Erika Olsson1, Liisa Byberg2, Brita Karlström3, Tommy Cederholm3, Håkan Melhus4, Per Sjögren3, Lena Kilander5. 1. Departments of Public Health and Caring Sciences/Clinical Nutrition and Metabolism, erika.olsson@pubcare.uu.se liisa.byberg@surgsci.uu.se. 2. Surgical Sciences, Orthopedics, erika.olsson@pubcare.uu.se liisa.byberg@surgsci.uu.se. 3. Departments of Public Health and Caring Sciences/Clinical Nutrition and Metabolism. 4. Medical Sciences, Clinical Pharmacogenomics and Osteoporosis, and. 5. Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden.
Abstract
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.
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.
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