Vitamin D is not associated with incident dementia or cognitive impairment: an 18-y follow-up study in community-living old men1–3

• Published in: The American journal of clinical nutrition Vol. 105; no. 4; pp. 936 - 943
• Main Authors: Olsson, Erika, Byberg, Liisa, Karlström, Brita, Cederholm, Tommy, Melhus, Håkan, Sjögren, Per, Kilander, Lena
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 01-04-2017
• Subjects: 25-hydroxyvitamin D; Alzheimer disease; cognitive impairment; cohort; dementia; Mendelian randomization; vascular dementia; vitamin D; AD; 25-hydroxyvitamin D; Alzheimer disease; vascular dementia; vitamin D; cohort; GRS; Mendelian randomization; MMSE; CYP2R1; 25(OH)D; dementia; cognitive impairment; DHCR7; GC
• DOI: 10.3945/ajcn.116.141531
• EISSN: 1938-3207
• ISSN: 0002-9165

Background: Vitamin D has been implicated as being important for maintaining cognitive function in old age. Results from longitudinal studies examining the association of vitamin D with incident dementia and cognitive impairment have been inconsistent.
Objective: We investigated the relation between vitamin D, assessed in 3 different ways, and the risk of dementia.
Design: We measured plasma 25-hydroxyvitamin D [25(OH)D] with the use of high-performance liquid chromatography–mass spectrometry, assessed dietary vitamin D intake with the use of 7-d dietary records, and created a vitamin D–synthesis genetic risk score (GRS) at baseline (1991–1995) in a cohort of 1182 Swedish men (mean age: 71 y). In a maximum of 18 y (median: 12 y) of follow-up, 116 men developed Alzheimer disease, 64 men developed vascular dementia, and 250 men developed all-cause dementia. An additional 80 men declined in cognitive function as assessed with the use of the Mini-Mental State Examination. Adjusted HRs and ORs were calculated with the use of Cox and logistic regressions.
Results: The mean ± SD plasma 25(OH)D concentration was 68.7 ± 19.1 nmol/L. Plasma 25(OH)D, dietary vitamin D intake, and vitamin D–synthesis GRS were not associated with any cognitive outcomes (crude and adjusted HRs and ORs were ~1.0 for all continuous exposures). The adjusted HR for all-cause dementia was 0.88 (95% CI: 0.59, 1.31) in men with plasma 25(OH)D concentrations ≤50 compared with >75 nmol/L. The adjusted HR for all-cause dementia was 0.92 (95% CI: 0.63, 1.32) for the lowest compared with highest tertiles of vitamin D intake. The adjusted HR for the continuous GRS for all-cause dementia was 1.04 (95% CI: 0.91, 1.19).
Conclusion: In this cohort study, we show that there is no association between baseline vitamin D status and long-term risk of dementia or cognitive impairment over an 18-y period of time.