03227nas a2200457 4500008004100000022001400041245006200055210006100117260001500178300001000193490000700203520200900210653000902219653002202228653001302250653001102263653002202274653001102296653001402307653000902321653003202330653001702362653001802379653001402397653002502411100002702436700002302463700001802486700002202504700002202526700002302548700001702571700002502588700002102613700002202634700002002656700001802676700001502694700002402709856003602733 2014 eng d a1526-632X00aVitamin D and the risk of dementia and Alzheimer disease.0 aVitamin D and the risk of dementia and Alzheimer disease c2014 Sep 2 a920-80 v833 a

OBJECTIVE: To determine whether low vitamin D concentrations are associated with an increased risk of incident all-cause dementia and Alzheimer disease.

METHODS: One thousand six hundred fifty-eight elderly ambulatory adults free from dementia, cardiovascular disease, and stroke who participated in the US population-based Cardiovascular Health Study between 1992-1993 and 1999 were included. Serum 25-hydroxyvitamin D (25(OH)D) concentrations were determined by liquid chromatography-tandem mass spectrometry from blood samples collected in 1992-1993. Incident all-cause dementia and Alzheimer disease status were assessed during follow-up using National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria.

RESULTS: During a mean follow-up of 5.6 years, 171 participants developed all-cause dementia, including 102 cases of Alzheimer disease. Using Cox proportional hazards models, the multivariate adjusted hazard ratios (95% confidence interval [CI]) for incident all-cause dementia in participants who were severely 25(OH)D deficient (<25 nmol/L) and deficient (≥25 to <50 nmol/L) were 2.25 (95% CI: 1.23-4.13) and 1.53 (95% CI: 1.06-2.21) compared to participants with sufficient concentrations (≥50 nmol/L). The multivariate adjusted hazard ratios for incident Alzheimer disease in participants who were severely 25(OH)D deficient and deficient compared to participants with sufficient concentrations were 2.22 (95% CI: 1.02-4.83) and 1.69 (95% CI: 1.06-2.69). In multivariate adjusted penalized smoothing spline plots, the risk of all-cause dementia and Alzheimer disease markedly increased below a threshold of 50 nmol/L.

CONCLUSION: Our results confirm that vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer disease. This adds to the ongoing debate about the role of vitamin D in nonskeletal conditions.

10aAged10aAlzheimer Disease10aDementia10aFemale10aFollow-Up Studies10aHumans10aIncidence10aMale10aProportional Hazards Models10aRisk Factors10aUnited States10aVitamin D10aVitamin D Deficiency1 aLittlejohns, Thomas, J1 aHenley, William, E1 aLang, Iain, A1 aAnnweiler, Cedric1 aBeauchet, Olivier1 aChaves, Paulo, H M1 aFried, Linda1 aKestenbaum, Bryan, R1 aKuller, Lewis, H1 aLanga, Kenneth, M1 aLopez, Oscar, L1 aKos, Katarina1 aSoni, Maya1 aLlewellyn, David, J uhttps://chs-nhlbi.org/node/701702884nas a2200277 4500008004100000022001400041245005400055210005300109260000900162300001300171490000700184520211400191100002702305700001802332700002302350700001802373700002202391700002202413700002302435700002502458700002102483700002202504700002002526700002402546856003602570 2016 eng d a1932-620300aVitamin D and Risk of Neuroimaging Abnormalities.0 aVitamin D and Risk of Neuroimaging Abnormalities c2016 ae01548960 v113 a

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.

1 aLittlejohns, Thomas, J1 aKos, Katarina1 aHenley, William, E1 aLang, Iain, A1 aAnnweiler, Cedric1 aBeauchet, Olivier1 aChaves, Paulo, H M1 aKestenbaum, Bryan, R1 aKuller, Lewis, H1 aLanga, Kenneth, M1 aLopez, Oscar, L1 aLlewellyn, David, J uhttps://chs-nhlbi.org/node/7126