The association between low serum 25-hydroxyvitamin D [25(OH)D] concentration and cognitive decline has been investigated by only a few studies, with mixed results. The objective of this cross-sectional population-based study was to examine the association between serum 25(OH)D deficiency and cognitive impairment while taking confounders into account.
The subjects, 752 women aged > or =75 years from the Epidémiologie de l'Ostéoporose (EPIDOS) cohort, were divided into 2 groups according to serum 25(OH)D concentrations (either deficient, <10 ng/mL, or nondeficient, > or =10 ng/mL). Cognitive impairment was defined as a Pfeiffer Short Portable Mental State Questionnaire (SPMSQ) score <8. Age, body mass index, number of chronic diseases, hypertension, depression, use of psychoactive drugs, education level, regular physical activity, and serum intact parathyroid hormone and calcium were used as potential confounders.
Compared with women with serum 25(OH)D concentrations > or =10 ng/mL (n = 623), the women with 25(OH)D deficiency (n = 129) had a lower mean SPMSQ score (p < 0.001) and more often had an SPMSQ score <8 (p = 0.006). There was no significant linear association between serum 25(OH)D concentration and SPMSQ score (beta = -0.003, 95% confidence interval -0.012 to 0.006, p = 0.512). However, serum 25(OH)D deficiency was associated with cognitive impairment (crude odds ratio [OR] = 2.08 with p = 0.007; adjusted OR = 1.99 with p = 0.017 for full model; and adjusted OR = 2.03 with p = 0.012 for stepwise backward model).
25-Hydroxyvitamin D deficiency was associated with cognitive impairment in this cohort of community-dwelling older women.
"In the studies showing a positive effect, subjects with low levels of vitamin D status had lower cognitive scores. Mild dementia was also associated with diminished vitamin D status  , while vitamin D deficiency increased the probability of cognitive impairment by more than 200% . "
[Show abstract][Hide abstract] ABSTRACT: The active form vitamin D is a seco-steroid with multiple neurotrophic and neuroprotective functions in the central nervous system. Robust evidence from studies in animals suggests that vitamin D deficiency may impair brain physiological functioning causing anatomical and behavioral adverse effects. On the other hand, vitamin D has been found to be protective against biological processes associated with Alzheimer's disease and cognition, including amyloid-β deposition, inflammation, calcium homeostasis, and corticosteroid-induced perturbations in cortical areas and the hippocampus. Human studies that examined the relationship between vitamin D status and cognitive function have provided inconclusive results. The majority of cross-sectional and longitudinal studies suggest a potentially protective association, whereas results from clinical trials are mostly negative, or at best, controversial. We review these studies in humans, with particular emphasis on randomized and observational prospective ones.
"It is of interest that some studies showed that low dietary calcium intake (< 700 mg/day) is associated with an increased risk of ischemic heart disease death in postmenopausal women . Several recent publications found a significant association between higher rate of cardiovascular disease and also cognitive impairment in the postmenopausal women and low vitamin D levels [12,13]. The mean of daily folate, vitamin B5 and B6 intake in our subjects was lower than RDA recommendations. "
[Show abstract][Hide abstract] ABSTRACT: Background
Evidence supports that increasing number of postmenopausal women are suffering from one or more chronic diseases. Dietary patterns have a pivotal role in maintaining human health. The aim of this study was to characterize the nutrients and energy intake in postmenopausal women, with the special focus on seasonal variation effect in their food intake.
The study population consisted of 30 postmenopausal women referred to Dr. Shariati Hospital, Tehran (Iran). Socio-demographic characteristics and BMI were registered. Dietary assessment was performed by a 3 day food records in each season through one year, allowing the estimation of energy, protein, carbohydrate, total fat, monounsaturated fatty acid (MUFA), polyunsaturated fatty acids (PUFA) and saturated fatty acids (SFA) intake. The mean of nutrient intake in each season was adjusted for energy intake. The effect of season on energy and nutrients intake was assessed based on the General linear model (GLM).
The mean of daily intake of vitamin C, B, B2, B12, iron, zinc, phosphorus and chromium was significantly higher than Recommended Dietary Allowance (RDAs ) (p < 0.05). The mean of vitamin D, E, B6, B5, folate, calcium, magnesium, potassium and selenium consumption was significantly less than RDAs (p < 0.05). All the participants meet the goal for vitamins A, K and B3 from food. The mean of energy intake was not different between seasons. However, the mean intake of fat, vitamin C, vitamin K and folate was significantly different between seasons.
These findings highlight some nutrients deficiency in postmenopausal women and therefore suggest nutritional education with emphasis on seasonal variation effect.
Journal of Diabetes and Metabolic Disorders 04/2014; 13(1):52. DOI:10.1186/2251-6581-13-52
"studies were also reported. Low levels of plasma 25-dihydroxyvitamin D 3 (25-hydroxycholecalciferol, abbreviated as 25(OH)D) were suggested to be associated with mood disorders, dementia, mild cognitive impairment, PD, AD, and cognitive decline         . "
[Show abstract][Hide abstract] ABSTRACT: Scientists have worked for over a century to uncover the basis of Alzheimer's disease (AD) with the ultimate goal of discovering a treatment. However, none of the approaches utilized have defined the exact cause of the disease or an ultimate treatment for AD. In this review, we aim to define the role of vitamin D in AD from a novel and fundamental perspective and attempt to answer the following question: Why should we seriously consider "simple" vitamin D as a "fundamental factor" in AD? To answer this question, we explain the protective effects of vitamin D in the central nervous system and how the action of vitamin D and AD-type pathology overlap. Furthermore, we suggest that the role of vitamin D in AD includes not only vitamin D deficiency and vitamin D-related genes but also the disruption of vitamin D metabolism and action. This suggestion is supported by evidence that the disruption of vitamin D pathways mimic amyloid pathology. We define the term "inefficient utilization of vitamin D" as any alteration in vitamin D-related genes, including receptors, the enzymes related to vitamin D metabolism or the transporters of vitamin D, and we discuss the potential correlation of vitamin D status with the vulnerability of neurons to aging and neurodegeneration. Finally, in addition to the current knowledge that defines AD, we suggest that AD could be the result of a long-term hormonal imbalance in which the critical hormone is vitamin D, a secosteroid that has long been misnamed.
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