Andreea M. Rawlings, MS; A. Richey Sharrett, MD, DrPH; Andrea L.C. Schneider, PhD; Josef Coresh, MD, PhD, MHS; Marilyn Albert, PhD; David Couper, PhD, MS; Michael Griswold, PhD; Rebecca F. Gottesman, MD, PhD; Lynne E. Wagenknecht, Dr PH, MPH; B. Gwen Windham, MD; Elizabeth Selvin, PhD, MPH
Note: Ms. Rawlings had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Acknowledgment: The authors thank the staff and participants of the ARIC study for their important contributions (staff members are listed in Appendix 2).
Grant Support: ARIC is a collaborative study supported by contracts HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C from the National Heart, Lung, and Blood Institute (NHLBI). Neurocognitive (ARIC-NCS) data are collected with support from NHLBI grants U01HL096812, HL096814, HL096899, HL096902, and HL096917, and previous magnetic resonance imaging examinations of the brain were funded by NHLBI grant R01HL70825. Ms. Rawlings and Dr. Schneider were supported by training grant T32HL007024 from NHLBI. Dr. Selvin was supported by grant R01DK089174 from the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Gottesman was supported by grant R01AG040282 from the National Institute on Aging.
Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M14-0737.
Reproducible Research Statement:Study protocol and data set: Protocols and data for the parent ARIC-NCS may be obtained by approved persons through written agreements with the ARIC Steering Committee and the research sponsor (NHLBI). Statistical code: Available from Dr. Selvin (e-mail, firstname.lastname@example.org).
Requests for Single Reprints: Elizabeth Selvin, PhD, MPH, Associate Professor of Epidemiology & Medicine, Welch Center for Prevention, Epidemiology and Clinical Research and the Johns Hopkins Bloomberg School of Public Health, 2024 East Monument Street, Suite 2-600, Baltimore, MD 21287; e-mail, email@example.com.
Current Author Addresses:Ms. Rawlings and Drs. Schneider, Coresh, and Selvin: Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, 2024 East Monument Street, Suite 2-600, Baltimore, MD 21287.
Dr. Sharrett: Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Room W6009, Baltimore, MD 21205.
Dr. Albert: Department of Neurology, Johns Hopkins University School of Medicine, Reed Hall West, Room 101B, 1620 McElderry Street, Baltimore, MD 21287.
Dr. Couper: Department of Biostatistics, University of North Carolina, 137 East Franklin Street, Suite 203, Chapel Hill, NC 27514.
Dr. Griswold: Center of Biostatistics and Bioinformatics, University of Mississippi Medical Center, 2500 North State Street, G551-07, Jackson, MS 39216.
Dr. Gottesman: Department of Neurology, Johns Hopkins University School of Medicine, Phipps 122 c/o Edna Gilliam, Meyer 6-109, 600 North Wolfe Street, Baltimore, MD 21287.
Dr. Wagenknecht: Division of Public Health Sciences, School of Medicine, Wake Forest University, Medical Center Boulevard, Room 2346, Winston-Salem, NC 27157.
Dr. Windham: Geriatrics Division, Department of Medicine, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216.
Author Contributions:Conception and design: A.L.C. Schneider, J. Coresh, B.G. Windham, E. Selvin.
Analysis and interpretation of the data: A.M. Rawlings, A.R. Sharrett, A.L.C. Schneider, J. Coresh, M. Griswold, R.F. Gottesman, L.E. Wagenknecht, E. Selvin.
Drafting of the article: A.M. Rawlings, E. Selvin.
Critical revision of the article for important intellectual content: A.M. Rawlings, A.R. Sharrett, A.L.C. Schneider, J. Coresh, M. Albert, D. Couper, M. Griswold, R.F. Gottesman, L.E. Wagenknecht, B.G. Windham, E. Selvin.
Final approval of the article: A.M. Rawlings, A.R. Sharrett, A.L.C. Schneider, J. Coresh, M. Albert, D. Couper, M. Griswold, R.F. Gottesman, L.E. Wagenknecht, B.G. Windham, E. Selvin.
Provision of study materials or patients: J. Coresh.
Statistical expertise: A.M. Rawlings, A.L.C. Schneider, D. Couper, M. Griswold, E. Selvin.
Obtaining of funding: J. Coresh, L.E. Wagenknecht.
Collection and assembly of data: A.M. Rawlings, J. Coresh, D. Couper, L.E. Wagenknecht.
Rawlings AM, Sharrett AR, Schneider AL, Coresh J, Albert M, Couper D, et al. Diabetes in Midlife and Cognitive Change Over 20 Years: A Cohort Study. Ann Intern Med. 2014;161:785-793. doi: 10.7326/M14-0737
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Published: Ann Intern Med. 2014;161(11):785-793.
Type 2 diabetes is associated with dementia risk, but evidence is limited for possible associations of diabetes and prediabetes with cognitive decline.
To determine whether diabetes in midlife is associated with 20-year cognitive decline and to characterize long-term cognitive decline across clinical categories of hemoglobin A1c (HbA1c) levels.
Prospective cohort study.
The community-based ARIC (Atherosclerosis Risk in Communities) study.
13 351 black and white adults aged 48 to 67 years at baseline (1990 to 1992).
Diabetes was defined by self-reported physician diagnosis or medication use or HbA1c level of 6.5% or greater. Undiagnosed diabetes, prediabetes, and glucose control in persons with diagnosed diabetes were defined by clinical categories of HbA1c level. Delayed word recall, digit symbol substitution, and word fluency tests were used to assess cognitive performance and were summarized with a global Z score.
Diabetes in midlife was associated with a 19% greater cognitive decline over 20 years (adjusted global Z-score difference, −0.15 [;95% CI, −0.22 to −0.08];) compared with no diabetes. Cognitive decline was significantly greater among persons with prediabetes (HbA1c level of 5.7% to 6.4%) than among those with an HbA1c level less than 5.7%. Participants with poorly controlled diabetes (HbA1c level ≥7.0%) had greater decline than those whose diabetes was controlled (adjusted global Z-score difference, −0.16; P = 0.071). Longer-duration diabetes was also associated with greater late-life cognitive decline (P for trend < 0.001). Rates of decline did not differ significantly between white and black persons (P for interaction = 0.44).
Single HbA1c measurement at baseline, 1 test per cognitive domain, and potential geographic confounding of race comparisons.
Diabetes prevention and glucose control in midlife may protect against late-life cognitive decline.
National Institutes of Health.
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Cardiology, Endocrine and Metabolism, Diabetes, Coronary Risk Factors.
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