SummaryBackground-Metformin might reduce insulin requirement and improve glycaemia in patients with type 1 diabetes, but whether it has cardiovascular benefits is unknown. We aimed to investigate whether metformin treatment (added to titrated insulin therapy) reduced atherosclerosis, as measured by progression of common carotid artery intima-media thickness (cIMT), in adults with type 1 diabetes at increased risk for cardiovascular disease.
Acute hypoglycaemia impairs cerebral function, and available data indicate that cognitive performance becomes impaired at a blood glucose level of 2.6-3.0 mmol/l in healthy subjects. Methodological problems limit comparisons between studies, but in general complex tasks are more sensitive to hypoglycaemia than simple tasks, and some cognitive abilities are completely abolished. The onset of hypoglycaemic cognitive dysfunction is immediate, but recovery may be considerably delayed. There is persuasive evidence of adaptation to hypoglycaemia, partly due to increased brain glucose uptake capacity, although other mechanisms may exist. Patients who are exposed to chronic or recurrent hypoglycaemia become remarkably tolerant to the state, but this is insufficient to prevent severe hypoglycaemia with neuroglycopenic decompensation, probably because symptomatic and counterregulatory responses adapt even more. During experimental hypoglycaemia, administration of non-glucose cerebral fuels preserves cognitive function. However, little progress has been made as yet towards protecting cognitive function during hypoglycaemia in clinical practice. The chronic effects of recurrent hypoglycaemia remain contentious. There are numerous case reports of hypoglycaemic brain damage and of cognitive deterioration attributed to repeated severe hypoglycaemia. The major prospective studies, including the Diabetes Control and Complications Trial, did not report cognitive declines in intensively treated patients, but had unrepresentative study populations and may have been too short to detect such effects. Structural and functional brain changes are not only associated with recurrent severe hypoglycaemia, but also with hyperglycaemia and early disease onset and may in part be due to hyperglycaemic microvascular disease. Children may be more prone to acute metabolic insults, and there is evidence of developmental disadvantage associated with hypoglycaemic episodes.
Compliance with statutory requirements to inform the licensing authority and motor insurer is good, and drivers' perceptions of the minimum safe blood glucose level for driving are encouraging. However, most drivers rely on symptoms to detect hypoglycaemia while driving, and seldom test blood glucose before driving. Patient education should emphasize the role of blood glucose monitoring in relation to driving, and highlight the potential deterioration in driving performance when blood glucose falls below 4.0 mmol/l.
OBJECTIVE-Recovery times of cognitive functions were examined after exposure to hypoglycemia in people with diabetes with and without impaired hypoglycemia awareness.RESEARCH DESIGN AND METHODS-A total of 36 subjects with type 1 diabetes were studied (20 with normal hypoglycemia awareness [NHA] and 16 with impaired hypoglycemia awareness [IHA]). A hyperinsulinemic glucose clamp was used to lower blood glucose to 2.5 mmol/l (45 mg/dl) (hypoglycemia) for 1 h or to maintain blood glucose at 4.5 mmol/l (81 mg/dl) (euglycemia) on separate occasions. Cognitive tests were applied during each experimental condition and were repeated at 10-to 15-min intervals for 90 min after euglycemia had been restored.RESULTS-In the NHA group, performance was impaired on all cognitive tasks during hypoglycemia and remained impaired for up to 75 min on the choice reaction time (CRT) task (P ϭ 0.03, 2 ϭ 0.237). In the IHA group, performance did not deteriorate significantly during hypoglycemia. When all subjects were analyzed within the same general linear model, performance was impaired during hypoglycemia on all tasks. Significant impairment during recovery persisted for up to 40 min on the CRT task (P ϭ 0.04, 2 ϭ 0.125) with a significant glycemia-awareness interaction for CRT after one hour of hypoglycemia (P ϭ 0.045, 2 ϭ 0.124). Performance on the trail-making B task was impaired for up to 10 min after euglycemia was restored (P ϭ 0.024, 2 ϭ 0.158). T he recovery of cognitive function following hypoglycemia has not received rigorous evaluation. Previous studies examined nondiabetic volunteers (1-3) in small numbers (3), did not include a euglycemia control arm (1,4), measured neurophysiological parameters rather than cognitive function (1,2,5,6), or restricted cognitive testing to one or two time points (3-5). The interval between restoration of euglycemia and cognitive testing was usually ill defined (2,4 -6). Controversy exists as to whether impaired awareness of hypoglycemia is associated with relative preservation (7-13) or exacerbation of the cognitive impairment induced by hypoglycemia (14 -16). The present study examined the time taken for recovery of cognitive function in adults with type 1 diabetes and assessed the effect of their state of awareness on the response to, and recovery from, hypoglycemia. CONCLUSIONS-Following RESEARCH DESIGN AND METHODSThe local medical research ethics committee approved the protocol, and subjects gave informed consent for participation.Inclusion criteria were a diagnosis of type 1 diabetes and age 18 -45 years. Exclusion criteria included pregnancy or any significant concurrent medical condition, history of head injury, epilepsy, or history of hypoglycemia-induced seizure.A total of 36 subjects with type 1 diabetes were recruited, 20 with normal hypoglycemia awareness (NHA) and 16 with impaired hypoglycemia awareness (IHA) confirmed by documenting their hypoglycemia history and using a validated hypoglycemia awareness scale (17). Microvascular complications were defined as any clinical diag...
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