Congenital hyperinsulinism is a rare condition characterized by unregulated insulin release from pancreatic beta cells, which can produce severe and unpredictable episodes of hypoglycaemia. Transient forms may occur with risk factors including perinatal stress, intrauterine growth restriction and maternal diabetes and often resolve within days or weeks, whereas genetic forms may result from a mutation in the insulin secretory pathway or from syndromes such as Beckwith-Wiedemann syndrome and tend to be persistent. The study examined children with genetically confirmed disease who had received a confirmed diagnosis between 2015 and 2025. Their management included diazoxide, surgical removal of a focal pancreatic lesion, subtotal pancreatectomy, octreotide or dasiglucagon, reflecting a range of disease severities and treatment pathways.

The children’s hospital admissions lasted between 58 and 211 days, an important feature of the context in which their feeding difficulties emerged. Many infants initially received intravenous fluids, parenteral nutrition or very small, scheduled oral feeds rather than uninterrupted opportunities to breastfeed or bottle-feed. Parents said that periods without oral intake, fasting, repeated blood-glucose checks and tightly controlled feeding schedules interrupted the establishment of typical feeding behaviours. One caregiver recalled that a child admitted for nearly four months was kept without oral intake for several weeks and was subsequently allowed only 10 to 15 millilitres every two or three hours. Another parent described prolonged hospitalization and repeated interventions as “blockers” that prevented the child from progressing with feeding.

Some parents believed that continuous glucose management also limited babies’ opportunities to experience hunger. Because blood glucose was monitored and maintained throughout the day, one parent said, the child did not develop the drive to feed that the parent associated with an ordinary baby. These accounts concern parents’ perceptions of how treatment affected feeding development; the study did not experimentally determine whether monitoring, fasting or any other medical factor caused a particular feeding outcome. It also could not separate the effects of hospitalization, repeated procedures, medication, tube feeding and close metabolic control. Nevertheless, the interviews show how clinically necessary interventions could alter the setting in which a child first learned to feed.

For many families, the practical demands continued after hospital discharge. Caregivers described learning to place and check nasogastric tubes, modify feeds, administer nutritional supplements and combine oral intake with pumped or tube-delivered nutrition. Some children received a nasogastric tube, while others had a percutaneous endoscopic gastrostomy; several continued enteral feeding alongside small amounts taken by mouth. The work was technically more demanding than these parents had anticipated for a newborn. Medication could also shape feeding: the article’s clinical background notes that diazoxide has an unpleasant taste and can cause vomiting and nausea, while octreotide can produce gastrointestinal dysmotility. The findings do not quantify the effect of any one treatment or establish which treatment was responsible for a child’s oral difficulties.

Oral feeding often progressed more slowly than families expected, and some children accepted less over time rather than improving with age. Parents reported gagging, vomiting, reduced bottle intake, refusal of new foods and prolonged dependence on enteral feeding. Some infants took a small amount by mouth and then needed the remainder delivered through a tube because blood glucose could not be allowed to fall. Other children stopped taking bottles before the usual transition to complementary foods. Caregivers described a persistent conflict between supporting development and protecting glycaemic stability: frequent prescribed feeds could leave a child too full to explore solids, while offering additional food raised concerns about vomiting or insufficient carbohydrate intake. “It’s trying to find a balance, but then unable to find a balance, because there’s no way,” one parent said.

Repeated unpleasant experiences also altered the emotional character of feeding. Several parents described anticipating distress before each feed, particularly when oral intake was followed by vomiting and further tube administration. One caregiver said the experience felt like force-feeding because the child had to receive the required amount to maintain blood glucose even when she resisted. Other parents reported anxiety, guilt or distress when they felt unable to distinguish ordinary infant refusal from a feeding decision with metabolic consequences. The study recorded these experiences through interviews and did not measure diagnoses of parental anxiety or depression, nor did it establish a causal pathway from individual feeding events to psychological outcomes. Its evidence is qualitative: the accounts show how clinical necessity and feeding development could pull families in opposing directions.

Across the interviews, glycaemic control became the main reference point for feeding decisions. Parents said they could not treat a missed feed with the same flexibility they had applied to other children, because maintaining the prescribed intake was necessary in CHI. Hunger, fullness and the infant’s willingness to eat therefore carried less weight in some decisions than the need to secure adequate nutrition for glucose stability. One parent explained that baby-led weaning was not compatible with the requirement that the child consume food because low blood glucose was possible otherwise. Continuous glucose monitoring was not raised spontaneously as a focus during the interviews, so the researchers did not speculate about how its use affected feeding management or caregiver wellbeing. The reported findings likewise do not quantify how often glycaemic control overrode infant cues.

The consequences of feeding extended well beyond individual meals. Families said leaving home required advance planning for milk, feeding pumps, medication, spare tubes and supplies for flushing or replacing lines. One caregiver described the preparation needed even for a trip to a shop, while others avoided public settings because of tube feeding, vomiting or unwanted attention. Some consequently stopped attending parent-and-infant groups and reduced social contact. The emotional burden included constant checking, anxiety about impending hypoglycaemia and uncertainty about the child’s future relationship with food. One participant became tearful when asked about the effect of feeding difficulties on family life and said, “I don’t think I want to look at that yet.” The interviewer did not pursue that topic further in order to respect the participant’s wellbeing.

The authors interpret the results as support for coordinated multidisciplinary care involving paediatric endocrinology, specialist nursing, dietetics, speech and language therapy and psychological support. They also emphasize education for healthcare teams outside specialist CHI services, noting that parents sometimes felt responsible for repeatedly explaining their child’s condition. This is a call based on participants’ experiences, not evidence that a particular programme has already been shown to improve feeding or family wellbeing. Recruitment was exploratory: 18 of 38 eligible families were invited, four declined, four could not be contacted and 10 completed interviews. The researchers used reflexive thematic analysis without statistical power calculations or a claim of data saturation. As the sample came from one centre and consisted of children with confirmed genetic CHI, milder forms may have been underrepresented, while feeding practices and support systems may differ in other healthcare settings. The study identifies experiences and service needs that require further evaluation; it does not establish how common these experiences are or demonstrate the effectiveness of an intervention.

Subject of Research: Caregiver experiences of feeding infants and children with congenital hyperinsulinism

Article Title: Parent experiences of infant feeding in congenital hyperinsulinism: a thematic analysis

Article References: Worthington, S., Ginbey, E., Otabor, O., Hall, C., Allchin, B., Auckburally, S. H., Salomon-Estebanez, M., Banerjee, I., & Worth, C. (2026). Parent experiences of infant feeding in congenital hyperinsulinism: a thematic analysis. Frontiers in Endocrinology, 17, Article 1955679. https://doi.org/10.3389/fendo.2026.1955679

Image Credits: AI Generated

DOI: 10.3389/fendo.2026.1955679

Keywords: congenital hyperinsulinism, infant feeding, feeding aversion, hypoglycaemia, enteral feeding, glycaemic control, parental stress, qualitative research, multidisciplinary care, family wellbeing, Parent, experiences

The scale of the problem is considerable. Across 44 controlled studies, depression affected roughly 19 percent of people with diabetes compared with 11 percent of those without the condition, an odds ratio of 1.76. The relationship runs in both directions. Depressive symptoms erode sleep, physical activity, diet, medication adherence and glucose monitoring, while the burdens of diabetes itself, including hypoglycaemia, treatment demands and complications, can sustain low mood. In type 2 diabetes, depression is associated with both microvascular and macrovascular complications, including cardiovascular events, and with higher mortality. Yet the review is careful to stress that observational associations cannot establish that treating depression prevents vascular events, a distinction that shapes the entire analysis.

The most striking technical finding concerns the direct evidence. The main pharmacotherapy network in type 2 diabetes comprised just 12 short-term trials with 792 participants, followed for only 8 to 24 weeks. Comparisons within this network are so sparse that the large effect estimates seen for some agents arise from a small evidence pool rather than a stable ranking. The authors also distinguish carefully between different kinds of evidence: direct evidence requires type 2 diabetes plus a stated depressive diagnosis or symptom threshold; mixed-diabetes studies count as only partially direct; general major-depression trials provide bridge efficacy evidence; and cardiac trials and regulatory information supply bridge safety evidence. This provenance labelling, applied to each claim rather than each paper, is the review’s key methodological contribution.

Among individual agents, the picture is heterogeneous. Sertraline has evidence for acute treatment and for recurrence prevention in diabetes: a maintenance trial randomised 152 patients who had recovered during open-label treatment, most of them with type 2 diabetes, and found that continued sertraline reduced recurrence while HbA1c did not differ from placebo in the randomised phase. Fluoxetine improved symptoms in an eight-week trial of 60 participants, only 34 of whom had type 2 diabetes, without a significant glycated-haemoglobin advantage. Escitalopram shows favourable short-term findings in the sparse network, but these require confirmation and must be weighed against its dose-related QTc liability. Bupropion was associated with improvements in depression, BMI and HbA1c in an uncontrolled cohort, and a secondary analysis of the same cohort reported improved sexual functioning, but without a control arm, recovery, self-management and weight change may all contribute.

Duloxetine occupies a special niche because depression in diabetes often coexists with painful neuropathy, yet the neuropathic-pain trials recorded modest fasting-glucose increases and a greater long-term HbA1c rise than routine care, and these samples were not selected for depression. Agomelatine has been examined in several small, comparator-dependent studies that point in conflicting directions: one open-label pilot favoured it over sertraline for symptoms and endpoint HbA1c, a randomised comparison found lower endpoint HbA1c than paroxetine without a symptomatic advantage, and another open-label study favoured escitalopram over agomelatine. Its principal safety concern is hepatotoxicity, requiring baseline and scheduled liver testing, which is particularly relevant given that diabetes, obesity and fatty liver frequently co-occur. Vortioxetine and trazodone rest on even weaker ground, with a severely attrition-limited pilot and expert consensus respectively, neither establishing glycaemic benefit or superior safety.

The review also scrutinises non-pharmacological options with the same provenance discipline. Psychological interventions can reduce depression in type 2 diabetes, but populations and components differ widely. Cognitive behavioural therapy for adherence and depression explicitly targeted medication use and glucose monitoring, so its HbA1c findings cannot be attributed to mood improvement alone. Digital delivery is not a single intervention: therapist-supported and guided web programmes showed benefit in mixed diabetes samples, whereas the unguided SpringboarD trial in type 2 diabetes did not outperform its active control. Exercise and behavioural programmes can improve mood and function, but glycaemic findings vary, and favourable subgroup results in Program ACTIVE II remain exploratory. Collaborative care, a service model combining care managers, systematic monitoring and stepped adjustment, improved psychiatric and medical outcomes in trials such as INDEPENDENT, but its composite endpoint required improvement in depression plus at least one cardiometabolic measure, and severe hypoglycaemia occurred in eight intervention participants and none receiving usual care.

On metabolism, the authors insist that an HbA1c change during antidepressant or collaborative-care treatment cannot be attributed to the drug without mediation evidence, because relief of depression may independently improve sleep, activity, adherence and self-management. Randomised SSRI studies suggest a small average glycaemic improvement, but most are short and treat glycaemia as a secondary outcome. Comparative rates of hypoglycaemia and hyperglycaemia are not reliably established for individual antidepressants in type 2 diabetes: case reports describe both directions of dysglycaemia, while a nested case-control study found no significant overall association with hypoglycaemia requiring hospital treatment. Fluoxetine labelling specifically notes hypoglycaemia during treatment and hyperglycaemia after discontinuation. The review’s blunt conclusion is that antidepressants are not glucose-lowering treatments, and favourable mean HbA1c changes do not establish freedom from hypoglycaemia or hyperglycaemia.

Cardiovascular interpretation receives equally careful treatment. Depression marks higher cardiovascular risk in type 2 diabetes, but that does not mean an antidepressant reverses it. The positive escitalopram trial after acute coronary syndrome, in which long-term follow-up found fewer major adverse cardiac events than placebo, is population-specific bridge evidence, not type 2 diabetes-specific cardioprotection, and mortality alone was not significantly reduced. Negative heart-failure trials, including MOOD-HF and SADHART-CHF, address different settings. Intermediate markers demand separate reading: SSRIs prolong the QTc interval by about 6 milliseconds on average, venlafaxine raises blood pressure in a dose-related fashion, and serotonin reuptake inhibition impairs platelet aggregation, linking SSRIs to upper gastrointestinal and intracranial bleeding, with absolute risk low but rising with antithrombotic or NSAID use. Drug interactions may matter more than small average differences between agents: paroxetine and fluoxetine can raise metoprolol exposure, and fluoxetine or fluvoxamine may reduce clopidogrel activation.

From this synthesis the authors propose an unvalidated conceptual checklist in which psychiatric urgency precedes cardiometabolic constraints, prior response and patient preferences. The first task is diagnostic triage, distinguishing major depressive disorder and subthreshold symptoms from diabetes distress, which may call for diabetes education rather than antidepressant prescribing. Imminent self-harm, psychosis, catatonia or inability to meet basic needs requires urgent psychiatric assessment before any metabolic refinement. The checklist then integrates weight profile, glycaemic control, hypoglycaemia history, cardiac disease, QT susceptibility, bleeding risk, polypharmacy and access, and it deliberately omits numerical weights and drug rankings because the evidence cannot justify them. Monitoring examples, such as a first antidepressant review within two weeks, are extrapolated from general depression guidance rather than tested in type 2 diabetes-specific schedules. The authors are explicit that the checklist is intended to structure clinical discussion, not to function as a guideline, validated decision aid or prediction rule.

The review closes with a research agenda that is as candid as its conclusions. The clearest gap is the absence of adequately powered, long-term active-comparator trials in type 2 diabetes stratified by phenotype, and the authors sketch a pragmatic trial of at least 12 months that would record psychiatric, metabolic, safety and patient-prioritised outcomes together, alongside mediation studies and implementation research on collaborative and digital care. They also acknowledge their own limitations: purposive selection, unreconstructable search histories, no formal risk-of-bias or GRADE assessment, and no stakeholder validation of the checklist. For clinicians, the practical takeaway is a disciplined humility: treat the depression according to psychiatric need, choose agents with the individual patient’s weight, glucose, cardiac and interaction profile in mind, measure rather than infer metabolic change, and remember that no current evidence establishes which antidepressant is best, or even reliably safer, for the millions of people living with both conditions.

Subject of Research: Selection of depression treatments for people with type 2 diabetes, integrating psychiatric efficacy, metabolic effects and cardiovascular risk

Article Title: Choosing depression treatment in type 2 diabetes: integrating psychiatric efficacy, metabolic effects, and cardiovascular risk. A narrative review

Article References: Tan, Y., Zhang, Y., Yuan, L., Huang, F., Cheng, Y., & Cheng, F. (2026). Choosing depression treatment in type 2 diabetes: integrating psychiatric efficacy, metabolic effects, and cardiovascular risk. A narrative review. Frontiers in Psychiatry, 17, Article 1976656. https://doi.org/10.3389/fpsyt.2026.1976656

Image Credits: AI Generated

DOI: 10.3389/fpsyt.2026.1976656

Keywords: type 2 diabetes, depression, antidepressants, HbA1c, cardiovascular risk, collaborative care, psychotherapy, SSRIs, hypoglycaemia, QTc prolongation, shared decision-making, narrative review

The study followed 97 children, adolescents, and young adults aged 1 to 25 years who attended routine follow-up at the BADAS Paediatric Diabetes Care and Research Centre at BIRDEM in Dhaka between March and November 2024. Each participant wore a blinded professional continuous glucose monitor, the Abbott FreeStyle Libre Pro iQ, on the upper arm for 14 days. Unlike the consumer devices increasingly common in high-income countries, the blinded sensor recorded interstitial glucose every 15 minutes without displaying any readings to the wearer. That design choice matters scientifically: when patients can see their glucose in real time, they tend to correct with extra insulin, adjust meals, or change activity, which artificially smooths the very fluctuations researchers want to measure. By keeping the sensor invisible, the team captured a less confounded estimate of true day-to-day glycaemic instability.

The central measure was the coefficient of variation, calculated as the standard deviation of glucose readings divided by the mean glucose and expressed as a percentage. International consensus guidelines, including those from the International Society for Paediatric and Adolescent Diabetes, recommend keeping this value at or below 36 percent, because higher variability is linked to more hypoglycaemic episodes, particularly dangerous overnight drops in blood sugar. In the Dhaka cohort, the mean coefficient of variation was 39.4 percent, with individual values ranging from 19.3 to 59.1 percent. Nearly 61 percent of participants exceeded the recommended threshold, meaning suboptimal variability was the norm rather than the exception. That mean is substantially above the 32 to 37 percent range typically reported in well-resourced paediatric cohorts, and because those comparison studies mostly used real-time devices that tend to lower observed variability, the true gap is likely even wider.

The contrast between diabetes types was stark. Participants with Type 1 diabetes, who made up just over 70 percent of the cohort, had a mean coefficient of variation of 41.9 percent, compared with 33.3 percent among those with Type 2 diabetes, a difference of 8.6 percentage points. More than three-quarters of the Type 1 group exceeded the variability target, against roughly a quarter of the Type 2 group. Time-in-range, the proportion of readings between 70 and 180 milligrams per decilitre, averaged just 52.5 percent in the Type 1 group versus 70.3 percent in the Type 2 group. Notably, time spent below range, which captures hypoglycaemia, was statistically similar between the two groups, at around 10 to 11 percent each, indicating that dangerous low blood sugar is not a concern confined to Type 1 diabetes in this population.

The study’s most intriguing finding concerns C-peptide, a byproduct of insulin production that serves as a marker of residual beta-cell function. When insulin-producing cells in the pancreas are destroyed, as in Type 1 diabetes, C-peptide falls to undetectable levels; when they survive, as in Type 2 diabetes or early Type 1 disease, measurable amounts persist. Fasting C-peptide was available for 46 of the 97 participants, and its relationship with glucose stability was striking. Higher C-peptide correlated strongly with lower variability, and in a multivariable regression adjusting for diabetes type, age, and insulin dose, each additional nanogram per millilitre of C-peptide was associated with a 1.94 percentage point reduction in the coefficient of variation.

Stratifying participants into three C-peptide categories revealed a clear dose-response pattern. The 20 participants with near-complete beta-cell depletion, defined as C-peptide below 0.2 nanograms per millilitre, had a mean coefficient of variation of 44.8 percent, time-in-range of only 42.1 percent, and time below range of 13.6 percent. The 13 participants with the best-preserved beta-cell function, above 1.0 nanograms per millilitre, achieved a mean variability of 32.2 percent and time-in-range of 65.8 percent, approaching international targets despite having no access to advanced insulin delivery technology. Time below range was nearly doubled in the lowest category compared with the highest, showing that hypoglycaemia risk, not just hyperglycaemia, tracks inversely with residual insulin secretion. The statistical trend across categories was significant for variability, time-in-range, time below range, and mean glucose.

The biology behind this relationship is coherent. Preserved endogenous insulin secretion provides meal-responsive, physiologically titrated insulin delivery that no injection regimen fully replicates, buffering the post-meal spikes that drive variability upward. Intact beta cells also support counter-regulatory glucagon responses that restrain hypoglycaemic swings. What makes the finding clinically important is its practicality: a single fasting C-peptide measurement costs roughly 5 to 10 US dollars in Bangladesh and can be run in ordinary hospital biochemistry laboratories, without the stimulation protocols or antibody assays that are often unavailable in low-resource settings. If confirmed in larger samples, the authors suggest, the test could help clinicians identify children who need prioritised access to glucose monitoring, more frequent clinical contact, or structured hypoglycaemia counselling.

The researchers are careful to frame the C-peptide results as hypothesis-generating. Because diabetes type was itself classified partly using fasting C-peptide, the two variables are partially collinear, and the association is best interpreted as a gradient of residual beta-cell function rather than a fully independent effect. Sensitivity analyses restricted to participants with Type 1 diabetes alone, and to those with at least 10 days of valid sensor data, produced consistent results, but C-peptide was missing for more than half the cohort, and although those with and without measurements differed on no measured baseline characteristic, residual selection bias cannot be excluded. The study was also single-centre, conducted at a tertiary referral facility where patients receive specialist care and may not represent all children with diabetes in Bangladesh. The 14-day monitoring window cannot capture seasonal or illness-related patterns, and the cross-sectional design precludes conclusions about cause and effect.

Even so, the findings carry weight for a region where diabetes in young people is rising and monitoring technology remains scarce and unevenly distributed. The authors point out that the elevated variability likely reflects a combination of resource-limited care realities: limited access to rapid-acting and long-acting analogue insulins, inconsistent meal timing, infrequent clinical contact, and practical barriers to rapid dose adjustment. Notably, even the Type 2 subgroup, which retained meaningful insulin secretion, showed variability exceeding values reported in comparably managed high-income country cohorts, suggesting the resource environment imposes a burden that operates across diabetes types. The team calls for multicentre studies across South Asia and sub-Saharan Africa to establish regionally appropriate benchmarks, for intervention trials testing whether variability-focused protocols reduce both high and low glucose excursions, and for cost-effectiveness analyses comparing professional glucose monitoring against standard HbA1c-only care. In the meantime, they argue, reducing variability, not merely lowering average HbA1c, should become an explicit treatment goal for young people with diabetes of both types in resource-limited settings.

Subject of Research: Glycaemic variability and residual beta-cell function in young people with Type 1 and Type 2 diabetes in Bangladesh

Article Title: Glycaemic Variability and C‐Peptide in Bangladeshi Children, Adolescents, and Young Adults With Diabetes: A Prospective Study

Article References: Flabe, A. H., Zabeen, B., Amirat, S., & Luo, J. (2026). Glycaemic Variability and C‐Peptide in Bangladeshi Children, Adolescents, and Young Adults With Diabetes: A Prospective Study. Endocrinology, Diabetes & Metabolism, 9(6), Article e70347. https://doi.org/10.1002/edm2.70347

Image Credits: AI Generated

DOI: 10.1002/edm2.70347

Keywords: continuous glucose monitoring, glycaemic variability, C-peptide, Type 1 diabetes, Type 2 diabetes, paediatric diabetes, hypoglycaemia, time-in-range, Bangladesh, low- and middle-income countries, beta-cell function, HbA1c

Type 1 diabetes is an autoimmune disease in which the insulin-producing beta cells of the pancreas are destroyed, meaning patients must rely on externally administered insulin for life. Because carbohydrate is the macronutrient with the most direct influence on blood glucose, the amount of carbohydrate a patient consumes has always been a central variable in insulin dosing. Conventional dietary guidance has generally encouraged moderate or higher carbohydrate intake combined with carefully matched insulin, partly out of concern that severe carbohydrate restriction could provoke dangerous metabolic disturbances in growing children. Yet in recent years a growing number of parents have begun experimenting with low and very low carbohydrate feeding strategies, often reporting striking improvements in their children’s glucose readings and a marked reduction in the amount of insulin needed each day.

Professor Christian Denzer, of the Department of Paediatrics and Adolescent Medicine, Division of Paediatric Endocrinology and Diabetes, at University Medical Center Ulm in Germany, who led the research together with Dr Belinda Lennerz of Boston Children’s Hospital and Harvard Medical School, explained the motivation behind the study. These diets are becoming more popular among people with diabetes, he noted, because patients themselves notice encouraging results, including much better blood sugar control and lower insulin needs. At the same time, he acknowledged that theoretical safety concerns have persisted, including the possibility of nutrient deficiencies, elevated cholesterol, low blood sugar episodes and ketoacidosis, a life-threatening complication of diabetes. In children, there is the additional worry that any restrictive diet could interfere with growth during critical developmental windows.

Until now, the evidence base for such diets in paediatric type 1 diabetes has been thin. Several observational studies and small interventional trials have corroborated the remarkable benefits on blood sugar and insulin requirements that patients report anecdotally, and no major safety events have been published to date. An earlier observational study led by Dr Lennerz, involving 316 children and adults, found major glycaemic benefits with mixed effects on cholesterol and no apparent adverse effect on growth or acute diabetes complications. But those studies were too small and too short to settle the question. What was needed, the researchers argued, was a large, long-term analysis capable of detecting rare complications and subtle effects on growth across a broad paediatric population.

To address this gap, the team turned to a diabetes prospective follow-up registry containing 25 years of longitudinal data collected from paediatric diabetes centres across Germany. From this resource they identified 45,569 children with type 1 diabetes, 55 percent of them male, with an average age of 10.3 years, whose carbohydrate intake had been recorded at least twice over a period of a year or more. This scale makes the analysis the largest of its kind ever performed, dwarfing previous investigations by orders of magnitude and providing the statistical power needed to examine both common outcomes and rare adverse events.

The children were grouped according to the carbohydrate percentage of their estimated energy intake. A very low carbohydrate group, comprising 219 children, consumed less than 10 percent of their energy from carbohydrate. A low carbohydrate group of 4,837 children obtained between 10 and less than 26 percent. The remaining 40,513 children followed a standard or higher carbohydrate diet of at least 26 percent. Average follow-up periods were 2.18 years for the very low carbohydrate group, 2.40 years for the low carbohydrate group and 3.67 years for the standard carbohydrate group. The researchers tracked height and weight, adjusting for the fact that the children were still growing, alongside changes in glycaemic trajectories, insulin use and the rates of the two most feared severe metabolic complications of diabetes: hypoglycaemia and diabetic ketoacidosis.

The analysis did not flag up any safety concerns in the areas examined. There was no evidence that a very low carbohydrate diet stunted growth, and no association between very low carbohydrate intake and either severe hypoglycaemia or diabetic ketoacidosis. This absence of harm signals is significant because both complications represent the principal acute dangers of type 1 diabetes. Severe hypoglycaemia, in which blood glucose falls to dangerously low levels, can cause seizures, loss of consciousness and, in extreme cases, death. Diabetic ketoacidosis arises when the body, starved of insulin, begins breaking down fat at an uncontrolled rate, producing acidic ketone bodies that overwhelm the blood’s buffering capacity and can rapidly become fatal without emergency treatment. Critics of carbohydrate restriction have long argued that pushing children into a state of relative ketosis might tip vulnerable patients toward ketoacidosis, but the registry data found no support for that fear.

On the benefit side, lower carbohydrate intake was associated with several favourable changes. Body mass index increased less over time in children following very low and low carbohydrate diets than in those on standard diets, meaning their weight remained closer to a healthier range as they grew. Levels of HbA1c, the laboratory measure that reflects average blood sugar over the preceding two to three months, were lower at the end of follow-up and rose less steeply over time in the lower carbohydrate groups. Doses of basal insulin, one of the two types of insulin typically prescribed for type 1 diabetes, followed the same pattern, being lower at the end of the observation period and increasing less over time among children eating less carbohydrate.

Most notably, the study examined a composite metric known as IDAA1c, which combines blood sugar levels with the amount of insulin a person requires. Dr Lennerz explained the significance of this measure: a lower IDAA1c means that better blood sugar control was achieved without simply using more insulin, strengthening the finding that very low and low carbohydrate diets were associated with both better glycaemic control and lower insulin requirements. This distinction matters because a patient could in principle achieve normal glucose readings by escalating insulin doses, but doing so increases the risk of hypoglycaemia and weight gain. A dietary approach that improves glucose control while simultaneously reducing insulin need therefore represents a genuinely favourable metabolic profile rather than a trade-off between competing risks.

The analyses were adjusted for factors including sex, age, migration background and diabetes duration, but the authors caution that the observational design leaves room for residual confounding. Families who choose very low carbohydrate diets may differ from other families in ways the registry cannot fully capture, including health consciousness, socioeconomic resources and the accuracy of self-reported dietary intake. Dr Lennerz concluded that reducing carbohydrate intake improved glycaemic control while reducing insulin needs without negatively impacting growth or increasing the rate of acute diabetes complications, describing the results as very encouraging but emphasising that they remain observational in nature. Additional research, she said, is needed to confirm the findings and establish the ideal amount of carbohydrate intake to maximise benefits while avoiding adverse effects and promoting food variety. For now, the study offers the strongest evidence yet that carbohydrate restriction in children with type 1 diabetes is not the hazard many clinicians feared, while leaving open the question of where the optimal balance lies.

Subject of Research: Effects of very low carbohydrate diets on growth and metabolic safety in children with type 1 diabetes

Article Title: Very low carbohydrate diets linked to health benefits in children with type 1 diabetes, largest study of its kind finds

Article References: Very low carbohydrate diets linked to health benefits in children with type 1 diabetes, largest study of its kind finds. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: type 1 diabetes, very low carbohydrate diet, paediatrics, HbA1c, IDAA1c, insulin requirement, hypoglycaemia, diabetic ketoacidosis, growth, registry study, EASD, nutrition

The study, led by Darshna Goordeen of Monash University’s Centre for Medicine Use and Safety together with collaborators at University College London and the University of North Carolina, is the first to examine glucose-lowering medication use in the final year of life specifically among people living with dementia in these two countries. Using linked hospital and administrative data, the team identified 10,088 individuals in the United Kingdom and 6,436 in Australia who had been diagnosed with both type 2 diabetes and dementia at least twelve months before their deaths between July 2013 and June 2018. In both cohorts, women made up the majority of participants, and a large proportion were aged 85 or older, with 55.8 per cent of the UK cohort and 37.7 per cent of the Australian cohort falling into this oldest age group.

The clinical rationale for stepping back from intensive diabetes treatment in advanced dementia is well established. Dementia guidelines in both the United Kingdom and Australia recommend individualising treatment according to changing goals when life expectancy is limited, and diabetes guidelines in both countries advise less strict glycaemic control, with higher glycated haemoglobin targets, for people living with dementia and limited life expectancy. Advanced dementia commonly brings poor nutrition, irregular eating and an inability to manage complex treatment regimens. These factors raise the risk of medication-related harm through administration errors and through a reduced ability to recognise, report or treat hypoglycaemia, the dangerous drops in blood sugar that glucose-lowering drugs can provoke. Deprescribing, defined as the planned and supervised process of reducing doses or stopping medications that may be causing harm or no longer offer benefit, is therefore widely endorsed for this population.

Despite this consensus, the evidence suggests overtreatment remains common. Earlier research found that among 161 patients with dementia and diabetes, 54 per cent were potentially overtreated, defined as having an HbA1c below 7 per cent despite mild functional or cognitive impairment or multiple comorbidities. In aged care homes, rates of potential overtreatment with glucose-lowering medications have ranged from 5 to 86 per cent. Against this backdrop, the new study set out to measure the prevalence of medication supply in the final 3, 6, 9 and 12 months of life and to identify which patient factors were associated with discontinuation in the six months before death.

The technical execution of the study drew on two of the world’s most comprehensive health data systems. In the United Kingdom, the researchers used the Clinical Practice Research Datalink, a primary care database sponsored by the Medicines and Healthcare products Regulatory Agency, linked to Hospital Episodes Statistics and mortality records from the Office for National Statistics. In Australia, they analysed linked data from the Victorian Admitted Episodes Dataset, the Pharmaceutical Benefits Scheme, which records every subsidised medication dispensed, and the National Death Index. Metformin emerged as the most commonly supplied medication class in both countries during the last year of life, used by 36 per cent of the UK cohort and 41 per cent of the Australian cohort, followed by insulin at 19.5 and 33.8 per cent respectively, sulfonylureas at 21.6 and 27.9 per cent, and newer agents including DPP-4 inhibitors, SGLT-2 inhibitors, GLP-1 receptor agonists and thiazolidinediones at 11.2 and 15.1 per cent.

The headline finding concerns insulin, the medication class most likely to be discontinued in both countries. Among people supplied insulin in the last twelve months of life, use fell by 25.6 per cent in the United Kingdom and 43.5 per cent in Australia in the final three months. In the UK, 97.1 per cent of those prescribed insulin in the last year received it within nine months of death, 90.8 per cent within six months and 74.4 per cent within three months. In Australia the decline was steeper, with supply falling from 92.5 per cent at nine months to 79.6 per cent at six months and just 56.5 per cent in the final quarter. The researchers suggest this pattern reflects growing clinical awareness of the particular hazards insulin poses in dementia, including difficulty with administration, diminished recognition of hypoglycaemic symptoms and reduced oral intake. Notably, this contrasts with Danish and American studies that reported stable or even increased insulin use near the end of life in older adults generally, though those studies did not focus specifically on people with dementia.

For metformin, the picture was more encouraging and revealed a striking alignment with clinical guidelines. Chronic kidney disease, a condition that makes metformin risky because of the small chance of lactic acidosis, was associated with higher odds of metformin discontinuation in the last six months of life in both countries, with an odds ratio of 1.05 in the UK and 1.60 in Australia. This suggests that clinicians are, at least in part, tailoring decisions to individual comorbidities rather than applying blanket rules. In Australia, male sex was associated with lower odds of metformin discontinuation, while for sulfonylureas, being aged 74 or younger was associated with higher odds of discontinuation compared with those aged 85 and older in both countries. For the newer medication classes, discontinuation was minimal, possibly because of lower initial supply rates, better tolerability or the absence of clear deprescribing recommendations in guidelines, even though recent work has flagged risks of malnourishment, dehydration, urinary incontinence and hypotension with SGLT-2 inhibitors and GLP-1 receptor agonists in frail older people.

Overall, among people supplied a glucose-lowering medication within six to twelve months of death, use fell by between 9.4 and 26.9 per cent in the final six months, with discontinuation occurring more frequently in Australia than in the United Kingdom. The authors interpret this as evidence of inadequate deprescribing overall. The gap between recommendation and practice may have several roots. Qualitative studies cited by the researchers indicate that clinicians generally feel comfortable deprescribing diabetes medications when harms clearly outweigh benefits, but some express hesitancy when a medication was initiated by a specialist. Healthcare professionals also report needing confidence that they are acting in the patient’s best interests and that the health system supports personalised care. Advance care planning, promoted in both countries as an integral component of dementia care, is intended to ensure that treatment preferences, including medication management, reflect individual values, yet the persistence of medication supply suggests these conversations are not translating into changed prescriptions.

The study’s strengths lie in its scale and its deliberate cross-national design. By applying identical methods to two large, population-level datasets, the researchers produced findings that can be directly compared, something single-country studies rarely achieve. The team acknowledged limitations, including differences in how age and comorbidities were captured across the two systems, the use of prescription records in the UK versus dispensing records in Australia, and a much lower documented prevalence of chronic kidney disease in the UK cohort, at 35 per cent versus 64.5 per cent in Australia, which may partly reflect under-ascertainment of kidney disease in UK diagnosis codes. The researchers also could not assess the appropriateness of medication use at the individual level or examine clinical parameters such as HbA1c measurements, meaning that appropriateness of discontinuation was inferred from the balance of risk and benefit at the population level.

The implications reach well beyond the two countries studied. As populations age and the overlap between dementia and diabetes grows, the findings point to a pressing need for structured, patient-centred deprescribing pathways embedded in routine dementia care. The authors highlight tools such as the 4S pathway for realigning diabetes regimens in older adults, multidisciplinary medication reviews that give clinicians the support to initiate deprescribing, and electronic health record alerts that could prompt timely medication management reviews for people with dementia in aged care settings. Until such systems become routine, the study’s central message stands: for many people living with dementia, diabetes treatment continues until the very end of life, and the challenge now is to ensure that comfort, rather than glycaemic numbers, guides the final prescription.

Subject of Research: Glucose-lowering medication use and deprescribing in the last year of life among people with dementia and type 2 diabetes in the United Kingdom and Australia

Article Title: Diabetes medication use in the last year of life in people living with dementia in the United Kingdom and Australia

Article References: Goordeen, D., Hopkinson, O. K., Reeve, E., Niznik, J. D., Lau, W. C. Y., Wei, L., Ilomaki, J., & Bell, J. S. (2026). Diabetes medication use in the last year of life in people living with dementia in the United Kingdom and Australia. European Geriatric Medicine. https://doi.org/10.1007/s41999-026-01608-6

Image Credits: AI Generated

DOI: 10.1007/s41999-026-01608-6

Keywords: dementia, type 2 diabetes, deprescribing, end-of-life care, insulin, metformin, polypharmacy, geriatrics, hypoglycaemia, pharmacoepidemiology, chronic kidney disease, medication safety

The scale of the problem makes the details of the survey worth unpacking. Insulin remains the cornerstone of diabetes management when lifestyle modification and oral agents fail to achieve glycaemic targets. Physiologically, the hormone performs two essential tasks: it drives glucose uptake into peripheral tissues such as muscle and fat, and it suppresses the liver’s production of glucose. When these actions are insufficient, chronic hyperglycaemia insidiously damages blood vessels and nerves, setting the stage for cardiovascular disease, nephropathy, retinopathy, neuropathy and premature death. Yet despite well-defined guidelines and decades of evidence, clinicians worldwide delay insulin initiation, a phenomenon researchers call therapeutic inertia. In Lahore, that inertia has now been measured with statistical precision, and the results suggest it is driven by a dense web of patient, physician and health-system factors that reinforce one another.

The research team, led from The University of Lahore, recruited physicians from Internal Medicine, Endocrinology, Gastroenterology and Nephrology at a public sector tertiary hospital. Using a calculated minimum sample of 384, they invited 910 eligible doctors and achieved a remarkable 88.8 percent response rate, with 808 completed questionnaires. The instrument, refined through a pilot study of 20 physicians and content-validated by a panel of 10 endocrinologists, achieved a content validity index of 0.90 and acceptable internal consistency, with Cronbach’s alpha values of 0.73 for the barriers section and 0.79 for the feedback section. Respondents were demographically diverse: 54.3 percent were women, 58.5 percent were aged 41 to 55, and the largest qualification group held the FCPS fellowship, followed by MBBS, MRCP and MRCS credentials. Most participants managed panels in which 11 to 30 percent of patients required insulin.

The barrier data, collected on four-point Likert scales and dichotomised for analysis, paint a picture of systemic strain. Beyond the twin giants of poor education and hypoglycaemia fear, physicians reported complex administration techniques as a barrier in 84.1 percent of cases, inadequate communication in 84 percent, fear of needles in 83 percent, misconceptions about weight gain in 81.5 percent and financial constraints in 81.4 percent. Patient resistance to insulin itself was ubiquitous. These figures resonate strikingly with international comparisons cited by the authors: in Trinidad, primary care physicians flagged needle fear in 98.6 percent of cases; in Saudi Arabia’s Jazan region, 80.5 percent reported injection phobia among patients; and in Nigeria, fear of hypoglycaemia topped the list at 81.3 percent. The consistency across such different health systems suggests that the psychology of insulin refusal is close to universal, even if its intensity varies with local literacy and economic conditions.

Statistical testing revealed that the experience of barriers was not evenly distributed across the medical workforce. Kruskal-Wallis tests with Bonferroni adjustment found highly significant differences by qualification in several domains. Patients’ resistance to insulin, difficulty explaining the differences between short-acting and long-acting formulations, the influence of cultural beliefs, and hesitation rooted in hypoglycaemia fear and regimen complexity all varied significantly across degree holders, with p values below 0.001. Binary logistic regression added a demographic dimension: male physicians were significantly more likely than female colleagues to report barriers, with an adjusted odds ratio of 1.392. Holders of the MRCP qualification faced elevated odds of 1.657 after adjustment, while physicians with 5 to 10 years of clinical experience were markedly less likely to report barriers than those with fewer than 5 years, with an adjusted odds ratio of 0.588. The authors caution that the reasons underlying the gender difference remain unclear and may reflect differences in clinical experience or practice patterns rather than any intrinsic factor.

The experience gradient deserves particular attention. That mid-career physicians encounter fewer obstacles than their juniors suggests a learnable skill set: the counselling techniques, cultural fluency and regimen-management strategies that accumulate with practice. Conversely, the finding that MRCP holders reported more barriers may reflect the complexity of the patients they manage or differing thresholds for perceiving problems. Either way, the authors argue, the pattern points toward targeted professional development rather than one-size-fits-all training. In a country where literacy rates lag behind those of many comparison nations, the dominance of patient education as the leading barrier, reported by 85.8 percent of respondents, takes on added weight. A parallel study from Singapore found that educational level was significantly associated with patients’ willingness to accept insulin, and the Lahore data are consistent with that relationship operating at population scale.

Perhaps the most actionable portion of the study is the physicians’ own prescription for reform. When asked what support was lacking in helping patients understand insulin therapy, the most common answer, endorsed with highly significant differences across qualification groups, was access to diabetes educators. For improving adherence, regular follow-up appointments dominated, and for sustaining patient responses over time, regular follow-up and support was the leading recommendation, chosen by 156 FCPS holders and 105 MRCP holders. On communication, an overwhelming majority across all credential groups selected a combined approach: written instructions, verbal counselling and shared decision-making. When asked how to improve the prescribing process itself, most favoured an all-of-the-above package of streamlined electronic prescribing systems, better patient education resources, improved access to formulary information and closer collaboration with diabetes specialists.

These recommendations align with a growing evidence base. A 2025 systematic review by Aslam and colleagues found that behavioural intervention programmes incorporating patient education, counselling and structured follow-up are effective in preventing and managing diabetes in adults. Pakistan’s rapidly expanding telecommunications infrastructure offers a plausible delivery channel for such programmes, potentially extending education and follow-up beyond hospital walls. Meanwhile, screening initiatives such as the Risk Assessment of Pakistani Individuals for Diabetes aim to identify high-risk individuals before complications develop. The survey’s authors also situate their findings within the broader literature on therapeutic inertia, which attributes roughly 20 percent of clinical delay to health-system factors, including medication cost, resource limits, discontinuity of care and workforce overload, and about 30 percent to patient-related factors such as injection phobia, fear of weight gain and low health literacy.

The study is not without limitations, and the authors are candid about them. Convenience sampling at a single urban tertiary hospital limits generalizability, particularly to rural settings where the majority of Pakistan’s population receives care. Self-reported data carry the risk of recall and social desirability bias. The inclusion of an all-of-the-above response category may have introduced overlap in the chi-square analyses, and the regression models did not formally assess multicollinearity or clustering by department. Crucially, because only physicians were surveyed, the barriers documented are physician perceptions, which may not fully mirror patients’ lived experience. The cross-sectional design identifies associations but cannot establish causation, and the interventions physicians recommended were not tested within the study itself.

Even with those caveats, the research delivers a clear message at a moment when Pakistan’s diabetes epidemic is accelerating. Insulin works; the obstacle is everything surrounding it. The Lahore survey transforms anecdote into quantified evidence, showing that the path to better glycaemic control runs through diabetes educator access, structured follow-up, culturally attuned communication and financial support, tailored to the experience level and professional background of the prescriber. Future intervention-based studies, the authors conclude, must now test whether these physician-endorsed strategies actually reduce barriers and improve outcomes. For a country where one in four urban adults lives with diabetes, the cost of therapeutic inertia is measured not in percentages but in amputations, blindness and lost years of life. What 808 physicians have described is, in effect, a map of where the system is failing, and a first draft of how to fix it.

Subject of Research: Barriers to insulin prescribing and physician-recommended interventions in diabetes care in Lahore, Pakistan

Article Title: Insulin Prescribing Challenges and Physician‐Suggested Interventions: Evidence From a Tertiary Care Hospital in Lahore, Pakistan

Article References: Aamir, M., Nafeesa, B., Aslam, A., Ghulam Mustafa, A., Elahi, M., Elahi, A., Barkat, K., Ashraf, M. U., Wahab, M. S. A., & Akhtar, S. S. (2026). Insulin Prescribing Challenges and Physician‐Suggested Interventions: Evidence From a Tertiary Care Hospital in Lahore, Pakistan. Endocrinology, Diabetes & Metabolism, 9(5), Article e70337. https://doi.org/10.1002/edm2.70337

Image Credits: AI Generated

DOI: 10.1002/edm2.70337

Keywords: insulin therapy, type 2 diabetes, Pakistan, therapeutic inertia, patient education, hypoglycaemia, physician survey, diabetes educators, cross-sectional study, tertiary care, medication adherence, health systems

The research team set out to address a practical gap in diabetes care. Existing questionnaires tend to measure self-care as a broad construct, aggregating many activities into a single score, and subjective judgements about personal glucose levels have been shown to predict distress more strongly than objective continuous glucose monitoring data. Clinicians, meanwhile, face time-pressured consultations packed with glycaemic metrics but often lack a rapid way to pinpoint which concrete behaviours might be driving a patient’s results. To fill that gap, the investigators used the Behavioural Diabetes Care Record, or BDCR, a questionnaire of 18 items that can be completed in under five minutes, with separate versions tailored to multiple daily injections and continuous subcutaneous insulin infusion pump therapy.

Most BDCR items ask respondents to give a number describing how often a specific behaviour occurred in the preceding 14 days. Questions include how many times per day blood glucose was tested, on how many days a main meal was eaten without administering insulin, and on how many days hypoglycaemia treatment food was carried for most of the day. Pump users are asked about cannula and infusion line changes, while injection users are asked about missed doses. The record also asks individuals to rate, on a scale of one to ten, how well they are achieving their personal diabetes self-care goals and how willing they are to make changes. Previous work has shown the measure responds to behavioural intervention, with medium to large effect sizes, and that improvements in individual behaviours correspond with improvements in HbA1c and distress.

The cross-sectional study recruited 105 adults aged 18 to 40 who had lived with type 1 diabetes for at least six months and were independently managing their condition, drawing participants from consecutive outpatient appointments over eight months. The cohort, 53 percent male with an average age of 27 and average diabetes duration of 12.6 years, had a mean HbA1c of 8.7 percent. Two-thirds used multiple daily injections and about a third used insulin pumps, while 29 percent used some form of continuous glucose monitoring. Alongside the BDCR, participants completed the 17-item Diabetes Distress Scale, the Acceptance and Action Questionnaire-II, reverse scored to index psychological flexibility, and a short form of the Behavioural Activation for Depression Scale. Point-of-care HbA1c values were taken from the medical record.

The behavioural frequencies told a clear story. Participants with HbA1c below 8 percent checked their glucose a median of four times per day, compared with three times among those at or above 8 percent, a statistically significant difference. Days on which prandial insulin was missed were also associated with glycaemic outcome, with a median of zero missed main-meal doses in the better-controlled group versus two in the higher HbA1c group. Among injection users, more frequent insulin administration, around four times per day, was associated with lower HbA1c. Those with better control also detected or tested for hypoglycaemia more often, a median of four times versus two, and were more likely to carry fast-acting treatment food throughout the day.

Distress painted its own distinct picture. Clinically significant diabetes distress, defined as a mean Diabetes Distress Scale score of three or above, was associated with more days on which insulin was skipped for main meals and for snacks, and with less frequent glucose checking before meals. Notably, distress and HbA1c did not move entirely in lockstep: some behaviours separated the groups on one measure but not the other, reinforcing the idea that emotional burden and glycaemic control are related but separable entities. Perceived achievement of personal self-care goals and psychological flexibility were both significantly associated with lower HbA1c and lower distress, while behavioural activation alone was not.

To see whether these signals clustered into recognisable profiles, the researchers applied latent class cluster analysis, guided by statistical fit criteria and input from consumers with lived experience of type 1 diabetes and clinicians from medical, nursing and nutrition disciplines. Three subgroups emerged. Half of participants fell into the first cluster, characterised by near-daily glucose checking, checking before insulin doses, few missed mealtime boluses, ready availability of hypoglycaemia treatment, higher psychological flexibility and strong perceived goal achievement. Only 30 percent of this group had HbA1c at or above 8 percent, and just 4 percent reported clinically significant distress.

The second cluster, about a third of the sample, showed moderate engagement: three-quarters checked glucose daily, but 72 percent had HbA1c at or above 8 percent and roughly 29 percent reported significant distress. The third cluster, nearly 18 percent of participants, stood out as clearly at risk. Ninety-nine percent had HbA1c at or above 8 percent and 72 percent reported clinically significant distress. They checked glucose on only about a third of days, missed main-meal insulin on a mean of nearly six days out of 14, checked before meals only about a quarter of the time, carried hypoglycaemia treatment least often, and recorded the lowest psychological flexibility and goal achievement scores. The authors note that this kind of stratification could allow clinicians to direct attention and resources to those most in need, particularly when glucose levels are suboptimal or distress is evident.

The findings carry implications for how routine consultations are structured. Because the BDCR items are observable and measurable, they can be repeated over time to track behavioural change and response to intervention, and triangulating them with HbA1c and continuous glucose monitoring data may offset some limitations of self-report, such as recall inaccuracy and social desirability bias. The authors suggest the instrument could guide personalised conversations, tailored goals, decisions about diabetes technology, or timely referral to dietitians and clinical psychologists. They also caution that the cross-sectional design limits causal inference and that findings from a tertiary-centre cohort may not generalise to wider populations, including people seen by telehealth or those not attending scheduled appointments.

Even in an era of continuous glucose monitoring and hybrid closed-loop systems, the behaviours highlighted here remain pillars of standard care: checking glucose or a trend arrow before dosing, announcing and administering mealtime insulin, and keeping hypoglycaemia treatment within reach. By showing that a five-minute set of plain questions can flag both metabolic risk and emotional strain, and by linking those patterns to psychological flexibility, the study offers a low-cost foundation for more person-centred, goal-oriented diabetes consultations. The team calls for prospective research to test whether routinely collecting these behavioural data genuinely improves outcomes for adults living with type 1 diabetes.

Subject of Research: Associations between type 1 diabetes self-care behaviours, glycaemic control, diabetes distress and psychological flexibility in adults

Article Title: Frequency of Key Type 1 Diabetes Self‐Care Behaviours Are Associated With Psychological Flexibility, Distress and Glycaemic Outcome

Article References: Nicholas, J. A., Yeap, B. B., Cross, D., Bear, N., & Burkhardt, M. S. (2026). Frequency of Key Type 1 Diabetes Self‐Care Behaviours Are Associated With Psychological Flexibility, Distress and Glycaemic Outcome. Endocrinology, Diabetes & Metabolism, 9(5), Article e70336. https://doi.org/10.1002/edm2.70336

Image Credits: AI Generated

DOI: 10.1002/edm2.70336

Keywords: type 1 diabetes, diabetes self-care, HbA1c, diabetes distress, psychological flexibility, Behavioural Diabetes Care Record, insulin regimen, glucose monitoring, cluster analysis, hypoglycaemia, behavioural intervention, Frequency

The study is notable less for its size than for its novelty. Until now, all evidence on this topic came from questionnaires and interviews rather than measured physiology. In one frequently cited survey of 53 young adults with type 1 diabetes, roughly one third reported fearing hypoglycaemia during sexual activity. But no one had ever tracked what actually happens to blood glucose in the hours surrounding sex. The Warsaw team set out to close that gap by combining real-time CGM data with participant-reported events, creating the first objective physiological picture of glucose dynamics during and after sexual intercourse in people with type 1 diabetes.

Dr Orłowska explained the clinical reasoning behind the research. On paper, sex is physical exertion like any other, and exertion lowers glucose. In practice, however, it behaves differently from planned exercise. A person preparing for a workout can reduce an insulin dose, eat carbohydrates beforehand, or activate an exercise mode on an insulin pump. Sexual activity, by contrast, is usually spontaneous, and it typically occurs in the evening or at night — precisely the window in which severe and unnoticed hypoglycaemia is most likely. Compounding the problem, she noted, is silence: patients routinely discuss exercise with their diabetologists and receive concrete advice, but almost nobody asks about sex, so the fear is never addressed. Yet sexual life is central to quality of life, and fear of hypoglycaemia can lead people to avoid intimacy entirely.

To investigate, the researchers enrolled 12 adults with type 1 diabetes — seven women and five men — in a prospective observational study. Participants had a median age of 36 years, ranging from 21 to 64, and a mean body mass index of 24 kg/m². All wore CGM devices, either the FreeStyle Libre 2 or the Guardian 4. Six were treated with multiple daily insulin injections and six with insulin pump therapy, including two using automated insulin delivery systems. None of the five male participants reported erectile dysfunction. Over a three-month period, participants marked each instance of sexual intercourse in their CGM application, allowing the researchers to analyse glucose data from two hours before to six hours after every event.

In total, 110 sexual intercourse events were recorded. A telling behavioural detail emerged: all participants using insulin pump therapy reported removing their devices during sex, meaning glucose readings during the events themselves came from the surrounding CGM trace rather than pump-integrated data. Despite the potential for exertion-related glucose drops, no clinically significant hypoglycaemia was observed anywhere in the dataset. Blood sugar changes were also unrelated to insulin therapy mode or to how long a participant had lived with diabetes, suggesting the response pattern is broadly consistent across treatment approaches.

The most striking finding was the bidirectionality of the glucose response. In 64 events, representing 58 percent of the total, mean post-intercourse glucose fell by 27 percent, from 180 to 132 mg/dL — a statistically significant decrease. In the remaining 46 events, or 42 percent, glucose rose by 34 percent, from 122 to 164 mg/dL, also statistically significant. Both increasing and decreasing patterns were observed within every single participant, meaning no individual could be classified as a consistent

The direction of the glucose response was not random. Higher glucose levels before intercourse were associated with a greater subsequent fall when glucose declined, and with a smaller rise when glucose increased, suggesting the body’s response may partly depend on the starting metabolic state. This bidirectional pattern echoes what is known about exercise physiology more broadly: physical activity typically lowers glucose by increasing muscle glucose uptake, but factors such as adrenaline, anticipatory stress, and circulating insulin levels can push glucose in the opposite direction. Sexual activity combines elements of exertion with emotional arousal, and the new data suggest these competing forces can net out in either direction in any given encounter.

Timing emerged as a meaningful variable. Of the 110 recorded events, 66 occurred at night, defined as between 20:00 and 06:00, and these nighttime events were associated with a statistically significant reduction in glucose levels, from a mean of 165 to 147 mg/dL. Daytime events, numbering 44, produced essentially no change, with mean glucose moving only from 144 to 143 mg/dL. The researchers also found no difference between mean glucose measured two hours after intercourse and six hours after, indicating that any glucose effects of sexual activity had largely settled within the first two hours rather than producing delayed drops hours later. That detail matters clinically, since delayed-onset hypoglycaemia is a well-recognised hazard after vigorous exercise and a common source of anxiety among people using insulin.

Body composition appeared to influence the response as well. Participants with a body mass index of 25 or higher showed a statistically significant post-intercourse glucose decrease of 10.7 percent, from 150 to 134 mg/dL, while those with a BMI under 25 showed a smaller, non-significant decline of 5.6 percent, from 159 to 150 mg/dL. The authors suggest this may reflect differences in energy expenditure, insulin sensitivity, or muscle mass, though the small sample size makes it impossible to draw firm conclusions. Diabetes duration, meanwhile, had no detectable effect on glucose responses, and neither did the mode of insulin delivery, whether multiple daily injections, conventional pump therapy, or automated insulin delivery.

The study’s limitations deserve emphasis. Twelve participants and 110 events are enough to generate hypotheses and provide reassurance, but not enough to establish definitive risk estimates for subgroups. All participants were adults in mid-life on average, with a normal mean BMI, and none of the men reported erectile dysfunction, so the findings may not extend to people with diabetes-related sexual dysfunction, older adults, or those with hypoglycaemia unawareness, a condition in which the normal warning symptoms of falling glucose are blunted. People with impaired awareness of hypoglycaemia are generally considered at higher risk during any unplanned activity, and clinicians may reasonably advise more cautious monitoring for them regardless of these results.

There is also the question of what the CGM trace can and cannot capture. Because every pump user removed their device during intercourse, the analysis relied on interstitial glucose readings from the surrounding period, and interstitial glucose lags behind blood glucose by several minutes to more than a quarter of an hour. Rapid changes during the event itself could therefore be somewhat smoothed or delayed in the recorded data. The researchers defined clinically significant hypoglycaemia according to standard thresholds used in diabetes research, and no readings crossed those thresholds, but the study was not powered to detect rare events. A single severe episode among hundreds of encounters would not necessarily appear in a dataset of this size.

Even with those caveats, the findings carry practical weight for clinical counselling. Diabetes care guidelines encourage clinicians to discuss the impact of physical activity on glucose, but sexual activity is rarely mentioned, and patients rarely raise it themselves. Dr Orłowska and her colleagues argue that the silence itself is harmful: fear of hypoglycaemia during sex can lead to avoidance of intimacy, strain on relationships, and reduced quality of life, all of which are recognised concerns in diabetes care yet seldom addressed in routine consultations. Objective evidence that intercourse does not typically provoke dangerous glucose lows gives clinicians a concrete, evidence-based starting point for those conversations.

The results also offer a framework for individualised advice rather than blanket reassurance. Because starting glucose level, time of day, and BMI all appeared to shape the glucose response, people with type 1 diabetes and their clinicians can use these factors when thinking about personal risk. Someone beginning sexual activity with a glucose level already trending low at night may reasonably choose to check a reading beforehand or keep fast-acting carbohydrates within reach, while someone starting from a higher glucose level may see little change or even a rise. The observation that glucose effects settled within two hours, with no delayed divergence at the six-hour mark, may further ease worries about overnight lows following evening intimacy.

The authors close with a reminder about technology access. In an ideal world, they note, every person with type 1 diabetes would use continuous glucose monitoring; those who do not may have no way of knowing whether they experience hypoglycaemia during sex or in any other setting. For the growing number of CGM users, however, the device itself offers a simple tool: marking events and reviewing the surrounding trace can turn an abstract fear into personal data. As the first study to measure glucose objectively in this context, the Warsaw work transforms a question that has lived only in surveys and unspoken anxieties into an answerable physiological one, and it opens the door to larger studies in more diverse populations.

Subject of Research: Glucose responses to sexual intercourse in adults with type 1 diabetes measured by continuous glucose monitoring

Article Title: Sex is safe in type 1 diabetes, shows small study using continuous glucose monitoring devices

Article References: Sex is safe in type 1 diabetes, shows small study using continuous glucose monitoring devices. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: type 1 diabetes, continuous glucose monitoring, hypoglycaemia, sexual intercourse, EASD, blood glucose, insulin therapy, quality of life, observational study, Medical University of Warsaw, nocturnal hypoglycaemia, diabetes counselling

Completing a marathon with type 1 diabetes is a metabolic balancing act of unusual complexity. Every kilometre of running consumes muscle glycogen and blood glucose, while carbohydrate intake, insulin sensitivity, adrenaline, dehydration and core temperature all push glucose levels in different directions at different times. Too much circulating insulin, or too little carbohydrate on board, risks hypoglycaemia, a dangerous drop in blood sugar that can cause confusion, collapse or worse. Too little insulin risks hyperglycaemia and ketoacidosis. Despite the well-documented health benefits of regular exercise, fear of these low-glucose episodes remains the single biggest barrier to physical activity for people with type 1 diabetes, affecting up to 45 per cent of those living with the condition.

To examine how amateur runners actually manage this challenge, the researchers designed an observational study built around the 2025 Poznań Marathon, a standard 42-kilometre road race. They recruited 20 amateur runners: 10 with type 1 diabetes of at least one year’s duration and 10 controls without diabetes. The two groups were well matched, showing no significant difference in age (a mean of 35.4 years in the diabetes group versus 39.7 years in the controls), and each group contained eight men and two women. Among the runners with type 1 diabetes, the median duration of the condition was 16.5 years and median glycated haemoglobin, a measure of long-term glucose control, stood at 6.4 per cent, indicating generally well-managed diabetes.

Before the race, each runner with type 1 diabetes followed an individualised insulin strategy agreed in advance. The target pre-race glucose range was set at 140 to 200 mg/dL, deliberately above the normal fasting range to create a safety buffer for the exercise-induced drops to come. Runners using multiple daily injections reduced their basal insulin dose by 25 per cent, while those using non-hybrid insulin pumps cut basal delivery by 50 per cent. Participants on hybrid closed-loop systems, which automatically adjust insulin delivery, instead set a target glucose of 150 mg/dL. Five runners used multiple daily injections, three used continuous subcutaneous insulin infusion pumps, and two used automated insulin delivery systems, reflecting the full spectrum of modern insulin therapy.

Glucose was assessed at five checkpoints along the course: the start line, 10 km, 19 km, 30 km and the finish. At each point, capillary glucose was measured with a standard fingerstick glucometer and compared against readings from two different CGM systems, one intermittently scanned and one transmitting in real time. Carbohydrates or insulin were administered as required throughout the race. The researchers also evaluated the accuracy of the CGM devices using mean absolute relative difference, or MARD, a standard metric that expresses the average absolute percentage difference between sensor readings and reference glucose values. The lower the MARD, the more faithfully the sensor tracks true blood glucose.

The headline performance result was striking in its ordinariness. Marathon completion times did not differ significantly between the groups, with a median finishing time of 228 minutes for the runners with type 1 diabetes and 248 minutes for the controls. In other words, with careful preparation, the runners with diabetes were not merely surviving the distance; they were racing it on equal terms. During the race, they consumed a median of 53.5 grams of carbohydrate per hour, equivalent to 2.61 grams per kilogram of body weight across the entire marathon, a fueling rate consistent with general endurance-sport guidance.

The glucose traces themselves told a reassuring story. Median capillary glucose measured by glucometer stood at 183.5 mg/dL at the start, within the planned pre-race target, then fell to 119.5 mg/dL at 10 km, rose to 142.5 mg/dL at 19 km, dipped to 121.5 mg/dL at 30 km and finished at 108.5 mg/dL. These values remained within or close to a safe range throughout, showing that the pre-race insulin reductions and steady carbohydrate intake kept the runners’ blood sugar from collapsing under the metabolic demands of the distance. Only two hypoglycaemic measurements occurred, and both were in the same participant, who nevertheless completed the race. Notably, that runner had started with a glucose level below 140 mg/dL, beneath the study’s recommended pre-race floor, and consumed 49.5 grams of carbohydrate per hour, slightly less than the group median.

But the study also delivered a caution about the very technology that made it possible. CGM accuracy deteriorated substantially during the marathon. The intermittently scanned system differed from glucometer measurements by an average of approximately 43 per cent, and the real-time system by approximately 37 per cent. Both sensors overestimated capillary glucose, by +32.2 mg/dL and +50.4 mg/dL respectively. This matters because a runner who trusts an inflated sensor reading may believe their glucose is safe when it is in fact falling toward hypoglycaemia. Sensor error during prolonged exercise is thought to arise from a combination of factors, including reduced subcutaneous blood flow as the body shunts blood to working muscle, sweat interfering with sensor adhesion, compression of the sensor site, and the lag between interstitial fluid glucose, which CGM devices measure, and blood glucose, which changes fastest during rapid metabolic swings.

The authors drew a practical conclusion from this discrepancy. In a statement, they said: In this small observational study, all runners with type 1 diabetes completed the marathon, with performance comparable to controls. The runner who experienced low blood sugar had started the race with a glucose level below 140 mg/dL. During the marathon, CGM readings differed from glucometer measurements. For longer endurance events, runners should therefore consider checking their glucose with a glucometer, especially when the sensor reading does not match how they feel. That advice effectively reframes CGM as a trend-monitoring tool rather than a standalone decision-making instrument during ultra-endurance efforts, with fingerstick confirmation reserved for moments when symptoms and sensor numbers diverge.

The research team emphasised that the findings should not be read as a green light for unsupervised endurance racing. They noted that fear of hypoglycaemia is the main barrier to physical activity and affects up to 45 per cent of people with type 1 diabetes despite the major health benefits of regular exercise, and that managing glucose is challenging when levels change rapidly and responses vary between individuals. Their message was nonetheless an optimistic one: with appropriate education and careful blood sugar management, people with type 1 diabetes can successfully take part in even very demanding endurance exercise. They advised anyone with type 1 diabetes preparing for a marathon to discuss an individual glucose, carbohydrate and hydration plan with their doctors before the event, stressing that the most important element is an appropriate insulin management strategy, including reductions in basal and prandial insulin, and that baseline glucose control, exercise experience, diabetes duration and complications all shape individual risk. Some people, they added, should consult a cardiologist before starting endurance training. The team, which supports many athletes with type 1 diabetes, including competitors at the Olympic Games, Ironman triathlon finishers and a runner who completed ten marathons in ten consecutive days, presents the study as further evidence that the condition need not disqualify anyone from the marathon start line, provided the science of glucose management is respected as rigorously as the training plan itself.

Subject of Research: Glucose management, carbohydrate intake and CGM accuracy in amateur marathon runners with type 1 diabetes during a real-world 42 km race

Article Title: Running marathons with type 1 diabetes can be safe, shows small study using continuous glucose monitoring devices

Article References: Running marathons with type 1 diabetes can be safe, shows small study using continuous glucose monitoring devices. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: type 1 diabetes, marathon, continuous glucose monitoring, hypoglycaemia, endurance exercise, insulin adjustment, carbohydrate intake, CGM accuracy, MARD, EASD, sports medicine, glucose management

A team at Guy’s and St Thomas’ NHS Foundation Trust in London set out to close this gap with a structured, age-adapted initiative known as the GOLD diabetes enhanced monitoring pathway, developed within the Geriatric Oncology Liaison Development clinic. Reporting their work in the European Geriatric Medicine journal, the researchers describe a quality improvement project conducted between February 2022 and June 2025, in which a multidisciplinary group of geriatricians, oncologists, diabetologists and clinical nurse specialists translated national guidance from the UK Chemotherapy Board and the Joint British Diabetes Societies for Inpatient Care into a practical, locally tailored system for older patients at intermediate risk of steroid-induced hyperglycaemia.

The pathway began with careful risk stratification. Patients were classified as low risk if they had an HbA1c below 48 mmol/mol and no history of diabetes, and were followed by their oncology team and general practitioner. High-risk patients, including those on insulin, those with HbA1c of 64 mmol/mol or above, glucose readings of 15 mmol/L or higher, pancreatic cancer, or a previous episode of steroid-induced hyperglycaemia, were referred directly to specialist diabetes services. The intermediate group, typically those with HbA1c between 48 and 63 mmol/mol or capillary glucose between 11 and 14.9 mmol/L, or patients with diabetes managed on oral agents who did not meet high-risk criteria, became the focus of the GOLD pathway.

Once enrolled, each patient received a capillary blood glucose meter and personalised education from a geriatric clinical nurse specialist, delivered face to face or by telephone within days of referral, because the interval between referral and the start of systemic anti-cancer therapy is often extremely short. Education covered the symptoms of high and low blood sugar, how to recognise diabetes emergencies, glucose targets, and practical demonstrations of the meter, all calibrated to each patient’s health literacy, cognition and physical abilities, with caregivers involved where necessary. During every treatment cycle, patients checked their glucose on the day of steroid administration and the following two days, before breakfast and before the evening meal, a schedule designed to capture the late-afternoon and evening peaks characteristic of steroid-induced hyperglycaemia.

Telephone follow-up by nurse specialists after each cycle formed the backbone of the monitoring system. The team reviewed all glucose readings, assessed food intake and treatment side effects, and applied decision-making algorithms for intervention. Hyperglycaemia was defined as at least two readings above 15 mmol/L, and hypoglycaemia as any reading below 4 mmol/L. When medication was required, the protocol favoured gliclazide, a sulphonylurea that directly stimulates insulin secretion and thereby counteracts the steroid-driven suppression of pancreatic beta-cell function. The team deliberately adopted a higher intervention threshold of 15 mmol/L, compared with the 12 mmol/L in national guidance, reflecting broader glycaemic targets for older people and a conscious effort to avoid hypoglycaemia and its consequences, particularly in patients with poor oral intake or renal impairment.

The implementation itself was iterative. The pathway was refined through seven Plan-Do-Study-Act cycles between 2022 and 2023, each incorporating feedback from healthcare professionals and addressing specific local barriers such as the feasibility of glucose measurement, intervention thresholds and the medication titration process. Risk criteria were sharpened over successive cycles, with the glucose range adjusted from 12–20 to 11–15 mmol/L and the HbA1c range expanded from 48–59 to 48–64 mmol/mol. Fortnightly multidisciplinary meetings were introduced from January 2023 to review complex cases, and the geriatric nursing team grew increasingly autonomous in managing intermediate-risk patients, reducing the burden on specialist diabetes services while retaining rapid access to expert advice.

In total, 126 patients were enrolled, with a median age of 74 years, 58% male, and 77% living with pre-existing diabetes. The most common tumour sites were the oesophagus, colon and breast, and 94% received chemotherapy as their primary systemic anti-cancer therapy, most commonly supported by dexamethasone at a median daily dose of 8 mg for the first four days of each cycle, chiefly for its anti-emetic and anti-allergic properties. Comprehensive geriatric assessment data, available for 81% of participants, revealed a largely pre-frail population with a median Clinical Frailty Scale score of 3, and identified malnutrition in 46% of the cohort, alongside social isolation, functional impairment and recent falls in smaller proportions. Personalised geriatric interventions, spanning physiotherapy, occupational therapy, dietary support and medication management, were implemented for the vast majority of those with identified impairments.

The results paint a picture of a pathway that is both feasible and safe. Clinical advice on diabetes management was provided to 89% of patients, and diabetes medication intervention was required in 32%, with gliclazide initiated or escalated in 92% of those cases. Women and patients with pre-existing diabetes were significantly more likely to need medication. Critically, only three hypoglycaemic events occurred, all asymptomatic and all managed without clinical consequences. Among 35 unplanned hospital admissions within a year, only two were related to hyperglycaemia, and there were no episodes of diabetic ketoacidosis or hyperosmolar hyperglycaemic syndrome, and no admissions for hypoglycaemia. During a median follow-up of 300 days, 41 patients died, but mortality was associated with metastatic disease, malnutrition and social isolation rather than with glycaemic control or diabetes intervention, suggesting that proactive metabolic monitoring did not add risk in this fragile population.

The pathway also influenced cancer treatment itself in measurable ways. Steroid regimens were modified for 24% of patients, almost always involving dose reductions driven by hyperglycaemia, and in 80% of those cases the adjustment was linked to the need for diabetes medication. While steroid reduction triggered treatment toxicity symptoms in four patients, leading to early discontinuation or dose reduction of the anti-cancer protocol in two, the overall signal was one of balance: oncologists could taper steroids with confidence knowing that a safety net existed for the metabolic consequences. Notably, secondary referrals to the diabetes team fell dramatically over the project period, from 36% of patients enrolled in 2022 to just 5% in 2025, evidence that the geriatric team’s growing expertise was absorbing demand that would otherwise have overwhelmed specialist services.

The authors are candid about limitations. The single-centre design, the predominance of pre-frail patients, the absence of a comparator group and the use of clinical rather than validated tools for some geriatric domains all constrain generalisability, and under-ascertainment of nocturnal or asymptomatic glycaemic excursions cannot be excluded with intermittent fingerstick testing. Even so, the team argues that the GOLD pathway offers a robust, patient-centred model for integrating geriatric, oncology and diabetes care, aligned with national and international recommendations for multidisciplinary management of older adults with complex needs. Future priorities include multi-centre validation, comparative and randomised designs to confirm effectiveness, integration of continuous glucose monitoring and digital health tools to reduce nursing workload, evaluation of patient-reported outcomes and cost-effectiveness, and incorporation of patient feedback to improve usability for those who struggle with glucometer technology. If those steps succeed, structured diabetes monitoring could become a standard component of geriatric oncology, ensuring that the steroids that help fight cancer no longer silently undermine the patients receiving them.

Subject of Research: A quality improvement project evaluating an age-adapted, multidisciplinary diabetes monitoring pathway for older adults with cancer undergoing steroid-based systemic anti-cancer therapy.

Article Title: Improving diabetes management in older adults with cancer: a quality improvement project to enhance monitoring during steroid-based systemic anti-cancer therapy

Article References: Liuu, E., Evans, R., Bassas-Letissier, N., Amaratunga, G., Compton, S., Georgiou, A., Kalsi, T., Liu, Y.-F., Maguire, J., Nottage, C., Rush, H. L., & Welch, C. (2026). Improving diabetes management in older adults with cancer: a quality improvement project to enhance monitoring during steroid-based systemic anti-cancer therapy. European Geriatric Medicine. https://doi.org/10.1007/s41999-026-01585-w

Image Credits: AI Generated

DOI: 10.1007/s41999-026-01585-w

Keywords: geriatric oncology, diabetes, steroid-induced hyperglycaemia, systemic anti-cancer therapy, quality improvement, multidisciplinary care, gliclazide, blood glucose monitoring, older adults, comprehensive geriatric assessment, hypoglycaemia, cancer treatment