Ambient Heat Significantly Elevates Hypoglycemia Risk in Type 1 Diabetes Patients
A study of 679 adults with T1DM using 33 million CGM readings identified a U-shaped risk curve between heat and hypoglycemia. Lowest risk was at 13C; at 25C temperature, the odds of hypoglycemia rose by 30%. Clinicians must advise dose adjustments in heat. Future automated insulin delivery systems should incorporate ambient temperature data to better predict and prevent hypoglycemic events.
KEY FINDINGS: Physicians should proactively educate patients with T1DM about the heightened risk of hypoglycemia during periods of increased ambient temperature. Managing glycemic levels in hot weather may require anticipatory reductions in insulin dosages to prevent dangerous declines. These findings also suggest that ambient temperature should be considered a dynamic variable within automated insulin delivery (AID) and hybrid closed-loop algorithms to optimize patient safety during seasonal heat waves.
BACKGROUND: As global temperatures continue to rise, understanding the impact of environmental factors on metabolic stability is increasingly critical for clinicians. Patients with Type 1 Diabetes (T1DM) often report seasonal fluctuations in glucose control, yet clinical guidelines remain ambiguous regarding whether high ambient temperatures primarily elevate the risk of hyperglycemia or hypoglycemia. This study was conducted to clarify the short-term relationship between outdoor temperature and the incidence of hypoglycemic events.
DETAILS: Researchers employed a case time series analysis using 33 million continuous glucose monitoring (CGM) data points collected between 2017 and 2024. The study cohort included 679 adults with T1DM residing in Sussex, UK. The primary exposure was the daily mean outdoor temperature at the participants' residential postcodes. Hypoglycemia was defined as a sensor glucose reading below 3.9 mmol/L (70 mg/dL) for a minimum of 15 minutes. The analysis revealed a non-linear, U-shaped association between ambient temperature and hypoglycemia risk. The lowest risk was observed at a daily mean temperature of 13°C. Risk significantly increased at temperature extremes, with the strongest effect seen during hotter weather. Specifically, at a daily mean temperature of 25°C, the odds of experiencing hypoglycemia were approximately 30% higher compared to the reference temperature of 13°C.
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Source: Daultrey, H. E., Oliver, N. S., Chakera, A. J., et al. The Association Between Ambient Temperature and Hypoglycemia in People Living With Type 1 Diabetes: A Case Time Series Analysis Using Real-Time Continuous Glucose Monitoring. Diabetes Care. 2026; 49(8):1323-1329. Published: August, 2026. DOI: 10.2337/dc25-2383
Somatic Diseases May Affect the Brain Primarily Through Vascular Injury and Neuronal Loss
A narrative review found that common age-related somatic diseases were consistently associated with brain atrophy, neuronal loss, and cerebrovascular lesions. Evidence linking these diseases to amyloid and tau pathology was limited and inconsistent. The findings suggest that systemic diseases may contribute to dementia primarily through non-Alzheimer's mechanisms, particularly vascular injury and neuronal loss. The review underscores the importance of recognizing mixed dementia and considering systemic health in the assessment of cognitive decline.
KEY FINDINGS: Common age-related somatic diseases appear to be more consistently associated with cerebrovascular injury, brain atrophy, and neuronal loss than with amyloid or tau pathology. These findings suggest that the relationship between systemic disease and dementia may involve multiple non-AD pathways rather than a direct effect on classical AD pathology. The review highlights the importance of recognizing mixed dementia and considering systemic health when evaluating brain aging and cognitive decline.
BACKGROUND: Several common age-related somatic diseases are associated with an increased risk of dementia, but the neuropathological pathways underlying these associations remain incompletely understood. This narrative review examined evidence linking heart disease, type 2 diabetes, kidney disease, liver disease, lung disease, and anemia with brain pathology, including Alzheimer's disease (AD)-related amyloid and tau pathology and non-AD changes such as neuronal loss, brain atrophy, cerebrovascular lesions, neuroinflammation, and non-AD proteinopathies.
DETAILS: The authors conducted a PubMed search for human studies investigating associations between somatic diseases and brain pathology using postmortem examinations, brain imaging, or cerebrospinal fluid biomarkers. The available evidence was qualitatively synthesized and graded according to its strength. The review specifically evaluated whether common systemic diseases were associated with AD-related pathology or with other forms of brain injury that may contribute to cognitive impairment and dementia.
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Across the conditions examined, the strongest and most consistent associations were between somatic diseases and global neuronal loss or brain atrophy, as well as cerebrovascular lesions. In contrast, associations between somatic diseases and amyloid or tau deposition were limited and inconsistent. The review found no systematic studies examining neuroinflammation or non-AD proteinopathies in relation to somatic diseases.
Overall, the available evidence suggests that systemic diseases may contribute to brain damage predominantly through non-AD mechanisms, particularly cerebrovascular injury and diffuse neuronal loss, rather than by directly driving the characteristic amyloid and tau pathology of AD. The authors emphasize that these processes may contribute to the complex combination of pathologies frequently underlying dementia in older adults.
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Source: Grande, G., Valletta, M., Gasparini, F., et al. Brain pathology in relation to somatic diseases: Exploring the body–brain crosstalk. Journal of Internal Medicine. 2026; 300(3): 223–237. Published: June 2, 2026. DOI: 10.1111/joim.70119.
Hypertension at 5 Months Postpartum in Women With Gestational Diabetes
Among 678 women with recent gestational diabetes mellitus, 26.4% developed hypertension by 5 months postpartum. Higher early-pregnancy weight and blood pressure, Black or mixed ethnicity, and gestational hypertension or pre-eclampsia were associated with increased risk. Postpartum hypertension was also associated with greater adiposity and dyslipidemia. The findings support structured postpartum screening for blood pressure and broader cardiometabolic risk after GDM.
KEY FINDINGS: Approximately one in four women with recent GDM developed hypertension by 5 months postpartum. Higher maternal weight and blood pressure early in pregnancy, as well as Black or mixed ethnicity, were associated with increased risk, while gestational hypertension or pre-eclampsia was also associated with postpartum hypertension. Women with postpartum hypertension had greater adiposity and more frequent dyslipidemia, highlighting the broader cardiometabolic abnormalities present after GDM. Because early-pregnancy characteristics provided only modest prediction, the findings support structured postpartum assessment that includes blood pressure and broader cardiometabolic risk evaluation rather than focusing solely on dysglycemia.
BACKGROUND: Gestational diabetes mellitus (GDM) is associated with an increased risk of later cardiometabolic disease, including hypertension. However, the occurrence and determinants of hypertension soon after pregnancy complicated by GDM have not been well defined. This prospective study evaluated the incidence and predictors of hypertension at 5 months postpartum and examined its relationship with other cardiometabolic abnormalities in women with recent GDM.
DETAILS: This single-center observational prospective cohort study was conducted at King's College Hospital, London, between September 2023 and January 2025. Women with GDM who received routine prenatal care at 12 weeks' gestation were invited for a postpartum assessment at approximately 5 months after delivery; women with chronic hypertension were excluded. The assessment included blood pressure, BMI, waist circumference, glucose status, lipid profile, and renal function. Hypertension was defined as systolic BP ≥ 130 mmHg, diastolic BP ≥ 80 mmHg, or receipt of antihypertensive treatment. Of 912 women with GDM invited for postpartum review, 696 (76.3%) attended. After excluding 18 women with chronic hypertension, 678 women constituted the study cohort. Follow-up occurred at a median of 5.1 (IQR, 4.4-6.7) months after birth.
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Among the 678 women with previous GDM, 179 (26.4%) developed hypertension at a median of 5.1 (IQR, 4.4-6.7) months postpartum. Women who subsequently developed hypertension had higher early-pregnancy weight and blood pressure. At 12 weeks' gestation, median weight was 79.3 kg versus 69.3 kg among women who remained normotensive, while median systolic BP was 121.8 versus 115.5 mmHg and median diastolic BP was 74.5 versus 70.3 mmHg, respectively. Obesity at this stage was also more frequent among women who later developed hypertension (50.3% vs 28.5%). Pregnancy hypertensive disorders were more common among women who developed postpartum hypertension. Gestational hypertension occurred in 8.4% versus 3.8%, and pre-eclampsia in 9.5% versus 1.8%, among women who developed postpartum hypertension compared with those who remained normotensive.
Multivariable analysis identified higher maternal age, Black or mixed ethnicity, higher weight, and higher systolic and diastolic BP at 12 weeks as predictors of postpartum hypertension. Black ethnicity was associated with an adjusted OR of 1.88 (95% CI, 1.19-3.00), mixed ethnicity with an adjusted OR of 2.75 (95% CI, 1.21-6.24), and weight ≥ 73 kg with an adjusted OR of 1.57 (95% CI, 1.04-2.38). Each 1-mmHg increase in systolic BP was associated with an adjusted OR of 1.04 (95% CI, 1.02-1.07), and each 1-mmHg increase in diastolic BP with an adjusted OR of 1.04 (95% CI, 1.00-1.07). Development of gestational hypertension or pre-eclampsia was associated with an adjusted OR of 3.00 (95% CI, 1.69-5.34).
At the postpartum assessment, women with hypertension had a median BMI of 30.1 (IQR, 26.7-36.8) kg/m² compared with 27.0 (IQR, 23.5-30.6) kg/m² among normotensive women. A waist-to-height ratio > 0.5 was present in 87.7% versus 69.1%, and dyslipidemia in 35.8% versus 24.4%, respectively. Dysglycemia and renal dysfunction did not differ significantly between the groups.
The prenatal prediction model had only modest discriminatory ability. The AUC was 0.723 (95% CI, 0.680-0.766) using characteristics available at 12 weeks and 0.739 (95% CI, 0.697-0.782) after adding gestational hypertension or pre-eclampsia. At a 20% false-positive rate, detection rates were 49.5% and 53.7%, respectively.
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Source: Gomez Fernández, C., Charakida, M., Moser, M., et al. Hypertension at 5 months postpartum in women with gestational diabetes. Ultrasound in Obstetrics & Gynecology. 2026; 68(2): 202-210. Published: July 17, 2026. DOI: 10.1002/uog.70291.
Modified Delphi Consensus Defines a Practical Intravitreal Treatment Pathway for Centre-Involving Diabetic Macular Oedema
A Delphi panel of medical retina specialists reached consensus on 64/82 statements (78%) supporting personalised CI-DMO management. Early anti-VEGF response assessment at 3-6 months and consideration of corticosteroids after 9-12 months for persistent suboptimal response or high treatment burden may improve treatment consistency, but prospective validation is needed.
KEY FINDINGS: A two-round Delphi consensus involving medical retina specialists achieved agreement on 64/82 statements (78%) for managing CI-DMO. The framework supports personalised treatment, early assessment of anti-VEGF response at 3-6 months, and consideration of corticosteroid therapy after 9-12 months for persistent suboptimal response or high treatment burden. Prospective clinical validation is still required.
BACKGROUND: Management of centre-involving diabetic macular oedema (CI-DMO) can be challenging because treatment response varies and practical guidance on when to modify or switch therapy remains limited. Anti-vascular endothelial growth factor (VEGF) therapy is generally used first-line, while corticosteroids provide an alternative or second-line approach.
DETAILS: A two-round modified Delphi study was conducted among medical retina specialists in the National Health Service in England. A steering group developed 82 statements covering patient-centred care, baseline assessment and monitoring, definitions of treatment response, anti-VEGF switching criteria, corticosteroid use, and treatment stopping or switching criteria. Consensus was predefined as ≥75%.
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Thirty specialists responded in round one and 39 in round two. Overall, consensus was achieved for 64/82 statements (78%). The panel strongly supported personalised treatment and comprehensive baseline assessment, including best-corrected visual acuity, intraocular pressure, and macular optical coherence tomography with central retinal thickness measurement.
The consensus defined non-response as a reduction in central retinal thickness (CRT) by ≤10% and suboptimal response as a 10-20% reduction. A positive response was defined as a ≥20% reduction in CRT with improvement or stabilisation of diabetic macular oedema-related best-corrected visual acuity.
The panel recommended evaluating anti-VEGF response at 3-6 months and after treatment with two different anti-VEGF agents. For patients with persistent suboptimal response or high treatment burden, there was moderate consensus supporting consideration of corticosteroid therapy after 9-12 months.
For patients demonstrating a positive response after 1-2 injections of a short-acting corticosteroid, 63% strongly agreed and 27% tended to agree that transition to a long-acting corticosteroid should be considered. The panel also supported assessing anti-VEGF treatment burden after 9-12 months and considering corticosteroid therapy when treatment burden is high.
The recommendations emphasize that treatment decisions should incorporate anatomical response, visual outcomes, patient factors, treatment preferences, and tolerance. However, the authors noted that the pathway is based on expert consensus rather than prospective clinical validation, and all panellists were from England.
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Source: Gale, R., Bailey, C., Devonport, H., et al. Modified Delphi Expert Consensus on the Optimal Intravitreal Treatment Pathway for Centre Involving Diabetic Macular Oedema Patients Within the National Health Service. BMJ Open Ophthalmology. 2026; 11: ve002787. Published: August 20, 2026. DOI: 10.1136/bmjophth-2026-002787.
Potassium Binders May Support Continued RAAS Inhibitor Therapy in Chronic Kidney Disease and Heart Failure
Second-generation potassium binders were associated with greater persistence of RASi and MRA therapy than first-generation binders. Continued RASi use was associated with lower observed mortality and hospitalization, but not with a clear difference in 3P-MACE. These findings suggest potassium binders may facilitate sustained RAASi therapy in CKD and HF.
KEY FINDINGS: In this Swedish nationwide observational cohort, second-generation potassium binders were associated with greater persistence of RASi and MRA therapy at 6 months than first-generation binders. RASi persistence was also associated with lower observed all-cause mortality and hospitalization, although no clear difference in 3P-MACE was identified. The findings support the potential role of potassium binders in maintaining guideline-directed RAASi therapy in patients with CKD and/or HF.
BACKGROUND: Renin–angiotensin–aldosterone system inhibitors (RAASi) provide important cardiorenal benefits in chronic kidney disease (CKD) and heart failure (HF), but their use can increase the risk of hyperkalemia. Hyperkalemia frequently leads to RAASi discontinuation despite the benefits of continued therapy. This study evaluated whether potassium binders, particularly second-generation agents, were associated with greater persistence of RAASi and mineralocorticoid receptor antagonist (MRA) therapy.
DETAILS:
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Source: Furuland, H., Larsson, A. O., Uhde, M., et al. Potassium Binders and Continuation of Renin–Angiotensin System Inhibitors/Mineralocorticoid Receptor Antagonist in Chronic Kidney Disease and Heart Failure (the DEMONSTRATE Database. Journal of Internal Medicine. 2026; 300(2): 179-192. Published: Augusts, 2026. DOI: 10.1111/joim.70087.
Hyponatremia Treatment Guidelines: Maintain Cautious Correction to Prevent Osmotic Demyelination
Current hyponatremia correction safeguards should be maintained. For chronic hyponatremia with sodium 120 mmol/L or lower, correction should generally remain within 10-12 mmol/L in 24 hours and 18 mmol/L in 48 hours; high-risk patients require a stricter limit of 8 mmol/L in 24 hours. Frequent monitoring and desmopressin may prevent overcorrection.
KEY FINDINGS: Current safeguards for severe hyponatremia remain warranted despite recent evidence questioning restrictive correction limits. Correction should be particularly cautious in patients with sodium ≤105 mmol/L or other ODS risk factors. Frequent serum sodium measurement and urine-output monitoring are essential because spontaneous water diuresis can cause rapid sodium increases. Desmopressin may help prevent or reverse excessive correction.
BACKGROUND: Severe hyponatremia can cause life-threatening neurologic complications, while overly rapid correction can result in osmotic demyelination syndrome (ODS). Recent retrospective evidence has questioned whether existing correction limits are overly restrictive. This review reassesses the evidence supporting current treatment safeguards and emphasizes continued caution when correcting severe hyponatremia.
DETAILS: The review examines the evidence underlying international recommendations for limiting the rate of serum sodium correction, with particular attention to patients with severe or chronic hyponatremia. The authors discuss evidence linking rapid correction with ODS and review data that have challenged the need for conservative correction limits.
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For chronically hyponatremic patients with serum sodium ≤120 mmol/L who are at normal risk for ODS, the US/Irish expert panel recommends limiting correction to 10–12 mmol/L during any 24-hour period and 18 mmol/L during any 48-hour period, with a minimum correction of 4–8 mmol/L. Patients at increased risk of ODS—including those with sodium ≤105 mmol/L, alcohol use disorder, hypokalemia, malnutrition, or advanced liver disease—should have correction limited to 8 mmol/L in any 24-hour period, with a minimum daily correction goal of 4–6 mmol/L.
For patients with severe symptoms, European and US/Irish recommendations support bolus administration of hypertonic saline to increase serum sodium by approximately 5 mmol/L or 4–6 mmol/L, respectively, within a few hours. The review notes that this initial increase can substantially reduce intracranial pressure and may reverse impending brain herniation.
The review concludes that current safeguards for treating severe hyponatremia should not be abandoned. Excessive increases in serum sodium can occur because of sudden elimination of dilute urine rather than excessive saline administration. Water diuresis may increase serum sodium by more than 2 mmol/L per hour, emphasizing the need for frequent serum sodium measurements and close monitoring of urine output in patients with sodium ≤120 mmol/L.
Desmopressin can be used to prevent or reverse inadvertent overcorrection. A strategy involving scheduled desmopressin with controlled hypertonic saline administration, termed the "DDAVP clamp"", has been reported to help achieve correction targets, although comparative evidence remains limited.
The review highlights that patients with sodium ≤105 mmol/L and additional risk factors for ODS are particularly vulnerable. If correction exceeds 8 mmol/L in less than 24 hours in these high-risk patients, relowering the serum sodium should be considered.
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Source: Sterns, R. H., Rondon-Berrios, H., Adrogué, H. J., et al. Treatment Guidelines for Hyponatremia: Stay the Course. Clinical Journal of the American Society of Nephrology. 2026; 19(1): 129-135. Published: January, 2024. DOI: 10.2215/CJN.0000000000000244.
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