Andrea L C Schneider1, Di Zhao2, Pamela L Lutsey3, Rebecca F Gottesman4,2, A Richey Sharrett2, Andreea M Rawlings2, Alvaro Alonso5, David Knopman6, Thomas H Mosley7, Elizabeth Selvin2, Erin D Michos2,8. 1. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland, USAachris13@jhmi.edu. 2. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. 3. Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, Minnesota, USA. 4. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA. 5. Department of Epidemiology, Emory University Rollins School of Public Health, Atlanta, Georgia, USA. 6. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. 7. Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA. 8. Division of Cardiology, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Abstract
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.
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.
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