Early research in cognitive functioning focused on type 2 diabetes as a theoretical model of accelerated aging [e.g., Kent (101)] but, more recently, there has been interest in potential changes in cognition that might make patient adherence to treatment more difficult (102). Both chronically elevated high blood sugars and recurrent low blood sugar levels have the potential to independently contribute to cognitive dysfunction, for example through changes to the blood - brain barrier transport of glucose. Verbal learning and memory skills may be especially disrupted in type 2 diabetes, but mainly for patients older than 60 years of age (103 - 105).

Other cognitive skills, such as attention, executive function, and psychomotor efficiency, were less affected. Although most research on cognition in diabetes has been conducted with type 1 patients, studies show that middle-aged type 2 individuals are apparently protected, insofar as researchers have only infrequently reported learning and memory impairments in that age group. It is likely that older adults have an increased risk of diabetes-associated memory dysfunction as a consequence of a synergistic interaction between diabetes-related blood glucose changes and the structural and functional changes occurring in the central nervous system that are part of the normal aging process (106,107).

Multiple diabetes-related comorbid conditions (i.e., hyperinsulinaemia, hypertension, hypercholesterolaemia) may individually and synergistically impact learning and memory skills [see review by Ryan and Geckle (104)].  For example,  hyperinsulinaemia may independently affect the central nervous system.

Insulin levels usually rise with age, and are strong predictors of cognitive impairment in adults without diabetes.  Data from the Framingham study showed that both hypertension and diabetes independently affect cognition generally, and memory skills in particular. Given their high rates in type 2 diabetes, it is notable that hypertension and hypercholesterolaemia interacts with hyperinsulinemia to disrupt memory. Generally, there is evidence to support the view that verbal learning and memory skills are particularly vulnerable to disruption in type 2 diabetes compared with other cognitive skills as a result of diabetes and its comorbidities. Recent data has indicated a link between insulin resistance and Alzheimer’s disease (AD). Although the mechanism linking these conditions is unclear, the predominate hypothesis is that insulin resistance, accompanied by hyperinsulinemia and subsequent glucose metabolism disturbances, leads to neurodegen-eration, and ultimately, AD (108 - 110). This association suggests that future AD treatments should focus on reversing or preventing insulin abnormalities (111,112).

While mild and severe hypoglycemia rates are lower in type 2 diabetes compared with type 1, due to residual insulin production in type 2, patients who use sulfonylureas or progress to insulin therapy can experience acute low blood sugars (113). Such episodes cause both autonomic and neuroglycopenic changes. Neuroglycopenia appears to impact the cerebral cortex more than the deeper brain structures, in terms of cognitive functioning. Complex, attention-demanding and speed-dependent responses are most impaired, with accuracy often preserved at the expense of speed. Cognitive function does not recover fully until 40 to 90 min after blood glucose is returned to normal. Hypoglycemia also provokes changes in mood, including anxiety and depression, and increases fear of further hypoglycemia, which in turn can modify self-care behavior (e.g., over-treating with food) and thus blood sugar control (114).

In summary, there are a wide range of psychosocial issues important to address in the clinical management of type 2 diabetes. For some patients, these issues are serious enough to warrant active treatment by the clinician, or referral to other healthcare professionals. This section briefly discussed some of these psychosocial issues and suggested practical, patient- centered strategies to aid the busy clinician. We should not lose sight of the fact that both obesity and type 2 diabetes are preventable diseases that have major public health implications. As a society, we need to focus on the profound social and cultural changes that have occurred in our daily lives. These involve reduced habitual activity and increased food intake. Practical preventive strategies at the societal and cultural level must be generated to reverse these trends. This may be the greatest challenge we face in tackling the current epidemic of type 2 diabetes.

Garry W. Welch, Alan M. Jacobson, and Katie Weinger
Behavioral and Mental Health Research, Joslin Diabetes Center, Boston, Massachusetts, U.S.A.

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