Diabetes mellitus constitutes a significant public health concern in the United States (US), particularly for the aging and ethnically diverse. Approximately 26% of adults over the age of 65 have diabetes, and the condition has a higher prevalence in ethnic and racial minorities (Center for Disease Control and Prevention, 2014). Although several types of DM exist, in the US, most cases fall within two groups: Type 1 (T1DM) or Type 2 (T2DM) (American Diabetes Association, 2014; Gonder-Frederick & Clarke, p. 139). These categories differ in their pathophysiology, epidemiology, and treatment. For example, T1DM emerges due to the pancreas’ failure to produce sufficient insulin, and is most common amongst children and Whites. In terms of treatment, T1DM involves daily subcutaneous insulin injections that are indispensable for survival (Gonder-Frederick & Clarke, p. 139). In contrast, T2DM occurs due to insulin resistance and/or defective insulin secretion (Gonder-Frederick & Clarke, p. 139; Haffner, 1998). In the US, T2DM is most common among Native Americans, Hispanics, and African Americans. While T2DM can be managed with exercise and diet, most cases require oral medication and/or insulin (American Diabetes Association, 2014; Gonder-Frederick & Clarke, p. 139).
While cognitive decline is not pathognomonic of DM, the link between cognitive decline and DM is well documented. Specifically, adults with DM exhibit marked decrements in psychomotor abilities, verbal learning, visual memory, and aspects of executive functioning (Palta, Schneider, Biessels, Touradji, & Hill-Briggs, 2014). Additionally, diminished cognitive performance at baseline, when compared to their non-diabetic counterparts, (Bangen et al., 2015) and increased risk of vascular and Alzheimer’s dementia have also been noted (Biessels, Staekenborg, Brunner, Brayne, & Scheltens, 2006; Cukierman, Gerstein, & Williamson, 2005). Level of glycemic control, as measured by hemoglobin A1c, accounts for less than 10% of the variance in cognition (Geljselaers, Sep, Stehouwer, & Biessels, 2015) suggesting that the exact mechanisms leading to cognitive dysfunction in diabetes are poorly understood. Evidence indicates that cognitive deficit in DM is secondary to a number of factors including hyperglycemia, vascular disease, hypoglycemia, and insulin resistance (Kodl & Seaquist, 2008).
ABSTRACT: Relationship between type 2 diabetes mellitus and cognitive change in a multiethnic elderly cohort (2015).
OBJECTIVES: To examine the association between diabetes mellitus and cognitive functioning at baseline and cognitive change over time in a large, ethnically diverse sample of older adults.
DESIGN: Prospective cohort study.
SETTING: Washington Heights–Inwood Columbia Aging Project, a community-based, prospective study of risk factors for dementia in northern Manhattan, New York City.
PARTICIPANTS: Hispanic, non-Hispanic black, and non-Hispanic white men and women aged 65 and older without dementia at baseline (N = 1,493).
MEASUREMENTS: Participants underwent baseline and follow-up cognitive and health assessments approximately every 18 months. Generalized estimating equations were used to examine the longitudinal association between diabetes mellitus and cognition.
RESULTS: Diabetes mellitus was associated with poorer baseline cognitive performance in memory, language, processing speed and executive functioning, and visuospatial abilities. After adjusting for age, education, sex, race and ethnicity, and apolipoprotein-e4, participants with diabetes mellitus performed significantly worse at baseline than those without in language and visuospatial abilities. There were no differences between those with and without diabetes mellitus in terms of rate of cognitive change over a mean follow-up time of 6 years.
CONCLUSION: The rate of cognitive change in elderly persons with and without diabetes mellitus is similar, although cognitive performance is poorer in persons with diabetes mellitus. These findings suggest that cognitive changes may occur early during the diabetes mellitus process and highlight the need for studies to follow participants beginning at least in midlife, before the typical later life onset of dementia.
[Bangen, K. J., Gu, Y., Gross, A. L., Schneider, B. C., Skinner, J. C., Benitez, A., Sachs, B., Shih, R., Sisco, S., Schupf, N., Mayeux, R., Manly, J. J., & Luchsinger, J. A. (2015). Relationship between type 2 diabetes mellitus and cognitive change in a multiethnic elderly cohort. Journal of the American Geriatrics Society, 63(6). 1075-1083. http://dx.doi.org/10.1111/jgs.13441.]
FURTHER READING: Chung, C. C., Pimentel, D., Jor'dan, A. J., Hao, Y., Milberg, W., & Novak, V. (2015). Inflammation-associated declines in cerebral vasoreactivity and cognition in type 2 diabetes. Neurology, 85(5), 450-458. http://dx.doi.org/10.1212/WNL.0000000000001820.
PODCAST: Diabetes Prevention in Midlife Helps Protect Aging Brain- Scientific American 60 Second Health- by Dina Fine Maron http://www.scientificamerican.com/podcast/episode/diabetes-prevention-in-midlife-helps-protect-aging-brain/
American Diabetes Association. (2014). Diagnosis and classification of diabetes mellitus. Diabetes Care, 28, S37. templatelab.com/national-diabetes-report-2014/
American Diabetes Association. (2014). National Diabetes Statistics Report, 2014. Estimates of diabetes and its burden in the epidemiologic estimation methods. National Diabetes Statistics Report, 2009-2012. templatelab.com/national-diabetes-report-2014/
Bangen, K. J., Gu, Y., Gross, A. L., Schneider, B. C., Skinner, J. C., Benitez, A., Sachs, B., Shih, R., Sisco, S., Schupf, N., Mayeux, R., Manly, J. J., & Luchsinger, J. A. (2015). Relationship between type 2 diabetes mellitus and cognitive change in a multiethnic elderly cohort. Journal of the American Geriatrics Society, 63(6). 1075-1083. http://dx.doi.org/10.1111/jgs.13441
Biessels, G.J., Staekenborg, S., Brunner, E., Brayne, C., & Scheltens, P. (2006). Risk of dementia in diabetes mellitus: A systematic review. Lancet Neurology, 5(1), 64–74. http://dx.doi.org/10.1016/S1474-4422(05)70284-2
Center for Disease Control and Prevention. National Center for Chronic Disease Prevention and Health Promotion (2014). National diabetes statistics report: Estimates of diabetes and its burden in the United States, 2014. Atlanta, GA: US Department of Health and Human Services. templatelab.com/national-diabetes-report-2014/
Chung, C., Pimentel, D. Jor'dan, J., Hao, Y., Milberg, W., & Novak, V. (2014). Inflammation-associated declines in cerebral vasoreactivity and cognition in type 2 diabetes. Neurology, 85(5), 450-458. http://dx.doi.org/10.1212/WNL.0000000000001820
Cukierman, T., Gerstein, H.C., & Williamson, J.D. (2005). Cognitive decline and dementia in diabetes – systematic overview of prospective observational studies. Diabetologia, 48(12), 2460–2469. http://dx.doi.org/10.1007/s00125-005-0023-4
Geijselaers, S. L., Sep, S. J., Stehouwer, C. D., & Biessels, G. J. (2015). Glucose regulation, cognition, and brain MRI in type 2 diabetes: A systematic review. The Lancet Diabetes & Endocrinology, 3(1), 75-89. http://dx.doi.org/10.1016/S2213-8587(14)70148-2
Gonder-Frederick, L., Cox, D. J., & Clarke, W. L. (2008). Diabetes. In A. Christensen & M. H. Antoni (Eds), Chronic physical disorders: Behavioral medicine's perspective (pp. 137-154). Oxford, England: Blackwell Publishers.
Haffner, S. M., Lehto, S., Rönnemaa, T., Pyörälä, K., & Laakso, M. (1998). Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. New England Journal of Medicine, 339(4), 229-234. http://dx.doi.org/10.1056/NEJM199807233390404
Kodl, C. T., & Seaquist, E. R. (2008). Cognitive dysfunction and diabetes mellitus. Endocrine reviews, 29(4), 494-511. http://dx.doi.org/10.1210/er.2007-0034
Palta, P., Schneider, A. L., Biessels, G. J., Touradji, P., & Hill-Briggs, F. (2014). Magnitude of cognitive dysfunction in adults with type 2 diabetes: A meta-analysis of six cognitive domains and the most frequently reported neuropsychological tests within domains. Journal of the International Neuropsychological Society, 20(03), 278-291. http://dx.doi.org/10.1017/S1355617713001483