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Original Investigation |

Vitamin D Status and Rates of Cognitive Decline in a Multiethnic Cohort of Older Adults

Joshua W. Miller, PhD1,2; Danielle J. Harvey, PhD3; Laurel A. Beckett, PhD3; Ralph Green, MD, PhD2; Sarah Tomaszewski Farias, PhD4; Bruce R. Reed, PhD4; John M. Olichney, MD4; Dan M. Mungas, PhD4; Charles DeCarli, MD4
[+] Author Affiliations
1Department of Nutritional Sciences, Rutgers University, New Brunswick, New Jersey
2Department of Medical Pathology and Laboratory Medicine, University of California, Davis
3Division of Biostatistics, Department of Public Health Sciences, University of California, Davis
4Department of Neurology, University of California, Davis
JAMA Neurol. 2015;72(11):1295-1303. doi:10.1001/jamaneurol.2015.2115.
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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.

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Figure.
Trajectories of Cognitive Function Domains Over Time by Baseline Vitamin D Status

Trajectories across measured cognitive domains are shown for those with adequate, insufficient, and deficient vitamin D levels at baseline for episodic memory (A), semantic memory (B), visuospatial ability (C), and executive function (D). Slopes of decline differed significantly from adequate for both insufficient and deficient levels for episodic memory (P < .001 and P = .049, respectively) and executive function (P = .008 and P = .01, respectively) after adjustment for covariates.

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Sunlight is the major source of VitD and affect body, mind and intellect.
Posted on September 17, 2015
Dr.Rajiv Kumar, Dr.Jagjit Singh.
Faculty, Department of Pharmacology, Government Medical College & Hospital Chandigarh 160030. India.
Conflict of Interest: None Declared
Vitamin D (VitD), is the fat-soluble, steroid prohormone & sunshine vitamin. VitD has received increased attention due to the identification of extra-skeletal effect i.e beyond bone health. Vit D receptor (VDR) has been identified in skin, placenta, brain, pancreas, breast, prostate, colon cancer cells, and activated T cells. There are promising extra-skeletal therapeutic implications of Vitamin D beyond bone health, VitD has anticancer properties [1]. As per the Hindu Religion, Surya symbolizes the Sun God. The sun, source of light and energy for the entire solar system. Surya Namaskar (Salutations to the Sun) is experienced on three levels ? body, mind and intellect and exposure in sunlight is the major source of VitD [2]. Vitamin D is considered as a neurosteroid, the neuroprotective and immunomodulatory effects of VitD have been shown in experimental models, indicating the potential value in neurodegenerative and neuroimmune diseases [3]. Study has shown that VitD enhances mood in healthy subjects during winter [4] and results were consistent with the hypothesis that low VitD concentration is associated with depression [5]. VitD supplementation is effective in depression in adults [6]. However regarding cognitive function, well designed randomized controlled trials (RCTs) are needed to determine whether VitD supplementation is effective at preventing or treating Alzheimer's disease and dementia.

References:
1. KK Deeb, DL Trump, CS Johnson. Vitamin D signalling pathways in cancer: potential for anticancer therapeutics. Nat Rev Cancer. 2007;7(9):684-700.
2. http://www.suryanamaskar.info/guidelines.htm
3. E Garcion , N Wion-Barbot , CN Montero-Menei , F Berger, D Wion. New clues about Vitamin D functions in the nervous system. Trends Endocrinol Metab. 2002 Apr;13(3):100-5.
4. AT Lansdowne, SC Provost. Vitamin D3 enhances mood in healthy subjects during winter. Psychopharmacology (Berl). 1998 ;135(4):319-23.
5. RE Anglin , Z Samaan , SD Walter, SD McDonald. Vitamin D deficiency and depression in adults: systematic review and meta-analysis. Br J Psychiatry. 2013 ;202:100-7.
6. Li Guowei , M Lawrence, S Zainab , Z Shiyuan, DA Jonathan, P Alexandra, T Lehana. Efficacy of vitamin D supplementation in depression in adults: a systematic review protocol.Syst Rev. 2013; 2: 64.
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