hormonal pathway, the next generation of medicines is increasingly being designed to act on several signals controlling appetite, glucose and metabolism simultaneously.

Whether that produces better long-term health outcomes, rather than simply greater weight loss, will be the key question for the larger trials now planned.

Primary source: Eli Lilly – EloraTZP Phase 2b results, 30 September 2026

A new GLP-1 medicine taken as a daily tablet has produced substantial improvements in blood glucose in a phase 3 trial involving adults with type 2 diabetes.

Safiglipron is an experimental small-molecule GLP-1 receptor agonist designed to be swallowed without some of the fasting and dietary restrictions associated with existing oral GLP-1 treatments.

That distinction is becoming increasingly relevant in the UK. An oral Wegovy tablet was approved in the UK earlier this year, while a tablet form has subsequently become available privately.

The OUTSTAND-1 trial recruited 284 adults with type 2 diabetes across 46 centres in China.

Participants had an average starting HbA1c of 7.95% and had been living with diabetes for a median of 1.6 years.

Their diabetes was being managed with diet and physical activity alone rather than glucose-lowering medication.

Participants were randomly assigned to safiglipron at doses of 30mg, 60mg or 90mg once daily, or placebo.

After 32 weeks, average HbA1c fell by:

• 1.40 percentage points with 30mg
• 1.38 percentage points with 60mg
• 1.63 percentage points with 90mg
• 0.18 percentage points with placebo

HbA1c gives an indication of average blood glucose over the preceding two to three months and is one of the main measures used to assess type 2 diabetes control.

Around 71% to 78% of participants taking safiglipron reached an HbA1c below 7%, compared with 25% taking placebo.

Up to 68.1% reached 6.5% or below.

Fasting blood glucose also improved, with the 90mg dose producing a reduction of around 2.08 mmol/L compared with placebo.

What happened to body weight?

Weight loss was present, although it was more modest than that reported with some of the latest injectable treatments.

People taking the highest 90mg dose lost an average of 4.78% of their starting body weight, compared with 1.22% with placebo.

That means safiglipron may ultimately be positioned primarily as a glucose-lowering treatment rather than purely a weight-loss medicine.

Even so, weight remains clinically relevant because reducing excess body weight can improve insulin sensitivity and make blood glucose easier to control.

Why does another oral GLP-1 matter?

Most of the medicines that have driven the recent growth in GLP-1 treatment have been injections.

For some people, a tablet may be easier to accept and use consistently.

Safiglipron is also structurally different from peptide-based drugs such as semaglutide.

It is a small molecule, which may eventually make manufacturing and administration simpler.

However, it is important not to confuse this drug with existing oral semaglutide or the recently approved UK oral Wegovy formulation.

Safiglipron remains experimental.

What about side effects?

The most commonly reported adverse events were gastrointestinal, including nausea and other digestive symptoms.

This broadly mirrors the established side-effect profile of the GLP-1 drug class.

Diabetes.co.uk has previously covered the common and more serious side effects associated with GLP-1 treatments.

Treatment was stopped because of adverse events in:

• 1.4% of people taking 30mg
• 2.9% taking 60mg
• 6.9% taking 90mg
• none of those taking placebo

The higher discontinuation rate at 90mg suggests there may be a trade-off between stronger glucose lowering and tolerability.

What are the limitations?

This was a randomised phase 3 trial, so it provides considerably stronger evidence than an observational study.

But there are important caveats.

All participants were recruited in China and had relatively early type 2 diabetes.

Most were not already using diabetes medication.

The study therefore cannot tell us exactly how safiglipron would perform in a broader UK population, including people with longstanding diabetes, multiple medications or more advanced complications.

The placebo-controlled period also lasted only 32 weeks.

Longer studies are needed to establish whether the improvements are sustained and whether the drug has any effect on cardiovascular disease, kidney disease or other long-term complications.

What does it mean for people in the UK?

There is no immediate change to NHS treatment.

Safiglipron is not currently licensed in the UK.

People with type 2 diabetes already have a range of treatment options, and medication choice depends on factors including HbA1c, cardiovascular risk, kidney health, body weight and individual preference.

The wider significance is that oral GLP-1 treatment is developing rapidly.

The UK already has its first approved oral GLP-1 weight-loss treatment, and safiglipron suggests that considerably more oral incretin medicines could follow.

Primary study: https://www.nature.com/articles/s41591-026-04651-9

An experimental weekly injection targeting two metabolic hormone pathways has produced significant weight loss and improved blood glucose in adults with type 2 diabetes.

Survodutide activates both the GLP-1 and glucagon receptors.

That makes it different from semaglutide, which primarily acts on GLP-1, and Mounjaro (tirzepatide), which targets GLP-1 and GIP.

The phase 3 SYNCHRONIZE-2 trial investigated survodutide in adults with overweight or obesity and type 2 diabetes.

After 76 weeks, participants receiving the drug lost up to an average of 13.1% of their starting body weight, compared with 3.1% among people receiving placebo.

Up to 79.3% of people taking survodutide lost at least 5% of their starting weight, compared with 32.7% receiving placebo.

The findings add to a rapidly expanding body of evidence around GLP-1 and multi-hormone weight-loss medicines.

Blood glucose also improved

Participants began the study with an average HbA1c of around 7.4%.

Survodutide lowered HbA1c by up to 1.21 percentage points, compared with a reduction of only 0.03 percentage points with placebo.

HbA1c is one of the principal measures used to assess longer-term blood glucose control in type 2 diabetes.

Up to 29.5% of participants receiving survodutide reached an HbA1c below 5.7%, compared with 4% receiving placebo.

That is below the usual diagnostic range for diabetes.

However, it should not be described as permanent reversal or remission.

The participants were still receiving an active glucose-lowering medicine when their HbA1c was measured.

Why could weight loss help diabetes?

Body weight and type 2 diabetes are closely linked for many people because excess visceral fat can contribute to insulin resistance.

Reducing excess weight can improve the body’s response to insulin and make glucose easier to manage.

The survodutide study also reported reductions in waist circumference.

At the strongest response, waist circumference fell by around 11.1cm compared with 3.5cm with placebo.

This matters because abdominal or visceral fat is particularly strongly associated with insulin resistance and type 2 diabetes.

Fasting glucose and measures of insulin resistance also improved.

How is survodutide different?

The drug’s glucagon activity is one of the main reasons researchers are interested in it.

Glucagon is commonly known as a hormone that raises blood glucose.

However, glucagon receptor activation can also affect energy expenditure and fat metabolism.

When combined carefully with GLP-1 receptor activation, researchers hope this could increase weight loss while retaining glucose-lowering effects.

This follows the broader trend towards drugs that activate more than one metabolic pathway.

Tirzepatide targets GLP-1 and GIP, while several experimental medicines are now targeting two or even three receptors simultaneously.

How does it compare with Mounjaro or Wegovy?

It would be misleading to compare the percentages directly and conclude that one medicine is better.

SYNCHRONIZE-2 compared survodutide with placebo.

It did not directly compare survodutide with semaglutide or tirzepatide.

Different trials also involve different participants, treatment durations, doses and statistical methods.

Head-to-head studies provide much stronger evidence for comparisons between medicines.

The recent Diabetes.co.uk review of the wider field showed just how quickly GLP-1 and co-agonist treatments are evolving.

Side effects were important

The most commonly reported adverse effects were gastrointestinal.

These included:

• nausea
• vomiting
• diarrhoea
• constipation

This is broadly consistent with the wider GLP-1 class.

However, around 18% of participants receiving survodutide stopped treatment because of gastrointestinal side effects, compared with 1.2% of those receiving placebo.

That is not a trivial figure.

The developers have suggested that more flexible dose escalation may improve tolerability in future trials, but that still needs to be demonstrated.

People using existing GLP-1 medicines should also be aware that digestive symptoms are common and that a smaller number of complications require urgent assessment. Diabetes.co.uk has a fuller guide to when GLP-1 side effects may become more serious.

What happens when treatment stops?

This study does not answer that question.

It is particularly relevant because research across existing GLP-1 treatments suggests that a substantial amount of lost weight can return after medication is stopped.

If survodutide eventually reaches clinical practice, researchers will therefore need to establish whether it is best viewed as a long-term treatment and what happens after withdrawal.

What does it mean for the UK?

Survodutide is not currently available as a routine UK diabetes or obesity treatment.

It remains under clinical development.

For now, established therapies remain the relevant options for people with type 2 diabetes, including lifestyle changes, conventional glucose-lowering medicines and, where appropriate, treatments such as Mounjaro.

The more important question is whether survodutide eventually improves outcomes beyond weight and HbA1c.

Future evidence will need to show whether treatment reduces complications such as cardiovascular disease, kidney disease and premature death, while remaining tolerable enough for long-term use.

If those results are positive, survodutide could become another significant option in the rapidly expanding field of metabolic medicines.

Primary study: Survodutide Once Weekly in Adults with Obesity and Type 2 Diabetes. New England Journal of Medicine, 2026. DOI: 10.1056/NEJMoa2607219

The genetics behind obesity appear to change as we grow.

A large study published in Nature Genetics has identified hundreds of genetic variants influencing body weight during childhood, with many behaving differently later in life.

Researchers combined objectively measured BMI from more than 62,000 children with larger datasets containing information on childhood body size and puberty.

Their combined genetic analysis had an effective sample size approaching 600,000 people.

They identified 624 independent genetic signals associated with childhood adiposity.

What makes the study interesting is that almost one-third of those signals did not behave in the same direction during adulthood.

The researchers reported that 196 of the 624 signals – 31% – had no concordant effect on adult BMI.

That challenges the idea that childhood obesity is simply adult obesity beginning early.

Some biological pathways appear particularly important during specific stages of development.

Genes involved in the leptin-melanocortin system, which helps the brain regulate hunger and energy balance, featured prominently.

Researchers also identified childhood-specific effects involving GIPR and GLP1R, receptors involved in incretin signalling.

Those names may be familiar because the same broad hormonal system is targeted by some modern diabetes and obesity medicines.

Rare variants in genes including MC4R, POMC, ADCY3 and MRAP2 also appeared to have stronger effects on childhood body size than adult BMI.

This reinforces something researchers already suspected from studies of obesity-related genes and type 2 diabetes: people can reach a similar body weight through different biological routes.

It also helps explain why two children with apparently similar environments can have very different tendencies to gain weight.

That should not be interpreted to mean childhood obesity is predetermined.

The researchers also examined whether genetically influenced childhood adiposity translated into future conditions including type 2 diabetes and high blood pressure.

The initial association was largely lost once adult BMI was accounted for.

In other words, much of the later cardiometabolic risk appeared to operate through body weight remaining higher into adulthood rather than through childhood adiposity acting independently forever.

That is potentially encouraging.

Children with obesity should not be told their future health has already been decided by either their weight or their genes.

Previous research has shown that children with obesity can remain at increased cardiometabolic risk even when standard blood tests currently look normal, which is why early support matters.

But the new genetic findings suggest persistence into adult life is particularly important for long-term disease.

That is relevant to type 2 diabetes prevention because excess body fat can drive insulin resistance long before diabetes is diagnosed.

It also supports focusing on sustainable family-level changes rather than crash diets or blaming children.

Food quality matters – research has linked higher ultra-processed food intake in young children with less favourable cardiometabolic measures – but genetics, development, sleep, physical activity, social environment and food availability all play a role.

That complexity is exactly why childhood obesity cannot sensibly be reduced to “eat less and move more”.

Nor is this study a genetic test parents can order.

Polygenic research is useful for understanding biology across populations but is currently far less useful for predicting exactly what will happen to one individual child.

The practical message is simpler.

A child can carry genetic susceptibility without being destined to develop type 2 diabetes.

And the distinction between childhood and adult genetics strengthens the case for intervening early while development is still highly dynamic.

Study: Nature Genetics – Genome-wide mapping of common and rare variant effects on adiposity across childhood

A tablet that targets the blood vessels damaged in diabetic retinopathy has shown encouraging early results in people with diabetes.

Researchers at Trinity College Dublin and Breye Therapeutics tested an experimental drug called danegaptide, which is taken orally rather than injected into the eye.

The research focused on non-proliferative diabetic retinopathy, an earlier stage of diabetic eye disease in which high blood glucose damages small blood vessels in the retina.

In laboratory models, danegaptide reduced leakage from retinal blood vessels, protected the inner blood-retina barrier and reduced retinal swelling.

Researchers then tested the treatment in 24 people with non-proliferative diabetic retinopathy and mild centre-involved macular oedema.

The treatment was reported to be safe and well tolerated in this early study.

Around 55% of participants also showed what the researchers describe as early biological activity.

That included reductions in retinal leakage, decreased thickness in the centre of the retina and, in some participants, resolution of fluid-filled cysts inside the retina.

That is potentially important because fluid leaking into the macula can lead to diabetic macular oedema and maculopathy.

Current treatment for more advanced diabetic retinal disease can include injections directly into the eye.

Those injections, including anti-VEGF treatment, can be highly effective, but they usually need to be given repeatedly and require regular hospital appointments.

An oral treatment that could intervene earlier would therefore be attractive.

But this study is nowhere near proving that a tablet can replace eye injections.

Twenty-four patients is a very small trial.

The main purpose of phase 1 studies is generally to assess safety, dose and biological activity rather than prove that a treatment prevents sight loss.

There is also a major difference between making a retinal scan look better and showing that patients actually maintain better vision over several years.

That will require much larger randomised trials.

The researchers now plan to move into phase 2 testing, with a larger controlled study expected to investigate whether the promising biological changes translate into meaningful clinical benefit.

For people living with type 1 diabetes or type 2 diabetes in the UK, nothing changes yet.

The most effective approach remains detecting retinal changes before they affect sight.

That means attending diabetic eye screening when invited and not assuming that normal vision means the retina is healthy.

Retinopathy can develop without noticeable symptoms.

Managing HbA1c, blood pressure and other cardiovascular risk factors also remains central to reducing progression.

People with diabetes should also keep up with wider screening for diabetes complications rather than waiting until symptoms develop.

Danegaptide is therefore an interesting treatment to watch, not something patients can currently request.

If larger trials work, however, the idea of treating early diabetic retinal disease with a tablet rather than waiting until injections become necessary could represent a meaningful change in care.

Study: Science Translational Medicine – danegaptide in diabetic retinopathy

Researchers have identified a gut bacterial molecule that appears to switch up energy use in visceral fat.

The discovery comes from scientists at Duke University School of Medicine studying a newly identified human gut bacterium called Clostridium immunis.

The bacterium produces a complex sugar called an exopolysaccharide.

Attached to that sugar is a chemical group called phosphocholine.

In experiments with obese mice, the molecule reduced visceral fat – the metabolically active fat that surrounds internal organs and is strongly associated with insulin resistance and type 2 diabetes.

The mechanism was unusual.

The mice did not appear to eat less.

They also did not lose muscle.

Instead, metabolic activity increased specifically in visceral fat tissue, causing the animals to expend more energy.

Researchers showed that the phosphocholine component was essential.

When the bacterium was genetically altered so it could no longer make that part of the molecule, the protection against obesity disappeared.

The effect involved the immune system too.

The bacterial molecule altered signalling involving interleukin-22, or IL-22, and a group of immune cells called group 3 innate lymphoid cells.

That ultimately changed metabolic activity within abdominal fat.

This is another example of researchers discovering that fat tissue is not simply passive energy storage.

Excess visceral fat can actively influence inflammation and metabolic disease.

The gut microbiome may be part of that relationship.

Previous work has suggested that gut microbes influence how much energy is extracted from food, while other studies have linked changes in gut bacteria with obesity and metabolic health.

Research has even found associations between sugary drinks, gut bacteria and future diabetes risk.

But this new study is several steps away from a human treatment.

The obesity experiments were carried out in mice.

Nobody has been given C. immunis as an obesity therapy.

Nobody has been treated with the isolated bacterial molecule.

There is no established human dose, safety profile or evidence that deliberately changing IL-22 signalling would be beneficial over the long term.

The researchers did find an intriguing human association.

When they examined microbiome datasets from thousands of people, genes involved in making bacterial phosphocholine were less abundant among people with obesity or high triglycerides.

That provides a reason to continue the research.

It does not prove that lacking these bacteria caused their obesity.

The direction of the relationship could run either way.

Diet, body weight and metabolic disease themselves can change the microbiome.

This means there is currently no reason to buy a probiotic claiming to reproduce the effect.

C. immunis is not an established weight-loss probiotic, and the active compound is not a licensed medicine.

For people trying to reduce excess abdominal fat, the evidence still supports established approaches including sustainable weight loss, dietary change and regular exercise.

Those changes can also improve triglycerides and reduce cardiovascular risk associated with diabetes.

The importance of this study is what it tells us about biology.

Most current obesity treatments either reduce appetite, change nutrient absorption or alter hormonal signalling.

If future human research confirms that bacterial metabolites can safely increase energy expenditure within visceral fat, the microbiome could eventually offer a completely different treatment route.

That is an interesting possibility.

For now, it remains a mouse experiment.

Study: Cell Host & Microbe – A commensal-derived sugar protects against obesity by regulating immunometabolism

Genes influence the risk of developing type 2 diabetes, but they are not the whole story.

A UK Biobank study suggests diet and activity remain associated with diabetes risk even among people with a relatively high inherited susceptibility.

Researchers analysed 56,964 adults who did not have diabetes at the start of the study.

Over an average follow-up of 7.8 years, 926 developed type 2 diabetes.

Diet was assessed using repeated 24-hour food records, while physical activity was measured objectively using wrist-worn accelerometers.

Researchers also constructed a genetic risk score based on hundreds of variants associated with type 2 diabetes.

The analysis found that each 10 percentage-point increase in the proportion of the diet classed as ultra-processed food was associated with around a 7% higher relative risk of developing type 2 diabetes.

People who were more physically active had a lower risk.

Among participants with high genetic susceptibility, the combination of lower ultra-processed food intake and recommended levels of moderate-to-vigorous activity was associated with roughly half the risk seen in the less favourable lifestyle comparison group.

The findings fit with earlier studies linking high ultra-processed food intake with type 2 diabetes and other cardiometabolic conditions.

They also fit with the established relationship between exercise and diabetes prevention.

But some of the headlines around this research have gone too far.

This was not a trial in which people reduced their ultra-processed food intake and researchers watched their diabetes risk fall.

Participants’ existing habits were measured and then compared with future diagnoses.

That means the correct phrase is “associated with lower risk”, not “cuts your risk”.

Independent UK experts highlighted exactly this issue.

They also pointed out that people eating different amounts of ultra-processed food differed in other ways, including education, smoking, alcohol use and overall diet.

Researchers adjusted for many of those factors, but observational studies cannot remove every possible source of confounding.

There is another important wrinkle.

Ultra-processed food is an enormous category.

It includes products with very different nutritional profiles.

When the researchers separated the category into subgroups, ultra-processed drinks were the only individual category that remained significantly associated with diabetes after full adjustment.

That means the study does not prove that industrial processing itself is the problem.

This nuance matters because previous research has linked UPFs with a wide range of health outcomes, but the category can include everything from confectionery and sugary drinks to some packaged wholegrain foods.

Even studies where people consumed similar calories have found differences between ultra-processed and less processed diets, but scientists are still working out how much comes from processing, food structure, calorie density, fibre, additives or simply the types of foods people choose.

The genetic result is perhaps the most useful part.

Having a higher genetic susceptibility to diabetes did not make lifestyle factors irrelevant.

That fits with what we know about insulin resistance and obesity and type 2 diabetes: risk develops through an interaction between biology and environment rather than either one acting alone.

Physical activity deserves particular attention.

Unlike diet, it was measured using a wearable device, and experts commenting on the study noted that its association with lower diabetes risk was stronger and more consistently measured.

For someone trying to lower their diabetes risk, the evidence therefore supports a familiar combination: eat a good-quality diet, keep highly processed discretionary foods and sugary drinks limited, and stay physically active.

What this paper does not provide is a mathematical promise that replacing exactly 10% of your diet will cut your personal diabetes risk by a particular percentage.

Study: Diabetes – Associations of Ultraprocessed Food Intake, Wearable-Measured Lifestyle Factors and Genetic Susceptibility With Incident Type 2 Diabetes

Inflammation may help connect some of the biggest cardiovascular risk factors – including excess abdominal fat, smoking and psychological distress – with changes inside the heart.

Researchers from Imperial College London analysed data from up to 488,079 UK Biobank participants.

They used a blood marker called GlycA to estimate chronic systemic inflammation, then combined this with heart MRI scans, protein measurements, genetic data and long-term cardiovascular outcomes.

Higher levels of inflammation were linked with smaller volumes in the heart’s main pumping chamber, reduced stroke volume and compensatory increases in heart rate.

• Tomato-soy juice reduced inflammation markers in adults with obesity
• Natural brakes on inflammation could lead to new treatments for chronic disease

These are subtle structural and functional changes that can occur before someone is diagnosed with heart failure.

The difference in longer-term risk was also substantial.

Participants in the highest fifth for GlycA had a 43% higher adjusted risk of a major cardiovascular event compared with people in the lowest fifth.

These events included outcomes such as heart attacks and strokes.

Researchers also identified inflammatory proteins involving pathways such as interleukin-1 and tumour necrosis factor that may partly connect systemic inflammation with cardiac remodelling.

Among the strongest factors associated with higher inflammation were trunk fat, current smoking, psychological distress and lower socioeconomic status.

Genetic susceptibility also appeared to influence how strongly environmental factors translated into inflammation and cardiovascular risk.

But this remains observational research.

It does not show that reducing a GlycA result itself would prevent a heart attack, and GlycA is not a standard NHS diabetes blood test.

Nor should the results be interpreted as saying psychological distress directly “damages the heart”.

The relationships are complex and may run in both directions.

• Statin muscle side effects may involve inflammatory danger signals
• Fasting diet may reduce gum disease inflammation

The diabetes relevance is nevertheless strong.

People with diabetes already face an increased cardiovascular risk, and metabolic disease is closely tied to chronic low-grade inflammation.

The findings add another reason to focus on the fundamentals that can be changed: smoking, central obesity, physical activity, blood pressure, cholesterol and glucose control.

They also reinforce that social and psychological health cannot always be separated neatly from physical cardiovascular risk.

How long you sleep matters, but new research suggests how you sleep may matter too.

A large UK Biobank study has examined sleep stages, sleep duration and disrupted sleep in 95,559 middle-aged and older adults.

Instead of relying only on questionnaires, researchers used data from wrist-worn accelerometers and a deep-learning system called SleepNet to estimate REM sleep, light sleep and deep sleep.

Participants were then followed for a median of almost nine years.

Researchers identified 156 associations between sleep patterns and the later development of different health conditions.

Greater amounts of REM sleep were associated with a lower risk of dozens of diseases.

More deep, or N3, sleep was associated with lower risk of seven conditions, including type 2 diabetes.

Sleep duration showed a striking pattern too.

For 69 health outcomes, the lowest risk tended to fall within a window of around six to eight hours a night.

People sleeping for less than five hours showed the broadest pattern of increased disease risk.

That does not prove that getting an extra hour of deep sleep will prevent diabetes.

This was an observational study.

People who sleep badly may have other health conditions or behaviours that partly explain their future disease risk.

The sleep stages were also estimated from wrist movement using an algorithm rather than measured directly using a clinical overnight sleep study.

So there is no reason to obsess over the “deep sleep” number produced by a consumer smartwatch.

Those estimates are not a diabetes diagnostic test.

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For people with diabetes, however, sleep is increasingly difficult to dismiss as a lifestyle side issue.

Sleep disruption can interact with appetite, insulin sensitivity, physical activity, mental health and glucose management.

The useful target is still remarkably basic: enough regular, good-quality sleep rather than chasing a perfect wearable score.

And if someone regularly sleeps very little, wakes repeatedly, snores heavily or feels exhausted despite spending enough time in bed, that may be worth discussing with a GP rather than simply accepting poor sleep as normal.

Study link: Read the study in PLOS Medicine

A diagnosis of gestational diabetes is becoming more common – but the increase is not being shared equally across society.

Researchers at Karolinska Institutet analysed 938,798 singleton pregnancies recorded in Sweden between 2015 and 2023.

They linked pregnancy records with national information on income, education and country or region of birth.

Across that period, gestational diabetes prevalence increased from 1.5% to 6.6%.

The increase was steepest among women born outside Sweden, those with lower educational attainment and those living on lower incomes.

That is a substantial rise.

But it should not automatically be interpreted as evidence that diabetes suddenly became four times more common because people’s biology changed.

Screening practices and diagnostic criteria also changed during the study period, and these can affect how many cases are detected.

The researchers nevertheless found clear social differences even after accounting for a range of other characteristics.

Gestational diabetes develops when the body cannot produce enough insulin to overcome the increased insulin resistance of pregnancy.

It causes and can increase the risk of complications for both mother and baby.

The Swedish study found that gestational diabetes was associated with pregnancy, obstetric, postpartum and neonatal complications.

But the strength of those associations varied between social groups.

For example, among Swedish-born women, gestational diabetes was associated with 71% higher odds of obstetric complications compared with Swedish-born women without gestational diabetes.

The relative increase was smaller among women born in Africa and the Eastern Mediterranean region.

That does not mean those groups had healthier pregnancies.

Some groups, including women born in Africa and Southeast Asia, had higher overall – or absolute – rates of complications.

This distinction between relative and absolute risk is important when discussing health inequalities.

There are several possible explanations.

Access to healthcare, language, income, food environment, housing, employment conditions and differences in underlying health can all influence pregnancy outcomes.

Diagnostic practices may also differ between populations and regions.

Because this was a registry study, it cannot determine which of those factors caused the differences.

Researchers also lacked detailed data on factors such as sleep, physical activity and social support.

The results therefore show inequality, not a single biological explanation for it.

The findings are highly relevant to UK maternity services even though the exact Swedish figures should not be imported directly.

Taking basal insulin every day could eventually become unnecessary for some people with type 2 diabetes.

The US Food and Drug Administration has approved insulin efsitora alfa-gobe, marketed as Onswik, as a once-weekly basal insulin for adults with type 2 diabetes.

Instead of approximately 365 basal injections a year, a weekly treatment would mean around 52.

The drug is designed to release insulin slowly enough to provide background glucose control across seven days.

The FDA decision was based on four phase 3 QWINT trials involving more than 3,400 adults with type 2 diabetes.

Participants included people starting insulin for the first time as well as people who were already using basal or basal-bolus insulin.

Across the studies, once-weekly efsitora reduced HbA1c by a similar amount to once-daily insulin glargine or insulin degludec.

The trials therefore met their main goal of showing that weekly treatment was not inferior to the established daily insulins for glucose lowering.

That builds on earlier research showing that weekly insulin injections can control glucose similarly to daily treatment.

The attraction is straightforward.

Starting insulin can add another daily task to diabetes management.

Reducing that to one injection each week could make treatment simpler, particularly for people who need help administering insulin or struggle with a complicated medication schedule.

But weekly insulin creates different safety considerations too.

With a daily basal insulin, dosing errors can often be corrected relatively quickly.

A once-weekly dose is much larger and remains active for considerably longer.

The FDA specifically warns about medication errors and accidental overdose.

As with other insulin treatments, the most important side effect is hypoglycaemia.

Other reported adverse reactions include injection-site reactions, allergic reactions, swelling and weight gain.

That means understanding how to test blood glucose and recognise a low remains important even if injections become less frequent.

Weekly insulin is also not simply a longer version of someone’s existing basal-bolus insulin regimen.

Switching between preparations requires specific dosing instructions from the clinical team.

The FDA does not recommend Onswik for people with type 1 diabetes because trials identified an increased risk of severe hypoglycaemia.

For people with type 2 diabetes, measures such as Time in Range may eventually provide useful information about how evenly glucose is controlled across the seven-day dosing cycle.

The UK position is separate from the US approval.

NICE currently lists its appraisal of insulin efsitora for type 2 diabetes as in progress, with guidance expected on 22 October 2026.

That distinction matters.

A positive trial and an FDA approval do not mean somebody in England can simply ask their GP for the treatment tomorrow.

NHS availability depends on the UK regulatory and commissioning process, as well as final NICE guidance.

But once-weekly basal insulin is no longer a theoretical idea.

It is now an approved treatment in a major healthcare market, and the UK decision is close enough that people using diabetes medicines should expect to hear much more about it.

Primary source: FDA approval of once-weekly insulin efsitora

UK status: NICE appraisal of insulin efsitora alfa

Serious fatty liver disease is often associated with older age.

New research suggests that assumption may allow significant disease in younger adults to go unnoticed.

Researchers analysed 2,395 adults with biopsy-confirmed metabolic dysfunction-associated steatotic liver disease, or MASLD.

Of those, 234 had cirrhosis. One quarter of the cirrhosis cases occurred before age 50.

MASLD is closely linked with insulin resistance, obesity and type 2 diabetes.

• Non-Alcoholic Fatty Liver Disease

It ranges from excess fat in the liver through inflammation and fibrosis to cirrhosis.

Among participants younger than 50, people with cirrhosis were more likely to have type 2 diabetes and severe obesity than younger participants without cirrhosis.

After taking other demographic and metabolic factors into account, type 2 diabetes was associated with 3.74 times the odds of cirrhosis before age 50.

A higher genetic risk score was associated with more than twice the odds.

The genetic score incorporated variants in genes including PNPLA3, TM6SF2 and HSD17B13, which have previously been linked with liver disease.

This suggests that some younger people may have a combination of metabolic and inherited risk that allows MASLD to progress faster.

But the study does not show that type 2 diabetes directly caused cirrhosis.

It was observational and involved people already selected for liver biopsy through the NASH Clinical Research Network.

That is not the same population as everyone living with type 2 diabetes in primary care.

The finding does, however, challenge the idea that age provides reassurance on its own.

Current European guidance already recommends looking for significant liver fibrosis in people at cardiometabolic risk, particularly those with type 2 diabetes or obesity plus additional metabolic risk factors.

For a UK diabetes audience, that is the practical point.

Fatty liver is not simply an incidental scan finding and it is not limited to older people.

Someone with type 2 diabetes can have substantial liver fibrosis without obvious symptoms or dramatically abnormal liver enzymes.

The new study suggests clinicians should be especially cautious about dismissing liver risk simply because a patient is under 50.

Living with diabetes means making decisions about food, glucose, medication, exercise and health every day.

New guidance argues that the emotional burden of doing that should be treated as part of diabetes care rather than an optional extra.

The European Association for the Study of Diabetes has published an evidence-based guideline specifically focused on diabetes distress in adults with type 1 and type 2 diabetes.

Diabetes distress is different from clinical depression.

It describes the frustration, worry, guilt, exhaustion or sense of being overwhelmed that can come from living with and managing diabetes.

The guideline recommends that healthcare professionals ask about it using open questions about the challenges and emotional burden of living with the condition.

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Crucially, the authors say diabetes distress should be assessed at least once a year.

It should also be considered during major life events, the development of complications and significant treatment changes.

That puts emotional health much closer to HbA1c, blood pressure and cholesterol in the routine diabetes conversation.

For adults with type 1 diabetes, the guideline conditionally recommends psychological interventions, continuous glucose monitoring and automated insulin delivery as approaches that may reduce distress.

CGM had a small but measurable effect on diabetes distress compared with finger-prick monitoring in six randomised trials.

Automated insulin delivery also tended to improve distress, although the effect was smaller and borderline statistically significant.

For type 2 diabetes, psychological, psychoeducational and educational approaches received conditional recommendations.

That word — conditional — matters.

The quality of evidence varies substantially, and for several psychological interventions it remains low or very low.

This is therefore not evidence that one particular therapy works for everyone.

• Effective coping strategies for diabetes distress identified

It is stronger evidence for something more basic: diabetes distress deserves to be recognised, asked about and acted on.

For the UK, this is European guidance rather than a new NICE requirement.

But its recommendations fit naturally into annual diabetes reviews.

There is little value in telling someone their HbA1c needs to improve without also understanding whether diabetes has become exhausting, frightening or simply too difficult to manage.

Guideline link: Read the 2026 EASD diabetes distress guideline in Diabetologia.

One of the central mysteries of type 1 diabetes is not simply why the immune system attacks insulin-producing beta cells, but how that attack can persist for years.

New human-tissue research may have found part of the answer.

Scientists studied pancreatic lymph nodes from people with type 1 diabetes using mass cytometry, single-cell RNA sequencing and T-cell receptor profiling.

These lymph nodes sit close to the pancreas and are an important meeting point between the immune system and pancreatic tissue.

Researchers found an increased population of stem-cell-memory-like CD8 T cells in lymph nodes from people with type 1 diabetes.

These are not stem cells in the usual sense.

They are immune cells with the ability to self-renew while also producing more specialised T cells.

That makes them a plausible reservoir capable of sustaining an immune response over long periods.

The cells also showed altered inflammatory gene activity.

Analysis pointed towards IL-15 signalling as one pathway that may help drive this immune state.

Researchers found related effector CD8 T cells in both pancreatic lymph nodes and pancreatic tissue, with the cells inside the pancreas showing stronger signs of becoming terminal immune effectors.

That raises an intriguing model.

Instead of every destructive T cell persisting indefinitely, a smaller self-renewing population in nearby lymph nodes could continually replenish cells capable of travelling into the pancreas.

But that remains a hypothesis.

The researchers could not definitively prove that the stem-like cells identified were the specific autoreactive cells killing beta cells.

Human pancreatic and lymph-node tissue is also exceptionally difficult to obtain, so sample numbers were limited and donors differed in age and other characteristics.

This is therefore discovery science, not a treatment trial.

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Still, the finding could matter for the future of type 1 diabetes immunotherapy.

If the disease is sustained by a persistent immune-cell reservoir, temporarily suppressing mature attacking cells may not be enough.

Future treatments might need to interrupt the mechanism that continually replaces them.

For people living with type 1 diabetes today, nothing changes clinically.

But understanding where the autoimmune response is maintained could be an important step towards therapies designed to preserve remaining beta-cell function rather than only replacing the insulin those cells can no longer produce.

Study link: Read the study in the Journal of Clinical Investigation

GLP-1 medicines are increasingly being used to treat type 2 diabetes, severe obesity and related metabolic conditions.

As their use expands into younger age groups, researchers are asking an important question: are children receiving enough nutritional support alongside the medication?

A new US study suggests there may be room for improvement.

Researchers analysed insurance records from 2,031 young people aged 10 to 17 who started a GLP-1 receptor agonist between 2017 and 2022.

None had a recorded nutritional deficiency before starting treatment.

Within six months, 10.2% had been diagnosed with at least one nutritional deficiency or related complication.

By one year, that had risen to 16.8%, or around one in six.

The most common problem was vitamin D deficiency, diagnosed in 12.4%.

Nutritional anaemia affected around 1.6%, iron-deficiency anaemia around 1.4% and recorded muscle loss around 0.8%.

This matters because children and teenagers are still growing.

A treatment that reduces appetite can be useful for weight management, but calorie reduction should not come at the expense of protein, vitamins, minerals or normal development.

The study also found surprisingly limited access to nutrition support.

Only 5.8% had a nutrition consultation within 30 days of starting treatment.

By six months, the figure was still only 23.3%, with the average first consultation occurring around five months after treatment began.

That does not necessarily mean nutritional care prevents deficiencies.

In fact, deficiencies were diagnosed more often in young people who saw a nutrition professional, which may simply mean they were referred because a problem had already been identified or were tested more thoroughly.

There are other limitations.

Most participants were taking liraglutide, while only around 9% were taking semaglutide.

The data also came from 2017 to 2022, before newer GLP-1 treatment became as widely used as it is today.

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And because this was a claims study, it records diagnoses rather than detailed food intake or blood results.

So it cannot prove that GLP-1 medicines directly caused these nutritional problems.

But it raises a sensible clinical point.

When medication significantly changes appetite and weight loss, nutritional quality becomes more important, not less.

Young people using these medicines need treatment that includes food quality, adequate protein, micronutrients and healthy growth rather than focusing only on the number on the scales.

That fits with the wider principle that diabetes treatment works best when medication is combined with appropriate dietary and lifestyle support.

Anyone taking these medicines should also understand their known side effects and warning signs.

For younger people in particular, prescribing a GLP-1 medicine should be the beginning of structured support rather than the end of the conversation about nutrition.

Study link: https://doi.org/10.1177/21532176261486979

The development of type 1 diabetes appears to involve more than genetics alone.

A new study suggests the way the gut microbiome develops during the first years of life may interact with a child’s genes to influence future risk.

Researchers used data from TEDDY, one of the world’s largest long-running studies into the environmental triggers of childhood type 1 diabetes.

The team analysed 12,151 gut microbiome samples collected from 887 children in Finland, Germany, Sweden and the United States.

All of the children already had a higher genetic risk of diabetes.

Samples were collected repeatedly during the first years of life, allowing researchers to look at how each child’s gut bacteria developed over time rather than taking a single snapshot.

Three broad microbiome patterns emerged.

Researchers labelled them Early Matured, Late Matured and Early Plateaued.

Children in the Early Plateaued group had a microbiome that changed less over time and remained less diverse.

They had more than three times the risk of developing persistent islet autoantibodies or clinical type 1 diabetes compared with children whose microbiome matured earlier.

The adjusted risk ratio was 3.21 compared with the Early Matured group.

That is a substantial association, but it is not evidence that the gut microbiome directly caused type 1 diabetes.

Type 1 diabetes is an autoimmune condition in which the immune system gradually destroys the pancreatic beta cells that produce insulin.

Genetics plays an important role, but researchers have long suspected that environmental influences help determine why one genetically susceptible child develops the condition while another does not.

The new study adds the gut microbiome to that picture.

Researchers also found that certain genetic variants involved in antiviral and antimicrobial immune responses changed the relationship between microbiome development and diabetes risk.

That fits with the growing understanding from gene research that diabetes susceptibility reflects an interaction between inherited biology and the environment.

But parents should not read this as evidence that they need to manipulate their child’s gut bacteria.

The study did not test probiotics, supplements or a particular diet as a way to prevent diabetes.

Breastfeeding, antibiotics, probiotic use, introduction of solid foods and delivery method were considered in the statistical analysis, but the research cannot tell families that changing any one of these factors will alter the outcome.

The children were also specifically selected because they had high genetic risk.

That means the findings cannot automatically be applied to every child in the population.

The importance may eventually lie in prediction.

Research into screening children for type 1 diabetes is already moving quickly, with blood tests looking for autoantibodies before symptoms appear.

New international screening guidance has proposed testing at several stages of childhood.

The TEDDY programme itself has already transformed understanding of how type 1 diabetes develops in children.

In time, microbiome information could potentially add another layer to those risk models.

For now, however, this remains research rather than a test parents can request from their GP.

It tells us something important about type 1 diabetes biology, but not yet how to stop the process.

Study link: https://doi.org/10.1038/s42255-026-01614-9

“BPA-free” has become shorthand for safer packaging.

New research suggests the replacement chemicals deserve scrutiny too.

A study published in Acta Diabetologica examined exposure to bisphenol A, or BPA, and bisphenol S, known as BPS, in adults living with type 2 diabetes.

BPS is chemically similar to BPA and is used in some products marketed as BPA-free.

Researchers wanted to know whether either chemical was associated with HbA1c, the blood test used to estimate average glucose levels over the previous two to three months.

The analysis included adults with established type 2 diabetes who were taking oral diabetes medication.

Importantly, medication adherence was measured electronically rather than simply asking participants whether they took their tablets.

The researchers also assessed diet, physical fitness, BMI and levels of BPA and BPS in the blood.

Higher BPS concentrations were initially associated with higher HbA1c after accounting for factors including age, sex, race, diet and medication adherence.

BPA showed no equivalent relationship with HbA1c.

However, there is an important caveat.

When researchers added further variables including BMI, BPA and physical fitness to the statistical model, the BPS relationship was no longer statistically significant.

That makes the result much less definitive than a headline saying “BPS raises blood sugar”.

This was also an observational analysis.

Researchers measured exposure and diabetes control but did not randomly assign people to BPS exposure.

It therefore cannot establish whether BPS worsened blood glucose control, whether people with poorer metabolic health were exposed to more BPS or whether another factor explains both.

Laboratory and animal studies have previously raised questions about endocrine-disrupting chemicals and insulin resistance, but translating those findings into meaningful human risk is difficult.

Exposure is also hard to measure.

The dietary questionnaire used by the researchers did a poor job of predicting actual BPA or BPS concentrations in the blood.

That means simply asking someone how much packaged food they eat may not tell us how much of these chemicals they absorb.

For people with diabetes, this study should not distract from the factors with far stronger evidence behind them.

Taking prescribed anti-diabetic medicines, making sustainable lifestyle changes, maintaining an appropriate weight and monitoring HbA1c remain far more established ways of reducing the risk of diabetes complications.

There is no evidence from this study that throwing away plastic food containers will improve HbA1c.

Nor should people become anxious about occasional contact with BPA-free packaging.

What the research does show is that replacing one industrial chemical with a closely related substitute does not automatically make questions about metabolic health disappear.

BPS now deserves larger and longer-term studies.

For people managing diabetes today, the basics of type 2 diabetes treatment still matter much more.

Study link: https://doi.org/10.1007/s00592-026-02794-2

Heart disease, kidney disease and nerve damage dominate conversations about the long-term complications of diabetes.

New Danish research suggests cancer deserves more attention too.

Researchers used nationwide health records covering virtually the entire adult population of Denmark between 1996 and 2022.

Over those 27 years, 75,540 first cancers were recorded among people with type 2 diabetes, compared with more than 635,000 among people without diabetes.

The researchers then looked at how cancer incidence differed over time.

During 2010 to 2022, overall cancer incidence was 12% higher among men with type 2 diabetes and 22% higher among women compared with people without diabetes.

The equivalent differences during 1996 to 2009 had been 9% for men and 15% for women.

The gap was particularly large for cancers associated at population level with obesity.

In the later period, these cancers occurred 45% more often in men with type 2 diabetes and 30% more often in women.

Colorectal cancer incidence was 17% higher in men with type 2 diabetes and 14% higher in women.

Postmenopausal breast cancer was 8% higher.

Lung cancer incidence was also higher, by 23% in men and 25% in women with type 2 diabetes.

But the pattern was not uniform.

Prostate cancer incidence was actually 19% lower among men with type 2 diabetes.

This complexity is important.

Diabetes does not have one simple relationship with “cancer” as a single disease.

Different cancers have different biological and behavioural risk factors.

There are plausible links between insulin resistance, higher circulating insulin, excess body fat, inflammation and some forms of cancer.

The existing diabetes and cancer evidence has pointed in this direction for years.

But this study was not designed to work out why the difference exists.

Researchers did not have sufficient information to separate the contribution of body weight, smoking, alcohol, exercise and other lifestyle factors.

That means it would be wrong to say type 2 diabetes itself caused the additional cancers.

The study has also been presented for the EASD annual meeting rather than published as a full peer-reviewed paper at this stage.

For people living with diabetes in the UK, there is no recommendation here for special cancer screening beyond NHS programmes.

The practical message is to take up routine screening when invited and continue working on the same modifiable risk factors that protect against several diseases at once.

That includes maintaining good blood glucose control, addressing excess weight through sustainable weight management, being physically active and not smoking.

Those behaviours also reduce heart disease risk, which remains one of the most important threats associated with diabetes.

The emerging message is therefore not that people with diabetes should fear cancer.

It is that long-term diabetes care increasingly needs to look beyond glucose and consider the whole pattern of future health risk.

Sex is rarely discussed during routine diabetes appointments.

For some people living with type 1 diabetes, one of the unspoken concerns is whether physical activity during sex could trigger a hypo.

A small new study has used continuous glucose monitoring to provide some reassuring, if preliminary, data.

Researchers followed 12 adults with type 1 diabetes for around three months.

Participants recorded 110 episodes of sexual intercourse while wearing CGM devices.

Across those events, the researchers found no clinically significant hypoglycaemia.

That does not mean glucose stayed flat.

Far from it.

In 58% of encounters, glucose fell by an average of 27%, from around 10.0 mmol/L to 7.3 mmol/L.

In the remaining 42%, glucose rose by around 34%, from approximately 6.8 mmol/L to 9.1 mmol/L.

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Every participant experienced both rising and falling glucose on different occasions.

That makes sense.

Sex, like other forms of physical activity, can affect glucose differently depending on starting glucose, circulating insulin, stress hormones, timing and intensity.

Night-time encounters were associated with a modest fall in glucose overall.

Daytime encounters produced virtually no average change.

People with a BMI of 25 or above experienced a somewhat larger glucose reduction.

The researchers believe these findings could help address fear of hypoglycaemia, which can affect intimacy and lead some people to deliberately run glucose high.

That fear is not irrational.

People using insulin do need to think about hypoglycaemia during and after physical activity, and delayed lows are well recognised after exercise.

But this study suggests sex should not automatically be treated as a high-risk activity.

There are significant limitations.

Twelve participants is an extremely small sample.

All had CGM, so the results may not apply in the same way to someone relying on occasional finger-prick checks.

Six participants used injections and six used insulin pumps, but there were far too few people to make reliable comparisons between treatment methods.

The work has also been presented as conference research and has not yet been published as a full peer-reviewed paper.

People with hypo unawareness, recent severe hypos or highly unpredictable glucose should therefore continue to take their individual risk seriously.

CGM alerts can offer additional reassurance, and keeping fast-acting carbohydrate nearby is sensible for anyone vulnerable to lows.

If a hypo does occur, it should be treated in the usual way with fast-acting carbohydrate. Diabetes.co.uk has a practical guide on how to treat a hypo.

Perhaps the most useful part of the study is simply that the question was asked.

Diabetes and sexual health should be something people can discuss normally with their clinical team rather than work out alone.