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Author Notes:

Andrea L.C. Schneider, MD, PhD, Department of Neurology, Johns Hopkins School of Medicine, 2024 East Monument Street, Suite 2-634, Baltimore, MD 21287 (USA), achris13@jhmi.edu.

The authors acknowledge and thank the participants and staff for their important contribution to the ARIC study.

Dr. Knopman serves on a Data Safety Monitoring Board for Lundbeck Pharmaceuticals and for the DIAN study.

Dr. Knopman is also an investigator in clinical trials sponsored by the Alzheimer’s Disease Cooperative Study, TauRX Pharmaceuticals, and Lilly Pharmaceuticals.


Research Funding:

This work was supported by grant R01NS072243 from NIH/ NINDS to Dr. Erin D. Michos, by grant R01HL103706 from NIH/ NHLBI to Dr. Pamela L. Lutsey, and by grant R01HL103706-S1 from the National Institutes of Health Office of Dietary Supplements to Dr. Pamela L. Lutsey.

Additionally, Drs. Di Zhao and Erin D. Michos are supported by the Blumenthal Scholars Fund at Johns Hopkins for preventive cardiology research.

Dr. Andrea L.C. Schneider is supported by the NIH/NINDS via an administrative supplement to award R25NS065729.

The ARIC Study is collaboratively funded by NIH/NHLBI contracts HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HH-SN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C.

ARIC-NCS was funded by U01 HL096812, HL096814, HL096899, HL096902, and HL096917, with additional NIH/NINDS support.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Public, Environmental & Occupational Health
  • Clinical Neurology
  • Neurosciences & Neurology
  • Cognition
  • Vitamin D
  • Cohort study
  • DIET

Serum Vitamin D Concentrations and Cognitive Change Over 20 Years: The Atherosclerosis Risk in Communities Neurocognitive Study

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Journal Title:



Volume 51, Number 3-4


, Pages 131-137

Type of Work:

Article | Post-print: After Peer Review


Background/Aims: 25-hydroxyvitamin D (25[OH]D) concentrations have been associated with cognitive decline and incident dementia in elderly populations; however, these relationships are susceptible to reverse causation. Less is known about the association of midlife 25(OH)D with long-term cognitive decline. Methods: This was a prospective cohort study of 13,044 participants (mean age 57 years at baseline) in the Atherosclerosis Risk in Communities Study. 25(OH)D was measured from serum collected at baseline (1990-1992) using liquid chromatography tandem high-sensitivity mass spectrometry. Cognition was assessed using 3 neuropsychological tests at 3 time points, which were combined into a composite cognitive Z-score. Multivariable-adjusted linear mixed-effects models with random intercepts and slopes were used to estimate associations between 25(OH)D and cognitive change over 20 years. Results: Compared to persons with sufficient 25(OH)D (≥30 ng/mL), those with deficient (< 20 ng/mL) and intermediate (20-< 30 ng/mL) 25(OH)D concentrations had similar cognitive decline in composite cognitive Z-scores (deficient versus sufficient: -0.035 [95% CI -0.104 to 0.033] and intermediate versus sufficient: -0.029 [95% CI -0.080 to 0.023]). Conclusions: Lower concentrations of 25(OH)D measured in midlife were not significantly associated with more rapid cognitive decline over a 20-year follow-up period. The results of this prospective study are less susceptible to reverse causation than prior studies.

Copyright information:

© 2018 S. Karger AG, Basel. Copyright: All rights reserved.

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