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      Acute Hyperglycemia Alters Mood State and Impairs Cognitive Performance in People With Type 2 Diabetes

      , ,
      Diabetes Care
      American Diabetes Association

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          Abstract

          To examine the effects of acute hyperglycemia on cognitive function and mood in people with type 2 diabetes. Twenty subjects with type 2 diabetes, median age 61.5 years (range 53.1-72.0), known duration of diabetes 5.9 years (range 2.8-11.2), BMI 29.8 kg/m2 (range 22.0-34.6), and HbA1c 7.5% (range 6.7-8.4) were studied. Treatment modalities varied from antidiabetic medications to insulin. A hyperinsulinemic glucose clamp was used to maintain arterialized blood glucose at either 4.5 (euglycemia) or 16.5 mmol/l (hyperglycemia) on two occasions in a randomized and counterbalanced fashion. Tests of information processing, immediate and delayed memory, working memory, and attention were administered, along with a mood questionnaire, during each experimental condition. Speed of information processing, working memory, and some aspects of attention were impaired during acute hyperglycemia. Subjects were significantly more dysphoric during hyperglycemia, with reduced energetic arousal and increased sadness and anxiety. During acute hyperglycemia, cognitive function was impaired and mood state deteriorated in a group of people with type 2 diabetes. These findings are of practical importance because intermittent or chronic hyperglycemia is common in people with type 2 diabetes and may interfere with many daily activities through adverse effects on cognitive function and mood. Copyright 2004 American Diabetes Association

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          Most cited references18

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          Is type II diabetes associated with an increased risk of cognitive dysfunction? A critical review of published studies.

          Type II (non-insulin-dependent) diabetes may be associated with impaired cognitive function. A detailed search of the literature has identified 19 controlled studies in which cognitive function in type II diabetes has been examined. The studies vary widely with respect to the nature of the diabetic populations studied and the psychological tests used. Thirteen studies demonstrated that the diabetic individuals performed more poorly in at least one aspect of cognitive function. The most commonly affected cognitive ability was verbal memory. Psychomotor ability and frontal lobe function were affected less consistently. The remaining six studies showed no differences in cognitive ability between subjects with type II diabetes and nondiabetic control subjects, but none had adequate statistical power to detect a between-group difference in cognitive ability of 0.5 of a standard deviation (a medium effect size). These findings are consistent with type II diabetes being associated with an increased risk of cognitive dysfunction. However, the widespread differences in methodology between the studies should lead to a cautious interpretation of their conclusions. The etiology of any cognitive decrement in type II diabetes is likely to result from an interaction between metabolic abnormalities intrinsic to diabetes, diabetes-specific complications, and other diabetes-related disorders.
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            Cognitive efficiency declines over time in adults with Type 1 diabetes: effects of micro- and macrovascular complications.

            Mild cognitive dysfunction is not uncommon in adults with Type 1 diabetes, but its pathogenesis remains unclear. Previous cross-sectional studies had suggested that microangiopathy might affect brain integrity and lead to "central neuropathy." To assess the relationship between changes in cognitive performance and the incidence of new micro- and macrovascular complications, 103 young and middle-aged adults (mean age: 40 yrs) with childhood-onset Type 1 diabetes were followed over a 7-year period, and were compared to 57 demographically-similar adults without diabetes. All subjects completed a comprehensive battery of neurocognitive tests on two occasions. Diabetic subjects also received repeated medical assessments to diagnose the onset of clinically significant complications. Relative to control subjects, diabetic adults showed significant declines on measures of psychomotor efficiency; no between-group differences were evident on learning, memory, or problem-solving tasks. The development of proliferative retinopathy and autonomic neuropathy during the follow-up period predicted decline in psychomotor speed (p<0.01), as did incident macrovascular complications (p<0.05), systolic blood pressure at follow-up (p<0.01), and duration of diabetes (p<0.01). This study shows that cognitive efficiency may decline over time in diabetic adults, and that this neurocognitive change may be linked, at least in part, to the occurrence of complications like proliferative retinopathy and elevated blood pressure. Therapeutic interventions that reduce the risk of vascular complications may have a similarly beneficial effect on the brain and reduce the risk of neurocognitive dysfunction in diabetic patients.
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              The role of hyperglycemia in acute stroke.

              Ischemic stroke is a leading cause of death and long-term disability, and hyperglycemia is believed to aggravate cerebral ischemia. To review animal and human studies on the relationship between hyperglycemia and brain ischemia that elucidate some of the mechanisms for the deleterious effect of hyperglycemia. To discuss present and future clinical recommendations for glucose control. Computerized data sources and published indexes and articles from 1976 through 2000 were searched for human studies that evaluated the association between stroke and hyperglycemia, and studies focused on experimental models of hyperglycemic animals with focal and global brain ischemia. Most human studies have shown that in acute stroke, admission hyperglycemia in patients with or without diabetes is associated with a worse clinical outcome than in patients without hyperglycemia. This association is more consistent in the nonlacunar type of stroke. Animal studies support these findings by showing both in global and in focal postischemic models that hyperglycemia exaggerates the following damaging processes: intracellular acidosis, accumulation of extracellular glutamate, brain edema formation, blood-brain barrier disruption, and tendency for hemorrhagic transformation. Insulin treatment of hyperglycemic animals was found to have a beneficial effect in focal and global brain ischemia, which may be mediated by the glucose-reduction effect or by a direct neuroprotection. Most studies show the deleterious effect of early hyperglycemia, especially in patients with nonlacunar focal or global ischemia. Clinical trials of intensive insulin treatment are needed. Meanwhile simple measures to avoid excessive hyperglycemia are recommended.
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                Author and article information

                Journal
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                September 24 2004
                October 01 2004
                September 24 2004
                October 01 2004
                : 27
                : 10
                : 2335-2340
                Article
                10.2337/diacare.27.10.2335
                15451897
                54c4394e-ccb7-439a-be5c-80bef3512912
                © 2004
                History

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