Key result
Induced hypoglycemia in type 1 diabetes reduces prothrombin time and trends toward increased clot strength.
Why the study?
Hypoglycemia has been implicated in CVD in T1D through direct effects on coagulation proteins and indirect effects from disordered sleep, but the exact mechanisms remained to be determined.
Does induced hypoglycemia increase hypercoagulation and disordered sleep in adults with well-controlled type 1 diabetes?
Does induced hypoglycemia increase hypercoagulation and disordered sleep in adults with well-controlled type 1 diabetes?
Absolute Event Rate: 8.9% vs 6.8%
p-value: p=0.08
Induced hypoglycemia in well-controlled type 1 diabetes leads to persistent prothrombotic changes and reduced deep sleep, potentially contributing to elevated cardiovascular risk.
May link hypoglycemia to prothrombotic shifts in T1D; hypothesis-generating and should not yet change practice.
Introduction and Objective: Hypoglycemia is a common complication in type 1 diabetes (T1D). Hypoglycemia has been implicated in cardiovascular disease (CVD) in T1D via direct effects on coagulation proteins and indirect effects from disordered sleep. We used wearable sensors including continuous glucose monitoring (CGM) and smartwatch actigraphy to determine how hypoglycemia leads to hypercoagulation and disordered sleep. Methods: Adults with well-controlled T1D (mean A1c 6.3) completed 4 weeks of CGM and smartwatch actigraphy. Participants then underwent 40 minutes of induced hypoglycemia (glucose <60 mg/dL) via hyperinsulinemic-hypoglycemic insulin clamp. Functional clotting assays were measured at baseline and 24 hours after the clamp. Sleep actigraphy and CGM were measured for a week after the clamp to check for persistent sleep and glycemic dysregulation. Results: Prothrombin time was significantly reduced (p = 0.008) 24 hours after clamp (Figure) and thromboelastography trended towards increased clot strength (6.8 vs. 8.9 dynes/cm2, p = 0.08) after clamp. In the majority of participants, deep sleep duration was significantly reduced for the rest of the night after a nocturnal hypoglycemic event on CGM. Conclusion: Hypoglycemia leads to prothrombotic and sleep sequelae that persist after restoration of euglycemia. Recurrent hypoglycemia may contribute cumulatively to atherogenesis, helping to explain elevated CVD risk in T1D in patients with A1c <7. Disclosure R.L. Thomas: None. V. Hamidi: None. E. Giovannetti: None. C.F. Hsu: None. A.C. Ahn: Employee; Current; Labfront. M.X. Marcelli: Employee; Current; Quest Diagnostics. T. Ciaraldi: None. L.R. Castellanos: None. S. Boeder: None. J. Pettus: None. Funding National Institutes of Health DiabDocs National K12 Physician Scientist Career Development Program (K12DK133995), University of California, San Diego/University of California, Los Angeles National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
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THOMAS et al. (2026) studied Type 1 diabetes. Induced hypoglycemia via hyperinsulinemic-hypoglycemic insulin clamp vs. Baseline was evaluated on Thromboelastography clot strength (p=0.08). Induced hypoglycemia in adults with type 1 diabetes significantly reduced prothrombin time (p=0.008) and trended toward increased clot strength (8.9 vs. 6.8 dynes/cm2, p=0.08) 24 hours post-clamp.
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