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Significance Statement
A study conducted by Rutgers University and University of California, Davis researchers examined the relationship between vitamin D status and changes in cognitive function in a group of ethnically diverse older adults. The study enrolled 382 seniors in an outpatient clinic (February 2002 -August 2010). Their cognitive function was evaluated at baseline and yearly thereafter. The results showed that average vitamin D levels in the dementia group were lower compared with the mild cognitive impairment and cognitively normal groups. Moreover, the average vitamin D levels were significantly lower for African Americans and Hispanics compared to Caucasians. New clinical studies need to be conducted to evaluate whether vitamin D supplementation can slow cognitive decline.
Journal Reference
Miller JW1, Harvey DJ2, Beckett LA2, Green R3, Farias ST4, Reed BR4, Olichney JM4, Mungas DM4, DeCarli C4.
[expand title=”Show Affiliations”]1Department of Nutritional Sciences, Rutgers University, New Brunswick, New Jersey2Department of Medical Pathology and Laboratory Medicine, University of California, Davis.
2Division of Biostatistics, Department of Public Health Sciences, University of California, Davis.
3Department of Medical Pathology and Laboratory Medicine, University of California, Davis.
4Department of Neurology, University of California, Davis.
[/expand]Abstract
IMPORTANCE:
Vitamin D (VitD) deficiency is associated with brain structural abnormalities, cognitive decline, and incident dementia.
OBJECTIVE:
To assess associations between VitD status and trajectories of change in subdomains of cognitive function in a cohort of ethnically diverse older adults.
DESIGN, SETTING, AND PARTICIPANTS:
Longitudinal multiethnic cohort study of 382 participants in an outpatient clinic enrolled between February 2002 and August 2010 with baseline assessment and yearly follow-up visits. Serum 25-hydroxyvitamin D (25-OHD) was measured, with VitD status defined as the following: deficient, less than 12 ng/mL (to convert to nanomoles per liter, multiply by 2.496); insufficient, 12 to less than 20 ng/mL; adequate, 20 to less than 50 ng/mL; or high, 50 ng/mL or higher. Subdomains of cognitive function were assessed using the Spanish and English Neuropsychological Assessment Scales. Associations were evaluated between 25-OHD levels (as continuous and categorical [deficient, insufficient, or adequate]) and trajectories of cognitive decline.
MAIN OUTCOMES AND MEASURES:
Serum 25-OHD levels, cognitive function, and associations between 25-OHD levels and trajectories of cognitive decline.
RESULTS:
Participants (N = 382 at baseline) had a mean (SD) age of 75.5 (7.0) years; 61.8% were women; and 41.4% were white, 29.6% African American, 25.1% Hispanic, and 3.9% other race/ethnicity. Diagnosis at enrollment included 17.5% with dementia, 32.7% with mild cognitive impairment, and 49.5% cognitively normal. The mean (SD) 25-OHD level was 19.2 (11.7) ng/mL, with 26.2% of participants being VitD deficient and 35.1% insufficient. The mean (SD) 25-OHD levels were significantly lower for African American and Hispanic participants compared with white participants (17.9 [15.8] and 17.2 [8.4] vs 21.7 [10.0] ng/mL, respectively; P < .001 for both). The mean (SD) 25-OHD levels were similarly lower in the dementia group compared with the mild cognitive impairment and cognitively normal groups (16.2 [9.4] vs 20.0 [10.3] and 19.7 [13.1] ng/mL, respectively; P = .006). The mean (SD) follow-up was 4.8 (2.5) years. Rates of decline in episodic memory and executive function among VitD-deficient (episodic memory: β = -0.04 [SE = 0.02], P = .049; executive function: β = -0.05 [SE = 0.02], P = .01) and VitD-insufficient (episodic memory: β = -0.06 [SE = 0.02], P < .001; executive function: β = -0.04 [SE = 0.02], P = .008) participants were greater than those with adequate status after controlling for age, sex, education, ethnicity, body mass index, season of blood draw, vascular risk, and apolipoprotein E4 genotype. Vitamin D status was not significantly associated with decline in semantic memory or visuospatial ability. Exclusion of participants with dementia did not substantially affect the associations between VitD status and rates of cognitive decline.
CONCLUSIONS AND RELEVANCE:
Low VitD status was associated with accelerated decline in cognitive function domains in ethnically diverse older adults, including African American and Hispanic individuals who exhibited a high prevalence of VitD insufficiency or deficiency. It remains to be determined whether VitD supplementation slows cognitive decline.