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PLoS One. 2016 May 11;11(5):e0154896. doi: 10.1371/journal.pone.0154896. eCollection 2016.

Vitamin D and Risk of Neuroimaging Abnormalities.

Author information

1
Clinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom.
2
University of Exeter Medical School, University of Exeter, Exeter, United Kingdom.
3
Department of Neuroscience, Geriatrics Division, Angers University Hospital, Angers, France.
4
Herbert Wertheim College of Medicine, Florida International University, Miami, United States of America.
5
Kidney Research Institute, Division of Nephrology, University of Washington, Seattle, United States of America.
6
Department of Epidemiology, University of Pittsburgh, Pittsburgh, United States of America.
7
Division of General Medicine, University of Michigan Health System, Ann Arbor, Michigan, United States of America.
8
Institute for Social Research, Institute of Gerontology and Institute for Healthcare Policy and Innovation, University of Michigan, Ann Arbor, Michigan, United States of America.
9
Veteran Affairs Center for Clinical Management Research, Ann Arbor, Michigan, United States of America.
10
Department of Neurology and Psychiatry Division of General Medicine, University of Pittsburgh, Pittsburgh, United States of America.

Abstract

Vitamin D deficiency has been linked with an increased risk of incident all-cause dementia and Alzheimer's disease. The aim of the current study was to explore the potential mechanisms underlying these associations by determining whether low vitamin D concentrations are associated with the development of incident cerebrovascular and neurodegenerative neuroimaging abnormalities. The population consisted of 1,658 participants aged ≥65 years from the US-based Cardiovascular Health Study who were free from prevalent cardiovascular disease, stroke and dementia at baseline in 1992-93. Serum 25-hydroxyvitamin D (25(OH)D) concentrations were determined by liquid chromatography-tandem mass spectrometry from blood samples collected at baseline. The first MRI scan was conducted between 1991-1994 and the second MRI scan was conducted between 1997-1999. Change in white matter grade, ventricular grade and presence of infarcts between MRI scan one and two were used to define neuroimaging abnormalities. During a mean follow-up of 5.0 years, serum 25(OH)D status was not significantly associated with the development of any neuroimaging abnormalities. Using logistic regression models, the multivariate adjusted odds ratios (95% confidence interval) for worsening white matter grade in participants who were severely 25(OH)D deficient (<25 nmol/L) and deficient (≥25-50 nmol/L) were 0.76 (0.35-1.66) and 1.09 (0.76-1.55) compared to participants with sufficient concentrations (≥50 nmol/L). The multivariate adjusted odds ratios for ventricular grade in participants who were severely 25(OH)D deficient and deficient were 0.49 (0.20-1.19) and 1.12 (0.79-1.59) compared to those sufficient. The multivariate adjusted odds ratios for incident infarcts in participants who were severely 25(OH)D deficient and deficient were 1.95 (0.84-4.54) and 0.73 (0.47-1.95) compared to those sufficient. Overall, serum vitamin D concentrations could not be shown to be associated with the development of cerebrovascular or neurodegenerative neuroimaging abnormalities in Cardiovascular Health Study participants.

PMID:
27166613
PMCID:
PMC4864237
DOI:
10.1371/journal.pone.0154896
[Indexed for MEDLINE]
Free PMC Article

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