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Article Summaries for July–August 2015 Psychosomatic Medicine, Volume 77, Issue 6

doi: 10.1097/PSY.0000000000000225
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This special issue of Psychosomatic Medicine addresses “Diabetes, Obesity, and the Brain.” In the introductory editorial, Susan A. Everson-Rose and John P. Ryan highlight the increasing rates of diabetes and obesity, which in turn portend an accompanying rise in adverse consequences for brain structure and function. The editorial provides an overview of this special issue, noting the importance of the lifespan perspective to understand the influence of Type1 and Type 2 diabetes on brain metabolism, function, and structure.

Pages 612–615; Web:

In a comprehensive review article, Elizabeth R. Seaquist discusses how diabetes and treatment-induced hypoglycemia affect the human brain. Hyperglycemia and hypoglycemia have both been shown to impair cognitive function in children and adults. Dr. Seaquist describes research conducted using high magnetic field imaging and spectroscopy, which revealed microstructural changes in white matter regions, reduced gray matter density, and reduced activation of the thalamus in response to recurrent hypoglycemia in patients with Type 1 diabetes.

Pages 616–621; Web:

Using resting state functional MRI, Ryan et al. examined whether the age at which individuals develop Type 1 diabetes in childhood is related to functional brain connectivity in midlife. Later childhood age of onset was associated with lower connectivity. Given that people with diabetes are living longer, it is important to identify cognitive and neurological risks they face as they age.

Pages 622–630; Web:

With a meta-analysis of 60 studies, Corita Vincent and Peter A. Hall examined the association between Type 2 diabetes status and cognitive executive function. Findings indicate a small but reliable association between Type 2 diabetes diagnosis and lower executive function. Because diabetes management relies on self-care, and self-care requires adequate executive functioning, screening for cognitive impairments and providing additional support for self-care may help to reduce diabetes-related adverse health outcomes.

Pages 631–642; Web:

Dore et al. examined whether race and poverty modify associations between diabetes and cognitive functioning. Among African American men and women living near or below the US poverty level, people with diabetes performed poorer than those without diabetes on cognitive tasks evaluating verbal and working memory, executive function, and attention.

Pages 643–652; Web:

Previous studies have suggested that the onset of cognitive impairment related to diabetes begins before the age of 65 years. In a study by Luchsinger et al., Hispanic patients from ages 55 to 64 with diabetes and pre-diabetes were assessed for memory, executive function, and verbal fluency. Higher levels of glycemia and diabetes were related to worse memory and executive function, while pre-diabetes was only related to worsened executive abilities. Decreased executive functioning in individuals with pre-diabetes suggests that higher glycemia may have effects on cognitive processes earlier in the aging process.

Pages 653–663; Web:

Dianne P. Figlewicz summarizes the existing evidence for brain control in the rewarding properties of foods, which is potentially relevant for the development of obesity. Intrinsic endocrine systems and metabolic hormones relevant to energy homeostasis influence the brain control of reward-related food intake. These associations may differ by sex and across developmental stages. Extrinsic or environmental factors including ambient diet composition and stress or anxiety also contribute substantially to the expression of food reward behaviors. Contextual, behavioral, and psychological factors and central nervous system-related processes represent potential targets for multidisciplinary intervention.

Pages 664–670; Web:

Central adiposity is indicative of visceral fat, which is metabolically active and a stronger predictor of potential cognitive decline than body mass index. The mechanisms are poorly understood. Kaur et al. examined visceral fat and brain characteristics in middle age. Dual energy X-ray absorptiometry was used to quantify visceral fat and magnetic resonance imaging to assess brain measures. Findings indicate that higher visceral fat mass and volume were associated with a thicker cortex in the posterior cingulate gyrus. Results suggest that central adiposity is associated with significant metabolic changes that impinge upon the central nervous system in middle age.

Pages 671–678; Web:

Haley et al. provide an overview of the evidence that suggests that bariatric surgery, compared with nonsurgical interventions, tends to lead to greater weight loss, better glycemic control, and increased cognitive improvement during the first 1 to 2 years after intervention. Nonsurgical weight loss therapies, however, have been studied more extensively. The recognized benefits of nonsurgical approaches include positive health outcomes up to 10 years later with modest cognitive benefits. Long-term comparisons between bariatric surgery and nonsurgical weight reduction interventions are needed to establish sustained improvements in cognitive functioning.

Pages 679–687; Web:

The biobehavioral mechanisms underlying improved cognitive function after bariatric surgery are insufficiently understood. Hawkins et al. examined whether reduced inflammation after surgery plays a role in changes in cognitive function. In a study of 77 patients, they found no link between C-reactive protein levels before and after surgery with measures of cognitive function.

Pages 688–696; Web:

Gérard N. Bischof and Denise C. Park review the literature examining how obesity and aging interact to affect cognitive function. Obesity and aging are both associated with cognitive decline, but little is understood about how they interact to affect cognitive function across the lifespan. Of particular concern is whether there is a synergistic effect of obesity and older age that could accelerate normal aging processes or even increase the risk for pathological aging processes such as dementia. The data suggest that being overweight or obese in midlife may be more detrimental to subsequent age-related cognitive decline than being overweight or obese at later stages of the lifespan.

Pages 697–709; Web:

Copyright © 2015 by American Psychosomatic Society