Updating clinical guidelines does not necessarily mean every eligible patient immediately receives the treatments being recommended.

A new study published in JAMA Network Open has investigated how prescribing changed after American diabetes guidelines placed greater emphasis on medicines that can protect the heart and kidneys.

Researchers examined prescription records for 177,284 older adults with type 2 diabetes receiving care from 1,061 endocrinologists in the United States.

The analysis focused on changes following a 2019 American Diabetes Association guideline update.

It also explored whether prescribing patterns differed according to physicians’ later scores in a professional knowledge assessment. JAMA Network

What changed after the guidelines were updated?

The guidelines placed greater emphasis on using selected SGLT2 inhibitors and GLP-1 receptor agonists in people with particular cardiovascular or kidney-related conditions.

Researchers found that prescribing became more consistent with the guidance over time.

Between 2018 and 2022, the increase in adjusted SGLT2 inhibitor prescription-fill rates was 11.4 percentage points greater among patients targeted by the guidance than among those outside the targeted groups.

For GLP-1 receptor agonists, the corresponding difference was approximately 2.4 percentage points.

The findings indicate that prescribing changed after the guidance was updated, particularly for SGLT2 inhibitors.

However, they do not prove that the guideline revision alone caused the changes.

Other factors, including new evidence, medicine availability and reimbursement arrangements, were also changing during the period. JAMA Network

Did clinician knowledge make a difference?

The researchers compared prescribing trends with physicians’ scores on a subsequent professional knowledge assessment.

Doctors with higher scores tended to demonstrate larger increases in guideline-concordant SGLT2 inhibitor prescribing.

However, the study did not find the same statistically significant relationship for GLP-1 medicines.

There is also an important timing limitation.

The professional assessment scores were measured after the prescribing period.

That means the results cannot establish that achieving a higher score led to better prescribing.

The association may instead reflect broader differences in clinical practice, education or professional engagement.

Why does this matter for type 2 diabetes?

Diabetes treatment increasingly involves more than lowering HbA1c.

Certain medicines have demonstrated benefits for people with established cardiovascular disease, heart failure or chronic kidney disease.

For appropriate patients, these additional effects can influence which treatment is selected.

But the most suitable medicine still depends on individual health circumstances, contraindications, treatment preferences and access.

More prescriptions are not automatically better if medicines are given to people who are unlikely to benefit.

What is the UK angle?

The study used US Medicare data and American prescribing guidance.

Its findings cannot be treated as evidence that similar prescribing gaps exist within the NHS.

UK clinical decisions are informed by NICE recommendations, licensed indications and individual assessment.

Nevertheless, the research raises an important question for diabetes services: how effectively does new evidence translate into everyday clinical practice?

For people with type 2 diabetes, it reinforces the value of discussing cardiovascular and kidney health alongside glucose control during medication reviews.

The study highlights the challenges of implementing evidence-based treatment, rather than proving that any particular clinician or healthcare system is failing.

Primary study: JAMA Network Open – Prescribing SGLTis and GLP-1 RAs for Patients With Type 2 Diabetes, Guideline Updates, and Knowledge Assessment Scores

A virus detected in human gut samples for almost four decades may have been assigned to the wrong type of host.

Researchers have demonstrated that a member of the picobirnavirus family infects bacteria living in the gut, rather than directly infecting human intestinal cells.

The discovery, published in Nature Microbiology, changes how scientists may interpret earlier research linking these viruses to human illnesses.

Picobirnaviruses were first identified in human stool samples in 1988.

Since then, they have been detected in people and animals with a range of conditions.

However, scientists had never directly demonstrated which cells the viruses infected.

The new research provides the first experimental identification of a bacterial host for a human-associated picobirnavirus. Nature

How did researchers identify the virus’s host?

The team used human stool samples containing picobirnaviruses and transferred the associated gut microbes into germ-free mice.

They then established laboratory cultures containing communities of gut bacteria.

One of the viruses continued reproducing in these bacterial cultures.

Using specialised microscopy and genetic techniques, researchers identified viral material inside bacterial cells.

They subsequently traced the infection to a previously uncharacterised bacterial species, provisionally named Candidatus Anaerotignum faecalis.

The results establish that at least one member of the picobirnavirus family is a bacteriophage – a virus that infects bacteria. Nature

Why is this discovery important?

Picobirnaviruses have previously been detected in samples from people with illnesses including diarrhoea, inflammatory conditions and type 1 diabetes.

Because the viruses were found in human samples, researchers initially considered whether they might directly infect human cells.

The new work suggests a different explanation.

At least some picobirnaviruses may be present because the people being studied harbour bacteria that are infected with those viruses.

That changes the questions scientists need to investigate.

Rather than focusing exclusively on whether the virus attacks human tissue, researchers may need to examine whether it changes the behaviour of gut bacteria.

Does this explain type 1 diabetes?

No.

The study did not demonstrate that picobirnaviruses cause type 1 diabetes.

It also did not establish that removing or introducing the virus changes diabetes risk.

Earlier reports of associations between these viruses and type 1 diabetes should not be interpreted as evidence of causation.

Type 1 diabetes is an autoimmune condition involving the destruction of insulin-producing pancreatic beta cells.

Its development reflects genetic susceptibility and environmental influences that remain incompletely understood.

The gut microbiome is one area of investigation, but there is no established microbiome treatment that prevents type 1 diabetes.

What were the study’s limitations?

The researchers demonstrated bacterial infection for a particular picobirnavirus.

They have not established that every member of this diverse viral family infects the same bacterial species or that none can infect other organisms.

The mouse experiments and bacterial cultures also did not establish what happens to human health when the virus is present.

The research provides a major advance in microbiology, but its clinical implications remain uncertain.

What is the UK connection?

The research involved collaborators at Cambridge University Hospitals NHS Foundation Trust and received support linked to the NIHR Cambridge Biomedical Research Centre.

For UK diabetes researchers, it provides a new way to investigate relationships between gut bacteria, viruses and immune function.

However, it does not change current diabetes screening, prevention or treatment.

Its importance lies in correcting a long-standing assumption about how a common group of gut viruses behaves.

That could help researchers interpret future studies more accurately, including those examining potential connections between the microbiome and autoimmune disease.

Primary study: Nature Microbiology – A human gut-associated picobirnavirus establishes the Picobirnaviridae as the third clade of RNA bacteriophages

Around one in six adults living with type 1 diabetes experience moderate or severe symptoms of depression or anxiety, according to a nationally representative US study.

Researchers analysed data from 58,106 adults taking part in the US National Health Interview Survey.

The sample included 326 adults with type 1 diabetes and 5,802 with type 2 diabetes.

Moderate or severe depressive symptoms were reported by 17.1% of people with type 1 diabetes.

That compared with 12.4% among people with type 2 diabetes and 6.6% among adults without diabetes.

The pattern was similar for anxiety.

Moderate or severe symptoms of generalised anxiety disorder were reported by 16.2% of adults with type 1 diabetes, compared with 8.7% of those with type 2 diabetes and 6.1% of adults without diabetes.

Why might type 1 diabetes affect mental health?

Living with type 1 diabetes involves an unusually high level of day-to-day decision-making.

People may need to monitor glucose, calculate insulin doses, consider carbohydrate intake, respond to exercise, manage illness and continuously balance the risks of high and low glucose.

Technology such as continuous glucose monitoring can reduce some of that burden, but it can also create constant streams of information and alerts.

Fear of hypoglycaemia, worry about long-term complications and the pressure of maintaining glucose targets can all contribute to diabetes distress.

Diabetes distress is not the same condition as clinical depression or an anxiety disorder, although the two can overlap.

Who appeared most affected?

Within the type 1 diabetes group, moderate or severe depression and anxiety symptoms were particularly common among:

• women
• younger adults
• people with lower educational attainment.

The researchers argue that better mental health screening may therefore be particularly important in higher-risk groups.

However, only 326 survey participants had type 1 diabetes.

That is substantially smaller than the other comparison groups, meaning subgroup estimates are less precise.

What are the limitations?

The study was cross-sectional.

Researchers measured diabetes status and psychological symptoms at the same point rather than following people over time.

It therefore cannot establish that diabetes caused depression or anxiety.

Mental health could also influence diabetes management, while socioeconomic circumstances, access to healthcare and other medical conditions may affect both.

The research was conducted in the United States, where healthcare access and financial pressures differ substantially from the NHS.

The exact prevalence estimates should therefore not automatically be assumed to apply to the UK.

The UK diabetes angle

The findings nevertheless reinforce something increasingly recognised in diabetes care: psychological health is part of diabetes health.

Living with diabetes involves more than keeping HbA1c within a target.

Persistent anxiety, depression or severe diabetes distress can affect quality of life, sleep, relationships and someone’s ability to manage treatment.

Diabetes.co.uk has more information on diabetes and mental health.

People who find that low mood, anxiety or diabetes-related worry is interfering with everyday life should discuss it with their GP or diabetes team.

The new study does not mean depression or anxiety is inevitable with type 1 diabetes.

It does suggest these problems are common enough that they should not be treated as an afterthought.

Primary study: Annals of Internal Medicine – Depressive and Anxiety Symptoms in U.S. Adults With Type 1 Diabetes

Diabetes substantially increases the risk of a first heart attack in both women and men, but differences in cholesterol and blood pressure appear to explain much of the apparent additional relative risk in women.

Researchers analysed 42,907 participants in the long-running Tromsø Study in Norway.

The study followed adults across almost four decades, with 3,942 participants experiencing their first myocardial infarction – or heart attack – during follow-up.

Of these, 357 occurred among people with diabetes.

After accounting for age and birth cohort, diabetes was associated with a 2.26-fold heart attack rate in women and a 1.84-fold rate in men compared with people of the same sex without diabetes.

However, the statistical evidence that those two relative effects genuinely differed between women and men was not significant.

What happened when researchers considered cholesterol and blood pressure?

The difference became smaller still.

Once traditional coronary heart disease risk factors were included in the model, the heart attack rate associated with diabetes was approximately:

• 1.72 times higher in women
• 1.67 times higher in men.

The biggest contributor in both sexes was an unfavourable ratio between triglycerides and HDL cholesterol.

Accounting for this weakened the diabetes-heart attack association by around 19% in women and 17% in men.

High systolic blood pressure appeared particularly important among women.

Together, the conventional cardiovascular risk factors explained about one-third of the association in women and around one-sixth in men.

Warning signs appeared before diabetes

One particularly important finding was that unfavourable lipid levels and rising blood pressure were already present before diabetes was diagnosed.

That supports the idea that cardiovascular prevention should not wait until someone crosses the diagnostic threshold for type 2 diabetes.

People with prediabetes can already have metabolic abnormalities associated with future cardiovascular disease.

The study therefore strengthens the case for considering cholesterol and blood pressure alongside glucose rather than treating them as separate problems.

What does diabetes do to cardiovascular risk?

Persistently high glucose can damage blood vessels over time.

But diabetes frequently occurs alongside several other cardiovascular risk factors, including:

• high blood pressure
• raised triglycerides
• low HDL cholesterol
• obesity
• smoking.

That combination helps explain why heart disease is an important complication of diabetes.

The findings do not mean glucose control is unimportant.

They show that cardiovascular risk cannot be reduced to glucose alone.

What are the limitations?

This was a prospective observational study, not a clinical trial.

Researchers observed how risk factors and outcomes developed rather than assigning people to different treatments.

The study also spans several decades, during which diagnosis, smoking rates and treatment of diabetes, cholesterol and hypertension changed substantially.

Most participants came from a Norwegian population, which may limit how precisely the estimates apply to the UK’s more ethnically diverse population.

Residual confounding is also possible.

The findings therefore cannot prove that correcting a particular triglyceride-to-HDL ratio will remove a specific percentage of somebody’s diabetes-related heart attack risk.

What does this mean for people with diabetes in the UK?

The practical implications are familiar but important.

A good diabetes review should not focus only on HbA1c.

Blood pressure and cholesterol matter too.

For some people, that can mean taking medicines such as statins or blood-pressure treatments alongside glucose-lowering medication.

Smoking status, kidney health, weight and physical activity also contribute to cardiovascular risk.

The new study suggests that much of the apparent difference between women and men with diabetes can be understood by looking at those conventional risk factors.

The central message is therefore not that one sex is safe.

It is that cardiovascular prevention needs to begin early and address the whole risk profile, potentially even before type 2 diabetes is diagnosed.

Primary study: European Heart Journal Open – Sex differences in diabetes-related risk of myocardial infarction: the Tromsø Study

Researchers have nearly doubled the number of known genetic regions associated with fat accumulating in the liver.

The study, published in Nature Genetics, combined DNA information with MRI measurements of liver fat from 71,488 UK Biobank participants of European ancestry.

Researchers identified 60 independent genetic regions associated with liver triglyceride levels.

Thirty-one had not previously been reported for the trait.

The researchers estimated that common genetic variants collectively explain approximately 25% of the variation in liver fat between individuals.

Why does liver fat matter?

Metabolic dysfunction-associated steatotic liver disease, or MASLD, involves excessive accumulation of fat within liver cells.

It is strongly associated with obesity, insulin resistance and type 2 diabetes.

For many people the condition remains relatively stable, but in some it can progress to inflammation, fibrosis, cirrhosis and liver cancer.

Understanding why one person develops progressive disease while another does not is therefore an important area of research.

Researchers validated the findings in much larger datasets

The team did not rely entirely on the UK Biobank MRI analysis.

They tested the newly identified variants against genetic data involving 42,163 people with clinically diagnosed MASLD and more than 1.6 million controls.

Fourteen of the 31 newly identified genetic signals reached the study’s stringent validation threshold, while 22 showed nominally significant associations in the same direction.

Researchers also developed a polygenic risk score combining large numbers of genetic variants.

People in the highest tenth of genetic risk had 2.71 times the odds of cirrhosis and 7.47 times the odds of hepatocellular carcinoma, or primary liver cancer, compared with those in the lowest tenth.

Those are associations between genetic groups, not predictions that an individual person will develop either disease.

Most people in a high genetic-risk category will not necessarily develop liver cancer.

What did researchers see with diabetes?

When the genetic risk score was compared with a broad range of health conditions, liver disease had the strongest relationship.

Type 2 diabetes was also strongly associated.

That reinforces the substantial biological overlap between liver fat and metabolic disease.

The relationship runs in both directions.

People with type 2 diabetes have a particularly high prevalence of fatty liver disease, while excess liver fat is closely connected with impaired insulin sensitivity.

Could this become a genetic test?

Not yet.

Polygenic risk scores can identify differences in risk across large research populations, but their value for deciding what should happen to one individual patient is much less certain.

There is another important limitation.

The primary MRI analysis involved participants of European ancestry.

Genetic variants and their frequencies can differ across ancestry groups, so applying the same score indiscriminately to other populations could produce misleading estimates.

The researchers explicitly say larger studies in more diverse populations are required.

What is the UK angle?

The study was made possible by the UK Biobank, making this a particularly significant example of UK population data being used to investigate metabolic disease.

But there is no new NHS genetic test for fatty liver as a result.

For people with diabetes, established indicators remain much more useful clinically.

These include liver blood tests, metabolic risk factors and imaging where appropriate.

Weight management, physical activity, glucose control, blood pressure and cholesterol are also relevant to both liver and cardiovascular health.

The significance of this study is mainly what it gives scientists: 31 additional genetic clues pointing towards biological pathways that could ultimately help identify new treatments or explain why liver disease progresses in some people.

Primary study: Nature Genetics – Genome-wide analyses identify 60 loci associated with liver triglyceride content

Continuous glucose monitors may be useful for considerably more people with type 2 diabetes than those currently receiving insulin treatment, according to research published in the New England Journal of Medicine.

The CONNECT trial investigated whether continuous glucose monitoring (CGM) could improve blood sugar control in adults managing type 2 diabetes without insulin.

Researchers recruited 283 participants from 22 primary-care practices across the United States.

Participants were randomly assigned to use a real-time glucose sensor or continue with routine diabetes care.

After 26 weeks, the results showed meaningful differences between the groups. PubMed

What happened to HbA1c?

People using CGM started with an average HbA1c of 8.8%.

After 26 weeks, this had fallen to 7.2%.

In the usual-care group, HbA1c fell from 8.7% to 8.0%.

After statistical adjustment, the CGM group achieved a 0.9 percentage-point greater reduction in HbA1c.

That is equivalent to approximately 10 mmol/mol.

The difference was statistically significant.

HbA1c reflects average blood glucose over approximately two to three months and is one of the principal measurements used to assess longer-term diabetes control.

The study therefore suggests that people not receiving insulin may still benefit from seeing their glucose patterns throughout the day.

Five more hours within target range

Researchers also assessed time in range, which measures the proportion of time glucose remains within a specified target.

Participants using CGM spent an additional 21 percentage points of the day within the range of approximately 3.9–10 mmol/L.

That is equivalent to roughly five additional hours per day.

The improvement was largely driven by less time spent with elevated glucose.

No severe hypoglycaemia was reported during the trial. PubMed

Why might CGM work without insulin?

CGM provides frequent readings and shows how glucose changes after meals, during exercise and overnight.

People can identify patterns that would be difficult to detect through occasional finger-prick testing.

For someone managing diabetes through dietary changes or tablets, seeing the effect of particular meals may help inform everyday decisions.

Researchers also reported that 97% of participants assigned to CGM were still using the technology after 26 weeks.

However, the trial was open-label, meaning participants knew which treatment they were receiving. That could influence behaviour and engagement.

The study was also funded by Dexcom, the manufacturer of the device used.

What does this mean for the NHS?

The findings add to an emerging evidence base supporting wider CGM use in type 2 diabetes.

An earlier UK trial demonstrated benefits among people using basal insulin, while the new CONNECT trial extends the evidence to people who are not using insulin at all.

But a positive trial does not automatically change NHS prescribing criteria.

NICE and NHS commissioners would need to consider longer-term outcomes, clinical eligibility and whether the benefits justify the additional cost.

For people already managing diabetes without a sensor, existing approaches to blood glucose control remain important.

The new study provides evidence that CGM could improve glucose management in a wider population, but it does not yet prove that providing sensors to everyone with type 2 diabetes would be clinically or economically beneficial.

Primary study: New England Journal of Medicine – Continuous Glucose Monitoring in Non-Insulin-Treated Type 2 Diabetes

Gaining more weight during pregnancy than current recommendations suggest is associated with a higher risk of serious maternal complications, according to a study involving more than one million births.

Researchers analysed 1,035,927 singleton pregnancies recorded in Ontario, Canada, between 2012 and 2022.

They compared gestational weight gain with the US Institute of Medicine recommendations, which vary according to someone’s BMI before pregnancy.

More than half – 52.8% – gained above the recommended range, while 28.6% remained within it and 18.6% gained less.

Researchers identified 15,119 cases of severe maternal morbidity, equivalent to approximately 14.6 per 1,000 births.

The outcomes included serious complications such as severe bleeding, severe pre-eclampsia or eclampsia, intensive-care admission and hysterectomy.

What happened when women gained above the recommended range?

Excessive gestational weight gain was associated with higher rates of severe complications across every starting BMI category.

Compared with gaining within recommended ranges, adjusted rates were:

• 33% higher among people who began pregnancy underweight
• 24% higher among those with a BMI in the normal range
• 16% higher among those classified as overweight
• approximately 21–28% higher across the three obesity categories.

These percentages describe relative differences, not the absolute likelihood that an individual pregnancy will develop a complication.

The absolute severe-morbidity rate was 12.18 per 1,000 births among those gaining within recommendations and 16.09 per 1,000 among those gaining above them.

Too little weight was not always better

The results were more complicated than simply “less weight gain is healthier”.

Among people who began pregnancy at a normal weight or overweight, gaining less than recommended was also associated with higher rates of severe maternal morbidity.

The relationship therefore appeared U-shaped in some BMI groups, with higher risk at both extremes.

Among people with obesity, the increased risk was more concentrated at higher levels of weight gain.

This is important because pregnancy is not an appropriate time for people to independently pursue aggressive weight loss.

What about diabetes?

Pre-existing health conditions increased vulnerability.

The researchers specifically considered conditions including diabetes and high blood pressure when investigating how medical risk interacted with gestational weight gain.

People entering pregnancy with existing medical conditions had higher complication rates, and risks could increase further when gestational weight gain also fell outside recommended ranges.

This is particularly relevant for women with pre-existing diabetes and pregnancy.

Diabetes in pregnancy already requires careful management of glucose, blood pressure, fetal growth and maternal health.

The study does not provide a new pregnancy weight target specifically for women with diabetes.

What are the limitations?

This was a retrospective observational cohort study.

Researchers analysed existing pregnancy and hospital records rather than randomly assigning different weight-gain targets.

That means the study can identify associations but cannot prove that gaining more weight directly caused the complications.

For example, fluid retention caused by pre-eclampsia itself can increase body weight.

Researchers conducted additional analyses to reduce the effect of this problem, but it cannot necessarily be eliminated completely.

Prepregnancy weight and weight at delivery could also be either measured or self-reported, introducing potential measurement error.

The study used Canadian data and US Institute of Medicine weight-gain ranges.

UK maternity guidance is not identical.

What should women in the UK do?

Nothing in this study suggests that pregnant women should begin calorie restriction or attempt rapid weight loss.

Women with diabetes should continue to follow individual advice from their diabetes and maternity teams.

Maintaining good blood glucose control during pregnancy remains particularly important.

Women who develop gestational diabetes should likewise follow the dietary, glucose-monitoring and treatment advice agreed with their clinical team.

The study’s broader implication is that pregnancy weight guidance may eventually need to consider maternal outcomes – and individual health conditions – more explicitly rather than relying on broad BMI categories alone.

That question now needs prospective research before recommendations are changed.

Primary study: JAMA Network Open – Weight Gain During Pregnancy and Severe Maternal Morbidity

Differences in the prevalence of diabetes and high blood pressure may help explain why stroke occurs more frequently in some ethnic communities, according to new research from King’s College London.

Researchers analysed electronic primary-care records from 651,888 adults registered with 41 general practices in Lambeth, South London.

The records covered 2005 to 2021.

Rather than simply comparing overall stroke rates, the researchers investigated two separate stages of disease.

First, they examined who developed major cardiovascular risk factors.

They then assessed whether people with those conditions subsequently developed a stroke. Springer

Diabetes and hypertension showed substantial differences

Compared with White patients, Black patients were more than twice as likely to develop diabetes in the study’s statistical models.

Asian patients were around three times as likely to develop diabetes.

Black patients were also approximately twice as likely to develop hypertension, while Asian patients had around 50% higher risk.

Both conditions are major contributors to stroke risk.

Persistently high glucose can damage blood vessels, while high blood pressure increases the strain placed on the cardiovascular system.

The researchers therefore wanted to understand whether the increased frequency of these conditions could help explain differences in subsequent stroke.

What happened once risk factors were present?

Among patients who already had diabetes or hypertension, the researchers did not find a significant additional increase in progression to stroke associated with Black or Asian ethnicity compared with White ethnicity.

This suggests the higher burden of underlying cardiometabolic risk factors may explain an important part of the differences in overall stroke incidence.

However, there was an exception involving high cholesterol.

Among Black patients with hypercholesterolaemia, the analysis identified a slightly higher subsequent stroke risk.

The researchers said this deserves further investigation, including whether differences in access to cholesterol-lowering treatment may contribute. Medical Xpress

Why are these findings important?

The results support looking beyond ethnicity as a simple risk label.

Ethnic differences in disease outcomes reflect a complex interaction between socioeconomic circumstances, healthcare access, environment, behaviour, underlying biology and other factors.

Previous evidence has shown that South Asian communities in the UK experience higher rates of type 2 diabetes.

But no single mechanism explains every difference between populations.

The current study was observational and conducted within one urban area.

It cannot determine whether each difference arose from biological susceptibility, access to prevention, diagnostic practices or other influences.

Nor does finding no statistically significant additional stroke risk in one model prove that inequalities in healthcare have disappeared.

The first three months after starting certain antipsychotic medicines could be a particularly important period for monitoring blood glucose and body weight, according to a major UK study.

Researchers at University College London analysed anonymised NHS primary-care records from almost 97,000 adults aged 18–59 living with severe mental illness.

The participants had started one of four commonly prescribed second-generation antipsychotic medicines between 2000 and 2023.

These included olanzapine, quetiapine, risperidone and aripiprazole.

Researchers examined weight and HbA1c measurements recorded during the two years before treatment and the two years afterwards. University College London

Blood sugar and weight changed rapidly

The most pronounced changes occurred during the first 90 days after medication began.

During this period, the rate of HbA1c increase was approximately 14 times higher than before treatment.

The rate of weight gain was around nine times higher.

These are comparisons of the rates of change, not statements that HbA1c or body weight increased fourteenfold or ninefold.

This distinction matters because the actual changes were much smaller.

Nevertheless, the pattern suggests the early treatment period is particularly important for identifying emerging metabolic problems.

Weight alone may miss important changes

One of the study’s key findings was that rising glucose and weight gain did not always occur together.

Some people experienced changes in blood glucose without proportionate weight increases.

That means relying entirely on weight measurements could miss developing hyperglycaemia.

Of the medicines examined, olanzapine was associated with the largest early increases in both weight and HbA1c.

Participants with existing prediabetes were also particularly vulnerable.

Within two years, 19% of those with prediabetes developed type 2 diabetes, compared with 3% of participants whose glucose was initially normal.

Women experienced faster early increases in both measurements than men.

However, these findings describe associations within the study population rather than providing a personalised estimate of risk for everyone taking these medicines. Medical Xpress

Why do antipsychotic medicines affect diabetes risk?

Second-generation antipsychotics are important treatments for conditions including schizophrenia and bipolar disorder.

Some can increase appetite, affect energy balance and alter glucose metabolism.

Consequently, they may contribute to weight gain and insulin resistance.

People living with severe mental illness also face additional barriers to maintaining good physical health, making integrated care particularly important.

But antipsychotic treatment can be essential for managing serious psychiatric conditions.

The findings do not justify stopping or reducing medication without specialist advice.

What are the study’s limitations?

This was an observational analysis of existing medical records.

Researchers could not fully account for dietary changes, physical activity, other medicines or every factor influencing weight and glucose.

The analysis therefore cannot establish precisely how much of the observed change was caused directly by each antipsychotic.

There may also have been differences in which patients received particular medicines.

What does this mean for UK patients?

The findings directly concern NHS care because the records came from England.

They reinforce the importance of checking both weight and glucose before starting treatment and during the first few months afterwards.

People already taking antipsychotics should continue following their prescribed treatment and discussing any concerns with their clinical team.

The wider message is that mental and physical health need to be considered together.

Earlier recognition of rising glucose could allow clinicians to provide support before someone develops type 2 diabetes or experiences further metabolic deterioration.

Primary study: The Lancet Psychiatry – Change in HbA1c and weight after initiation of antipsychotic treatment

A commonly prescribed diabetes medicine may have effects on the immune system that help researchers better understand its cardiovascular benefits.

Scientists at Vanderbilt University Medical Center investigated whether empagliflozin, an SGLT2 inhibitor, changes inflammatory activity in the blood.

Empagliflozin is marketed as Jardiance and is already used to treat type 2 diabetes and certain cardiovascular and kidney conditions.

The new analysis focused on a possible biological mechanism behind some of these benefits.

Researchers studied 16 women with obesity and prediabetes who received empagliflozin for three months.

What changed in the blood?

The researchers measured structures called monocyte-platelet aggregates.

These form when platelets, which are involved in blood clotting, attach to monocytes, a type of white blood cell.

Monocyte-platelet interactions are associated with vascular inflammation and may contribute to processes involved in cardiovascular disease.

Within two weeks of starting empagliflozin, the researchers observed a reduction in these aggregates.

The reduction became more pronounced over 12 weeks.

Using detailed cell analysis, they also identified changes in monocyte metabolism consistent with a less inflammatory cellular state.

A comparison group following a low-calorie diet did not show the same reduction in monocyte-platelet aggregates.

Why could this matter?

SGLT2 inhibitors are already established treatments for certain people with type 2 diabetes.

They lower glucose by increasing the amount excreted through the urine.

Some medicines in this class have also demonstrated benefits for heart disease and kidney health in large clinical trials.

However, researchers are still investigating all the mechanisms responsible.

Changes in immune-cell activity could potentially be one explanation.

What are the limitations?

The findings need to be interpreted cautiously.

Only 16 women received empagliflozin, making this a very small pilot study.

The investigation was not a large randomised, placebo-controlled trial.

It also measured biological markers rather than clinical outcomes.

The researchers did not demonstrate fewer heart attacks, strokes or deaths.

Nor can the findings establish whether the same changes occur in men, people with established diabetes or patients with different metabolic conditions.

A larger randomised trial is needed to determine how reproducible and clinically meaningful the findings are.

Does this change NHS treatment?

No. Empagliflozin already has established uses, but the results do not create a new indication for treating inflammation or prediabetes.

People should not begin taking the medicine simply to reduce inflammatory markers.

SGLT2 inhibitors also have important safety considerations, including genital infections, dehydration and, rarely, diabetic ketoacidosis.

The study is most useful for understanding how medicines already used in diabetes care may influence pathways involved in long-term diabetes complications.

For patients, the more important evidence remains the large clinical trials demonstrating benefits for specific cardiovascular and kidney outcomes.

Primary study: SGLT2 Inhibitor Empagliflozin Reduces Circulating Monocyte-Platelet Aggregates: A Pilot Study – Circulation

Seeing a GP more frequently is not automatically better for everyone with type 2 diabetes, according to research investigating how primary-care appointments could be scheduled according to individual risk.

Two studies from researchers at the University of Massachusetts Amherst examined different parts of the type 2 diabetes pathway: how frequently people already diagnosed with diabetes should be reviewed, and how quickly an abnormal HbA1c result leads to a documented diagnosis.

The findings suggest that the organisation of primary care may matter alongside individual patient characteristics.

But they do not support simply replacing existing appointment schedules with an algorithm.

Should higher-risk patients be seen more frequently?

The first study used electronic health records from 10 primary-care practices to develop a mathematical model for choosing follow-up intervals.

Rather than automatically reviewing everyone after one, three or six months, the model adjusted the recommended interval according to the person’s current health and diabetes trajectory.

People in the higher-risk group tended to be older and have more existing conditions such as chronic kidney disease and cardiovascular disease.

When HbA1c increased, the model favoured more frequent follow-up in these patients.

For lower-risk people whose glucose remained stable, it allowed longer intervals between appointments.

The model performed better on its mathematical optimisation measure than fixed appointment schedules, including a benchmark based on American Diabetes Association recommendations.

The basic idea is straightforward.

Seeing someone again too soon may provide little new information because HbA1c reflects blood glucose over approximately the previous two to three months.

Waiting too long, however, could allow worsening glucose control to go undetected.

A personalised schedule tries to find the point between those two extremes.

This was a modelling study – not a trial of patient outcomes

That distinction is important.

Researchers did not randomly assign thousands of people to algorithm-selected appointment intervals and then show fewer diabetes complications.

Instead, they used existing electronic health records to build and evaluate a Markov decision model.

Its better performance refers to the model’s predefined optimisation criteria.

It does not yet prove that the approach reduces hospital admissions, kidney disease, cardiovascular complications or mortality in real clinical practice.

A prospective trial would be needed before drawing those conclusions.

A second study examined delays in diagnosis

A separate study investigated 594 adults attending two US primary-care clinics between 2017 and 2023.

All had recorded an HbA1c in the diabetes range – at least 6.5%, equivalent to 48 mmol/mol – before receiving a documented diagnosis of type 2 diabetes.

The median time from the first diabetes-range HbA1c to diagnosis differed between the two clinics, at approximately 1.6 months and two months.

The investigators found that the first few appointments following the abnormal HbA1c appeared to be particularly important opportunities for diagnosis.

However, this finding needs nuance.

After adjustment for other factors, the study did not find statistically significant associations between primary-care location, continuity of care or visit regularity and time to diagnosis.

It would therefore be too strong to conclude that staffing levels or the clinic someone attends have been proven to cause diagnostic delays.

The study was exploratory and involved only two practices.

The researchers argue that differences in staffing, appointment availability and local practice processes deserve further investigation.

Why might diagnosis be delayed?

An HbA1c result does not operate in isolation.

Clinicians may need to repeat tests, review symptoms, rule out factors that can distort HbA1c and consider whether another form of diabetes is possible.

Diabetes.co.uk has guides explaining how diabetes is diagnosed and how the HbA1c test is used in type 2 diabetes.

The healthcare system also has practical constraints.

Appointments may be missed or delayed, laboratory results need reviewing and primary-care teams differ in workload and staffing.

That makes the period immediately following an abnormal result an obvious place to examine whether patients are being lost between testing and treatment.

What could this mean for the NHS?

The studies were conducted using US healthcare data, so the results cannot simply be transferred to NHS general practice.

The UK has different diagnostic pathways, staffing structures, diabetes reviews and commissioning arrangements.

But the underlying question is relevant.

People with type 2 diabetes are highly heterogeneous.

Someone with stable glucose, few complications and a consistent treatment regimen may not need exactly the same follow-up frequency as someone whose HbA1c is rising rapidly alongside kidney or cardiovascular disease.

More appointments are not automatically better if they add workload without changing care.

Equally, leaving a higher-risk person too long between reviews may delay medication changes or recognition of complications.

The potential value of the research is therefore risk-based follow-up, rather than simply increasing or reducing appointment numbers for everyone.

Before an algorithm like this could be used in the NHS, it would need prospective UK validation and evidence that it improves clinically meaningful outcomes without widening inequalities or making access harder for people who need support.

The studies make a sensible case for personalising follow-up.

They do not yet prove the best schedule for doing it.

Primary studies:
Context-aware optimisation of follow-up intervals for type 2 diabetes care
A time-to-event analysis of delay in type 2 diabetes diagnosis in primary care

A new study suggests that differences in how the immune system ages may provide clues about future metabolic health.

Researchers from Washington University School of Medicine, Nationwide Children’s Hospital and King’s College London identified patterns in blood immune cells that were associated with later chronic disease and mortality.

The research, published in Immunity on 9 October, examined approximately 12.4 million individual immune cells collected from 2,609 adults.

Participants came from eight cohorts spanning North America, the UK, Asia and Australia.

The researchers then used information from UK Biobank to investigate whether the patterns could be associated with health outcomes many years later.

What did researchers find?

The study focused on two types of immune cells known as effector memory CD8 T cells.

Some of these cells produce granzyme K, while others produce granzyme B.

Granzymes are proteins involved in immune responses.

Researchers found that healthy ageing was generally associated with a greater relative abundance of granzyme K-producing cells.

By contrast, an immune profile dominated by granzyme B-producing cells was associated with a higher risk of later illness.

The findings suggest that chronological age does not necessarily reflect how someone’s immune system is functioning.

Two people of the same age may have substantially different patterns of immune activity.

How was diabetes involved?

Researchers developed a model using blood proteins to estimate the immune-cell patterns identified in the smaller study.

They then applied that model to approximately 50,000 UK Biobank participants.

Over subsequent years, people whose estimated immune profile was more strongly associated with granzyme B-producing cells were more likely to develop chronic conditions, including type 2 diabetes.

The same pattern was also associated with future high blood pressure, liver disease, kidney failure and mortality.

The findings add to growing evidence that chronic inflammation and immune activity are closely linked with metabolic health.

However, the immune-cell pattern itself has not been established as a cause of diabetes.

Could this become a blood test?

Potentially, but considerably more work is needed.

The researchers suggest that measuring these immune patterns could eventually help identify people whose biological ageing differs from their chronological age.

However, the UK Biobank analysis did not directly measure the relevant immune-cell ratios in every participant.

Instead, researchers used a model based on circulating proteins to estimate those patterns.

That introduces uncertainty.

The findings also do not establish whether the new measure adds useful predictive information beyond existing factors such as age, weight, blood pressure, glucose and cardiovascular history.

What are the limitations?

This was observational research.

It cannot show that increasing one type of immune cell, or reducing another, would improve health.

It also cannot determine whether the immune changes cause disease or whether early biological changes associated with disease alter the immune system.

The results therefore do not support commercial tests claiming to measure someone’s precise biological age or future diabetes risk from these markers.

Further validation is required across more diverse populations.

What does this mean for UK diabetes prevention?

There is no immediate change to diabetes screening or treatment.

Established factors such as insulin resistance, excess visceral fat, family history and blood glucose remain much more relevant to current clinical decisions.

People at increased risk should continue to use established healthcare pathways to assess prediabetes and type 2 diabetes.

Measures that support cardiovascular health, including regular physical activity and appropriate weight management, also remain important.

The study’s contribution is primarily scientific.

It suggests that certain patterns of immune ageing could eventually help researchers understand why some people develop chronic diseases earlier than others.

Whether those patterns can become useful clinical tests or treatment targets has yet to be established.

Primary study: Single-cell analyses of global cohorts outline determinants of immune aging and link the ratio of GZMK+ to GZMB+ Tem cells to health trajectories – Immunity

The order in which foods are eaten may influence how quickly blood glucose rises after a meal, according to new research from Kyoto University.

Scientists investigating the relationship between carbohydrates and blood glucose found that giving mice olive oil before glucose reduced the initial rise in blood sugar.

The study, published in the journal Diabetes on 8 October, examined how hormones and nerves contribute to this response.

Researchers were particularly interested in gastric emptying – the process by which food moves from the stomach into the small intestine.

This process can strongly influence post-meal blood glucose levels.

What did researchers discover?

Mice received olive oil before an oral glucose dose, after glucose, or water as a comparison.

When olive oil was given before glucose, the initial rise in blood sugar was smaller.

Researchers also observed slower gastric emptying.

At the same time, several hormones increased, including GLP-1, GIP and glucagon.

GLP-1 is particularly relevant to type 2 diabetes because it helps regulate glucose levels after eating.

The results were also observed in mouse models of diabetes and severe insulin deficiency.

Why was glucagon involved?

Glucagon is usually associated with increasing blood glucose by stimulating the liver to release stored glucose.

However, the researchers found that its role in this response was more complicated.

Blocking glucagon signalling alone did not eliminate the effect.

Neither did blocking GLP-1 signalling alone.

When both pathways were blocked together, the glucose-lowering response weakened and the effect on gastric emptying disappeared.

Further experiments suggested that signalling through the vagus nerve also contributed.

This indicates that meal sequencing may engage several overlapping mechanisms rather than simply changing how quickly nutrients are absorbed.

Does eating fat before carbohydrates improve glucose control?

There is some existing human research suggesting that consuming vegetables, protein or fat before carbohydrates can influence post-meal glucose responses.

However, the current study was specifically designed to investigate the biological mechanisms in mice.

It does not establish the ideal order in which people with diabetes should eat their meals.

It also does not show that consuming additional olive oil will improve HbA1c or reduce diabetes complications.

Olive oil contains substantial energy, so adding large quantities to the diet could increase calorie intake.

What does this mean for the UK?

For people managing diabetes through dietary changes, the findings provide another reason for researchers to investigate meal composition and food order.

However, the overall balance of a meal remains important.

That includes the type and amount of carbohydrate, the quality of dietary fats and the inclusion of fibre-rich foods.

Olive oil can form part of a Mediterranean-style diet, but this particular experiment does not justify drinking it before meals as a diabetes treatment.

People using insulin or other glucose-lowering medicines should not change their doses based on these findings.

The study provides a possible explanation for why the order of nutrients can affect glucose responses.

Whether deliberately changing meal order produces meaningful long-term benefits in people with diabetes remains a question for human trials.

Primary study: Olive Oil Before Oral Glucose Delays Gastric Emptying and Lowers Glycemia Through Partially Redundant Glucagon and GLP-1 Signaling in Mice – Diabetes

The trillions of microorganisms living in the gut may help explain why one person develops a fever after a vaccination while another feels almost nothing.

Researchers have found that people who developed stronger fever responses after COVID-19 vaccination already had measurable differences in their gut microbiome before receiving the vaccine.

The study, published in Science, involved 171 healthy adults receiving SARS-CoV-2 mRNA vaccines.

Participants provided stool samples for microbiome analysis and blood samples for immune measurements, while recording their temperatures before and after vaccination.

The researchers found that people who subsequently experienced stronger fever responses had greater activity in bacterial genes involved in producing flagella – whip-like structures that certain bacteria use to move.

Flagella contain proteins called flagellins.

The immune system can recognise flagellin as a potential danger signal, triggering inflammation.

Importantly, the microbiome differences were present before the vaccine was given, alongside evidence of a more inflammatory baseline state.

Researchers then tested the idea in mice

Observational findings in humans cannot on their own establish that the gut bacteria caused the stronger inflammatory response.

The researchers therefore carried out additional experiments.

Gut microbiomes from human participants were transferred into mice raised without their own intestinal microbes.

Mice receiving microbes from people who had experienced stronger fever responses subsequently developed more inflammation after vaccination than mice receiving microbiomes from participants with milder responses.

The effect was partly dependent on the animals’ ability to detect bacterial flagellin.

Researchers also tested the microbes in human intestinal organoids.

Together, the experiments provide stronger mechanistic evidence that gut bacteria can influence the inflammatory state of the immune system.

That does not mean exactly the same mechanism has been proven to cause fever in every vaccinated person.

Could diet change the response?

This is where the findings need particularly careful interpretation.

People reporting more plant-based diets tended to have weaker fever responses.

In laboratory experiments, certain food additives increased bacterial flagellin production, while a Western-style high-fat diet increased inflammatory vaccine responses in mice.

But the researchers explicitly did not demonstrate that changing diet alters vaccine reactions in people.

The human dietary findings were observational.

People who eat different diets also differ in many other ways, and the study did not randomly assign participants to different diets.

The high-fat-diet experiment was conducted in mice, while the food-additive findings came from laboratory experiments.

It would therefore be inaccurate to claim that eating a plant-based diet will prevent fever after a vaccine.

There is also no evidence from this study that probiotics, supplements or commercial microbiome tests can reduce vaccine side effects.

Diabetes.co.uk has more information on what the gut microbiome is and how it interacts with metabolism and immunity.

Recent research has also linked patterns in the early-life microbiome with future type 1 diabetes risk, although that study similarly did not show that deliberately changing gut bacteria prevents diabetes.

What does this mean for people with diabetes?

The study involved healthy young adults receiving COVID-19 mRNA vaccines in 2021 and 2022.

It did not specifically investigate people with diabetes and should not be used to predict whether someone with type 1 or type 2 diabetes will develop vaccine side effects.

It also did not examine seasonal flu vaccination.

That distinction matters in the UK, where people with diabetes are among the clinical risk groups eligible for an annual NHS flu vaccination during the 2026/27 season.

The results provide no reason to avoid vaccination.

Nor does developing a fever necessarily mean the vaccine is working better or worse.

A fever reflects inflammatory activity, but this study was primarily examining why inflammatory reactions differ between people rather than proving a relationship between fever and vaccine effectiveness.

People with diabetes may notice temporary changes in glucose when they develop a fever or feel unwell after a vaccination, just as they can during other illnesses.

Monitoring glucose more closely and following normal sick-day guidance is therefore sensible where needed.

What happens next?

The researchers suggest the gut microbiome could eventually become a target for reducing unwanted inflammatory reactions.

But that remains a research question.

Clinical trials would first need to deliberately alter the microbiome in people and show that doing so changes vaccine reactions without compromising protection against infection.

Until those trials happen, the practical message is limited.

The study provides an intriguing explanation for why immune reactions differ between individuals, but it does not provide a diet, probiotic or microbiome treatment that people should use before being vaccinated.

Primary study: Science – The human gut microbiome primes fever after vaccination

Helping children make one manageable dietary change could improve weight outcomes without requiring a complete overhaul of their lifestyle.

That is the finding of a randomised trial published in JAMA Network Open.

Researchers from Boston University tested a community programme called H2GO!, designed to encourage children to replace sugary soft drinks with water.

The trial involved 437 children aged eight to 13 attending 11 Boys & Girls Club sites in Massachusetts.

The participating centres were randomly assigned to deliver either the intervention or their usual activities.

What did the programme involve?

The intervention consisted of 12 group sessions delivered over six weeks.

Children took part in interactive activities, health education and creative projects aimed at helping them understand their beverage choices.

Parents and caregivers were also involved through activities designed to support healthier habits at home.

The programme focused on a single behaviour rather than attempting to change every aspect of children’s diets.

Researchers were particularly interested in reducing drinks containing added sugar.

These can contribute substantial energy without necessarily making children feel full.

What happened after one year?

Researchers measured height and weight at the beginning of the study and again during follow-up.

They calculated BMI z-scores, which account for children’s age and sex.

After 12 months, the adjusted difference in BMI z-score change between the two groups was -0.19.

This was statistically significant, although relatively modest.

Children receiving the intervention also reported drinking fewer sugary beverages and more water.

However, the differences in reported beverage consumption between the intervention and comparison groups were not statistically significant.

That means the study cannot confidently establish that reduced sugary drink consumption was the reason for the improvement in BMI.

Other aspects of the programme, including family engagement and changes in health awareness, may have contributed.

Why is the study relevant to diabetes prevention?

Childhood obesity is associated with a greater likelihood of developing type 2 diabetes later in life.

However, body weight is only one part of diabetes risk.

Genetics, physical activity, sleep, diet and socioeconomic circumstances also matter.

Replacing high-sugar drinks with water can reduce added sugar intake without requiring children to follow restrictive diets.

Families may also benefit from understanding the sugar content of fruit juices and sports drinks.

The research does not suggest that all sweet-tasting drinks are equivalent, nor does it establish that the programme prevented diabetes.

What are the limitations?

The trial was randomised by centre, rather than assigning individual children randomly within each centre.

It involved only 11 sites, and the results may not translate directly to other communities.

Beverage intake was self-reported, making those measurements less reliable than the directly measured height and weight outcomes.

The findings also do not establish whether the BMI improvement will persist for several years.

What could UK schools and communities learn?

The research suggests that relatively simple, structured interventions may be worth considering alongside wider approaches to childhood obesity.

For schools, community organisations and local health services, the attraction is that the programme did not require specialist medical equipment or a complicated clinical pathway.

It was delivered in a setting children already attended.

The study also reinforces the importance of supporting healthier choices through families and communities rather than placing responsibility entirely on individual children.

Combined with appropriate physical activity and broader nutritional support, similar approaches could form part of childhood health-promotion programmes.

The results are encouraging, but the effect was small and further studies are needed to establish how best to reproduce it.

Primary study: A Community-Based Behavioral Intervention and Body Mass Index in School-Aged Children – JAMA Network Open

Full Phase III results for the experimental weight-loss drug retatrutide have confirmed substantial reductions in body weight among people living with obesity and type 2 diabetes.

The TRIUMPH-2 trial involved 1,152 adults across 92 medical and research centres in eight countries.

Participants were randomly assigned to receive retatrutide at 4mg, 9mg or 12mg once a week, or placebo, for 80 weeks.

At the start of the study, participants had an average BMI of 38.2 and an average HbA1c of 7.71%. Most were already taking at least one oral glucose-lowering medicine.

The results, now published in The Lancet, provide fuller peer-reviewed evidence following earlier headline results from the development programme.

We previously reported on the earlier Phase III retatrutide findings and has a dedicated guide explaining how retatrutide works and its potential side effects.

How much weight did people lose?

After 80 weeks, average weight loss was:

• 11.9% with 4mg retatrutide
• 16.8% with 9mg
• 18.8% with 12mg
• 5.1% with placebo

At the highest dose, that translated to an average loss of roughly 20kg.

Among people who started with a BMI of 35 or above, average weight loss reached 21.9% with the 12mg dose.

Around three-quarters of people receiving the highest dose lost at least 10% of their starting body weight, while almost one-third lost 25% or more.

Those are substantial reductions, particularly because people with type 2 diabetes have often lost less weight in obesity-drug trials than participants without diabetes.

Blood sugar improved too

Retatrutide was developed as more than a weight-loss medicine.

Participants also experienced substantial improvements in HbA1c, a measure of average blood glucose over the preceding two to three months.

HbA1c fell by around 1.4 to 1.5 percentage points in the retatrutide groups, compared with approximately 0.45 percentage points with placebo.

For more information on how the measurement is interpreted, Diabetes.co.uk has a guide to HbA1c and diabetes.

Improvements were also reported in waist circumference, systolic blood pressure and triglyceride levels.

However, the study was not designed to establish whether retatrutide prevents heart attacks, strokes, kidney failure or premature death.

Those longer-term outcomes matter when assessing whether a new diabetes treatment offers benefits beyond changes on the scales and laboratory tests.

What makes retatrutide different?

Retatrutide targets three hormone receptors.

GLP-1 helps regulate appetite, gastric emptying and insulin secretion.

GIP also influences insulin secretion and works alongside GLP-1 in regulating metabolism.

Retatrutide additionally activates the glucagon receptor, which may increase energy expenditure and influence how the body processes fat.

That separates it from semaglutide, which primarily targets GLP-1, and Mounjaro, or tirzepatide, which targets GLP-1 and GIP.

It is tempting to compare headline weight-loss percentages between these medicines.

But TRIUMPH-2 compared retatrutide with placebo, not directly with tirzepatide or semaglutide.

The trial therefore cannot establish that retatrutide is superior to existing licensed treatments.

Head-to-head trials would be needed for that.

What were the side effects?

As with other medicines that activate GLP-1 pathways, gastrointestinal symptoms were common.

Diarrhoea affected up to 34% of participants receiving retatrutide, while nausea affected up to 28%.

Vomiting was also reported.

Treatment discontinuation because of adverse events or death occurred in 12% of participants receiving 9mg and 8% receiving 12mg, compared with 5% receiving placebo.

Hypotension and altered skin sensations, described as dysaesthesia, were also more common with retatrutide than placebo.

These figures matter because a medicine’s effectiveness needs to be balanced against whether people can tolerate taking it over the long term.

The trial was funded by Eli Lilly, which is developing retatrutide.

Is retatrutide available in the UK?

No.

Retatrutide remains an investigational medicine and is not currently approved for routine use in the UK.

This is especially important because products claiming to contain retatrutide are already being offered illegally online.

Diabetes.co.uk has previously warned about the risks from unregulated and counterfeit retatrutide products being sold in the UK.

Anything currently being sold as retatrutide outside a legitimate clinical trial should not be regarded as an approved medicine.

For people living with type 2 diabetes and obesity, the new Lancet publication nevertheless represents an important milestone.

Triple-hormone treatments may eventually become another major option alongside existing GLP-1 and dual-agonist medicines.

The next question is not simply how much additional weight retatrutide can produce, but whether those changes translate into durable improvements in cardiovascular, kidney and overall health.

Primary study: The Lancet – Retatrutide in adults with obesity and type 2 diabetes (TRIUMPH-2)

Complications during pregnancy may provide important clues about a woman’s future risk of diabetes, cardiovascular disease and kidney problems, according to a major study involving more than 1.4 million women in England.

Published in BMJ Medicine, the research examined whether complications occurring during a woman’s most recent or earlier pregnancies were associated with health problems developing in subsequent years.

Researchers analysed primary care and hospital records for 1,432,795 women aged 15 to 49 who had been pregnant between 2000 and 2022.

The analysis focused on four outcomes: type 2 diabetes, cardiovascular disease, high blood pressure and chronic kidney disease.

Gestational diabetes carried a particularly strong association

Women who had experienced gestational diabetes had approximately seven times the subsequent rate of type 2 diabetes compared with women without that history.

They were also more likely to develop high blood pressure and cardiovascular disease.

However, gestational diabetes was not significantly associated with subsequent chronic kidney disease after adjustment.

This distinction is important because different pregnancy complications were associated with different patterns of future risk.

High blood pressure during pregnancy also mattered

Women who experienced gestational hypertension or pre-eclampsia had substantially increased rates of high blood pressure later in life.

The rate was more than three times higher, with some analyses showing an even stronger association.

These complications were also associated with approximately twice the rate of chronic kidney disease.

Smaller associations were identified for future cardiovascular disease and type 2 diabetes.

Previous pregnancies were important too

One of the study’s notable findings was that complications from earlier pregnancies remained associated with later health problems.

Researchers also identified relationships involving miscarriage, stillbirth, premature birth and placental abruption.

Postnatal depression was associated with higher rates of all four health outcomes, with relative increases ranging from approximately 35% to 56% following the most recent pregnancy.

However, these findings should not be interpreted as evidence that depression directly causes cardiovascular or kidney disease.

The underlying relationships may involve shared biological, behavioural and socioeconomic factors.

What are the limitations?

The study was observational.

Although researchers adjusted for numerous risk factors, they could not account for everything that might influence health.

Dietary habits and physical activity data were limited, while ethnicity information was missing for approximately one fifth of participants.

The median follow-up was around four years, so the results describe risk over the years following pregnancy rather than lifetime outcomes.

Importantly, the study does not prove that pregnancy complications themselves cause later disease.

They may instead reveal an underlying susceptibility that was already present.

Why does this matter for NHS care?

The research has a direct UK relevance because it used English healthcare records.

It suggests that a woman’s full pregnancy and diabetes history could provide useful information when assessing future cardiovascular and metabolic risk.

For women who have experienced gestational diabetes, follow-up glucose testing remains important even when blood sugar returns to normal after childbirth.

Tests such as HbA1c may help identify subsequent diabetes or prediabetes.

The broader implication is that pregnancy care and longer-term preventive healthcare should not be treated as entirely separate.

A complication that occurred years earlier may still be relevant when assessing someone’s future health.

Primary study: Pregnancy complications and risk of cardiometabolic-renal conditions in 1.4 million women in England – BMJ Medicine

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