Vitamin D insufficiency and deficiency are a major health care problem. The association between vitamin D levels and cognitive function is still under debate. We conducted a systematic review to assess the association between levels of vitamin D and cognition. Therefore, the databases of Embase and Pubmed were searched through June 2012 for observational studies relating vitamin D levels to cognition. Our initial search yielded 2182 articles. After applying exclusion criteria, there were 28 studies eligible for inclusion: 25 cross-sectional and 6 prospective studies (3 studies show cross-sectional as well as prospective data). The main finding of the 25 cross-sectional studies was a statistically significant worse outcome on one or more cognitive function tests or a higher frequency of dementia with lower vitamin D levels or intake in 18 out of 25 (72%) studies, whereas 7 (28%) studies failed to show an association. Four out of 6 (66.7%) prospective studies showed a higher risk of cognitive decline after a follow-up period of 4-7 years in participants with lower vitamin D levels at baseline. In conclusion, this review supports the hypothesis that hypovitaminosis D is associated with worse outcome on one or more cognitive function tests or a higher frequency of dementia in cross-sectional as well as prospective studies. Further studies should focus on the role of vitamin D supplementation in the prevention of cognitive decline in participants with low vitamin D levels.
BACKGROUND: Hypovitaminosis D is associated with global cognitive impairment in adults. It remains unclear which domain-specific cognitive functions are affected with hypovitaminosis D.
OBJECTIVE: To systematically review and quantitatively synthesize the association of serum 25-hydroxyvitamin D (25OHD) concentrations with episodic memory and executive functions in adults.
METHODS: A Medline and PsycINFO libraries search was conducted on May 2012, with no limit of date, using the Medical Subject Headings (MeSH) terms "Vitamin D" OR "Hydroxycholecalciferols" combined with the MeSH terms "Memory" OR "Memory Disorders" OR "Executive Function" OR "Attention" OR "Cognition" OR "Cognition disorders" OR "Dementia" OR "Alzheimer disease" OR "Neuropsychological Tests". Fixed-effects meta-analysis was performed from 12 eligible studies using an inverse-variance method.
RESULTS: Of the 285 selected studies, 14 observational studies (including 3 prospective cohort studies) and 3 interventional studies met the selection criteria. All were of good quality. The number of participants ranged from 44-5,692 community-dwellers (0-100% women). In the pooled analysis, although episodic memory disorders showed only modest association with lower 25OHD concentrations (summary effect size of the difference (ES) = -0.09 [95%CI:-0.16;-0.03]), associations of greater magnitude were found with executive dysfunctions (processing speed: mean difference of Trail Making Test (TMT)-A score = 4.0 [95% CI:1.20;6.83]; mental shifting: mean difference of TMT-B score = 12.47 [95% CI:6.78;18.16]; information updating tests: ES = -0.31 [95% CI:-0.5;-0.09]). The pooled risk of incident decline of TMT-B score was OR = 1.25 [95% CI:1.05;1.48] in case of initial lower 25OHD concentrations. Vitamin D repletion resulted in improved executive functions (ES = -0.50 [95% CI:-0.69;-0.32] for before-and-after comparison), but exhibited no difference with control groups (ES = 0.14 [95% CI:-0.04;0.32] for between-group comparison after intervention).
CONCLUSION: Lower serum 25OHD concentrations predict executive dysfunctions, especially on mental shifting, information updating and processing speed. The association with episodic memory remains uncertain.
Poor vitamin B₁₂ status may lead to the development of cognitive decline and dementia but there is a large variation in the quality, design of and results reported from these investigations. We have undertaken a systematic review of the evidence for the association between vitamin B₁₂ status and cognitive decline in older adults. A database search of the literature to 2011 was undertaken, using keywords related to vitamin B₁₂ and cognition. All prospective cohort studies assessing the association of serum vitamin B₁₂ or biomarkers were included. Quality assessment and extraction of the data were undertaken by two researchers. The quality assessment tool assigns a positive, neutral or negative rating. Of 3772 published articles, thirty-five cohort studies (n 14 325 subjects) were identified and evaluated. No association between serum vitamin B₁₂ concentrations and cognitive decline or dementia was found. However, four studies that used newer biomarkers of vitamin B₁₂ status (methylmalonic acid and holotranscobalamin (holoTC)) showed associations between poor vitamin B₁₂ status and the increased risk of cognitive decline or dementia diagnosis. In general, the studies were of reasonable quality (twenty-one positive, ten neutral and four negative quality) but of short duration and inadequate subject numbers to determine whether an effect exists. Future studies should be of adequate duration (at least 6 years), recruit subjects from the seventh decade, choose markers of vitamin B₁₂ status with adequate specificity such as holoTC and/or methylmalonic acid and employ standardised neurocognitive assessment tools and not screening tests in order to ascertain any relationship between vitamin B₁₂ status and cognitive decline.
In view of the vital role of oxidative stress in the pathogenesis of Alzheimer's disease (AD), the potential of antioxidant supplements to prevent AD have gained much interest, while there are conflicting results on this topic in recent years. The purpose of the present study is to comprehensively evaluate the association between dietary intakes, instead of supplements, of the most common three antioxidants (vitamin E, vitamin C, and β-carotene) and the risk of AD on the basis of the meta-analysis studies published up to October 2011 in Medline and Scopus databases. In total, seven articles were included in the meta-analysis. According to the pooled relative risk [(95% CI) 0.76 (0.67-0.84) for vitamin E, 0.83 (0.72-0.94) for vitamin C, and 0.88 (0.73-1.03) for β-carotene], dietary intakes of the three antioxidants can lower the risk of AD, with vitamin E exhibiting the most pronounced protective effects. The findings will be of significance to the prevention and interventional treatment of AD.
OBJECTIVE: To examine the association between cognitive function and dementia with vitamin D concentration in adults. METHODS: Five databases were searched for English-language studies up to August 2010, and included all study designs with a comparative group. Cognitive function or impairment was defined by tests of global or domain-specific cognitive performance and dementia was diagnosed according to recognized criteria. A vitamin D measurement was required. Two authors independently extracted data and assessed study quality using predefined criteria. The Q statistic and I² methods were used to test for heterogeneity. We conducted meta-analyses using random effects models for the weighted mean difference (WMD) and Hedge's <i>g</i>. RESULTS: Thirty-seven studies were included; 8 contained data allowing mean Mini-Mental State Examination (MMSE) scores to be compared between participants with vitamin D <50 nmol/L to those with values ≥50 nmol/L. There was significant heterogeneity among the studies that compared the WMD for MMSE but an overall positive effect for the higher vitamin D group (1.2, 95% confidence interval [CI] 0.5 to 1.9; <i>I</i>² = 0.65; <i>p</i> = 0.002). The small positive effect persisted despite several sensitivity analyses. Six studies presented data comparing Alzheimer disease (AD) to controls but 2 utilized a method withdrawn from commercial use. For the remaining 4 studies the AD group had a lower vitamin D concentration compared to the control group (WMD = −6.2 nmol/L, 95% CI −10.6 to −1.8) with no heterogeneity (<i>I</i>² < 0.01; <i>p</i> = 0.53). CONCLUSION: These results suggest that lower vitamin D concentrations are associated with poorer cognitive function and a higher risk of AD. Further studies are required to determine the significance and potential public health benefit of this association. (PsycInfo Database Record (c) 2021 APA, all rights reserved)
BACKGROUND: Recent preventive strategies for patients with cognitive impairment include the identification of modifiable somatic risk factors like vitamin D deficiency. METHODS: A systematic literature research and meta-analysis were conducted to assess the association of cognitive impairment and vitamin D deficiency. RESULTS: Data from cross-sectional and longitudinal studies suggest an association between cognitive impairment and vitamin D deficiency. Meta-analysis of 5 cross-sectional and 2 longitudinal studies comprising 7,688 participants showed an increased risk of cognitive impairment in those with low vitamin D compared with normal vitamin D (OR 2.39, 95% CI 1.91–3.00; p < 0.0001). CONCLUSIONS: Methodological limitations of these studies comprise heterogeneity of study populations, different forms of cognitive assessment, the problem of reverse causality, different definitions of vitamin D deficiency and inconsistent control for confounders. As the value of vitamin D substitution in cognitive impairment remains doubtful, a long-time major placebo-controlled randomized trial of vitamin D supplementation in participants with mild cognitive impairment (MCI) should be started. (PsycInfo Database Record (c) 2024 APA, all rights reserved)
Elevated total plasma homocysteine has been linked to the development of cognitive impairment and dementia in later life and this can be reliably lowered by the daily supplementation of vitamin B6, B12, and folic acid.We performed a systematic review and meta-analysis of 19 English language randomized, placebo-controlled trials of homocysteine lowering B-vitamin supplementation of individuals with and without cognitive impairment at the time of study entry. We standardized scores to facilitate comparison between studies and to enable us to complete a meta-analysis of randomized trials. In addition, we stratified our analyses according to the folate status of the country of origin. B-vitamin supplementation did not show an improvement in cognitive function for individuals with (SMD = 0.10, 95%CI −0.08 to 0.28) or without (SMD = −0.03, 95%CI −0.1 to 0.04) significant cognitive impairment. This was irrespective of study duration (SMD = 0.05, 95%CI −0.10 to 0.20 and SMD = 0, 95%CI −0.08 to 0.08), study size (SMD = 0.05, 95%CI −0.09 to 0.19 and SMD = −0.02, 95%CI −0.10 to 0.05), and whether participants came from countries with low folate status (SMD = 0.14, 95%CI −0.12 to 0.40 and SMD = −0.10, 95%CI −0.23 to 0.04). Supplementation of vitamins B12, B6, and folic acid alone or in combination does not appear to improve cognitive function in individuals with or without existing cognitive impairment. It remains to be established if prolonged treatment with B-vitamins can reduce the risk of dementia in later life. (PsycInfo Database Record (c) 2024 APA, all rights reserved)
The increasing worldwide prevalence of dementia is a major public health concern. Findings from some epidemiological studies suggest that diet and nutrition may be important modifiable risk factors for development of dementia. In order to evaluate the strength of the available evidence of an association of dietary factors with dementia including Alzheimer's disease (AD), we systematically searched relevant publication databases and hand-searched bibliographies up to end July 2007. We included prospective cohort studies which evaluated the association of nutrient levels with the risk of developing dementia and randomized intervention studies examining the treatment effect of nutrient supplementation on cognitive function. One hundred and sixty studies, comprising ninety one prospective cohort studies and sixty nine intervention studies, met the pre-specified inclusion criteria. Of these, thirty-three studies (19 cohort and 14 randomized controlled trials) investigated the effects of folate, B-vitamins, and levels of homocysteine (a biomarker modifiable through B-vitamin supplementation) or fish/fatty acids and are the focus of the present report. Some observational cohort studies indicated that higher dietary intake or elevated serum levels of folate and fish/fatty acids and low serum levels of homocysteine were associated with a reduced risk of incident AD and dementia, while other studies reported no association. The results of intervention studies examining the effects of folic acid or fatty acid supplementation on cognitive function are inconsistent. In summary, the available evidence is insufficient to draw definitive conclusions on the association of B vitamins and fatty acids with cognitive decline or dementia, and further long-term trials are required.
