Among 942 individuals with type 2 diabetes who had a lacunar stroke, every 1% higher HbA1c was tied to a 0.06 drop in cognitive function at baseline measured by Cognitive Assessment Screening Instrument (CASI) z-score (95% CI -0.101 to -0.018), reported Tali Cukierman-Yaffe, MD, MSc, of Sheba Medical Center and the Sackler School of Medicine of Tel Aviv University in Israel.
This relationship was significant even after adjusting for demographic factors and clinical factors such as depression, hypertension, hyperlipidemia, body mass index, cardiovascular disease, obstructive sleep apnea, diabetic retinopathy, nephropathy, insulin use, and white matter abnormalities.
And those who started with higher average HbA1c levels at baseline tended to have lower cognitive functioning scores over time (P for interaction=0.037), Cukierman-Yaffe noted in her presentation at the virtual ENDO 2020 meeting sponsored by The Endocrine Society.
This association wasn’t stagnant either, as a 1% increase in HbA1c during follow-up was tied to a decrease in Cognitive Abilities Screening Instrument (CASI) score by approximately 0.021 points (95% CI -0.0043 to -0.038) over time.
This relationship between higher glucose levels and poorer cognitive functioning extended beyond just CASI z-score, as well, Cukierman-Yaffe noted. Higher HbA1c levels were also tied to significantly poorer performance in other psychological tests, including the clock making test of executive functioning, test of discriminative ability, and for the test of verbal fluency.
The prospective cohort analysis drew upon data from the individuals who participated in the Secondary Prevention of Small Subcortical Strokes (SPS3) trial. This included adults over the age of 30 — mean age of 63 — with an existing diagnosis of type 2 diabetes and a recent, symptomatic MRI-defined small subcortical ischemic stroke. These individuals had no evidence of cortical strokes, nor any evidence of severe cognitive functional impairment.
Many possible explanations could be underlying these significant associations seen in this study, she explained, also pointing out that this relationship is likely bidirectional.
“It may be that individuals with cognitive impairment have difficulty managing their [diabetes] disease, and thus have worse glucose control,” she stated, adding that “second, hyperglycemia may accelerate the rate of cognitive decline by either reducing capillary reperfusion or accelerating large vessel disease, or directly damaging the brain.”
But nonetheless, further research is needed to delve into these associations, she suggested. Future studies are not only needed to confirm these results, but also intervention studies should be done to delineate whether better glucose control could possibly slow the rate of cognitive declines in high-risk populations, such as this one.
In the meantime, Cukierman-Yaffe told MedPage Today that healthcare providers should be evaluating older patients with diabetes for cognitive decline, according to current guidelines from the American Diabetes Association, The Endocrine Society, and several more international societies.
“Cognitive assessment should be part of the routine check-up of older people with diabetes,” she said, noting that this is particularly important for two reasons: the relationship between cognitive dysfunction and self-care, and the fact that cognitive dysfunction is another one of many possible complications of diabetes posing a larger threat to older patients.
Disclosures
The study was supported by a grant from the National Institutes of Health.
Cukierman-Yaffe reported relationships with Sanofi, AstraZeneca, MSD, Lilly, and Medtronic.
Cukierman-Yaffe reported relationships with Sanofi, AstraZeneca, MSD, Lilly, and Medtronic.
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