Introduction Diabetic ketoacidosis (DKA) is a serious complication of diabetes. DKA is associated with poorer cognition in children with type 1 diabetes (T1D), but whether this is the case in older adults with T1D is unknown. Given the increasing life expectancy in T1D, understanding the role of DKA on brain health in older adults is crucial.
Research design and methods We examined the association of DKA with cognitive function in 714 older adults with T1D from the Study of Longevity in Diabetes. Participants self-reported lifetime exposure to DKA resulting in hospitalization; DKA was categorized into 0 hospitalization, 1 hospitalization or ≥2 hospitalizations (recurrent DKA). Global and domain-specific cognition (language, executive function/psychomotor speed, episodic memory and simple attention) were assessed. The association of DKA with cognitive function was evaluated via linear and logistic regression models.
Results Twenty-eight percent of participants (mean age=67 years; mean age at diagnosis=28 years; average duration of diabetes=39 years) reported a lifetime history of DKA resulting in hospitalization (18.5% single DKA; 9.7% recurrent DKA). In fully adjusted models, those with recurrent DKA had lower global cognitive function (β=−0.13; 95% CI −0.22 to 0.02) and lower scores on the executive function/psychomotor speed domain (β=−0.34; 95% CI −0.51 to 0.17). Individuals with recurrent DKA were also more likely to have the lowest level of cognitive function on the executive function/psychomotor speed domain (defined as 1.5 SD below the population mean; OR=3.26, 95% CI 1.43 to 7.42).
Conclusions Among 714 older adults with T1D, recurrent DKA was associated with lower global cognitive function, lower scores on the executive function/psychomotor speed domain and 3.3 times greater risk of having the lowest level of cognitive function in our sample on the executive function/psychomotor speed domain. These findings suggest that recurrent DKA may negatively impact the brain health of older patients with T1D and highlight the importance of DKA prevention.
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Presented at Preliminary results from this study were presented at the American Diabetes Association 79th Scientific Sessions, San Francisco, CA: 7–11 June 2019.
Contributors MEL conducted the analyses, wrote the manuscript and assisted with study design/data interpretation. PG, CWE, MSB and AJK assisted with study design/data interpretation and reviewed/edited the manuscript. RAW obtained funding, assisted with study design/data interpretation, and reviewed/edited the manuscript. MEL is the guarantor of this work.
Funding The study received funding from the National Institutes on Aging (NIA R01 AG047500; RAW). MEL and CWE were supported by the UCSF Training for Research on Aging and Chronic Disease (T32 AG049663). MEL was also supported through contract PPRN-1306-04709 from the Patient-Centered Outcomes Research Institute (PCORI).
Disclaimer The funders of the study had no role in study design, data collection, data analysis, data interpretation, or writing of this report.
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval This study was approved by the Kaiser Permanente Northern California Institutional Review Board (project number: 1276423).
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data are available upon reasonable request. Deidentified data from participants in the Study of Longevity in Diabetes (SOLID) are available upon request/approval. For information, please contact the Whitmer Lab at UC Davis: https://rachelwhitmer.ucdavis.edu/contact-0
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