Impact of supplementation with vitamins B₆, B₁₂, and/or folic acid on the reduction of homocysteine levels in patients with mild cognitive impairment: A systematic review

Abstract

Hyperhomocysteinemia is an independent predictor of the risk for cognitive decline and may be a result of low levels of vitamins B 12 , B 6 , and folate. Previous findings suggest that adequate intake of these vitamins may reduce homocysteine levels. This review aimed to assess the effects of treatment with vitamins B 6, B 12 , and/or folic acid in the homocysteine levels in patients with mild cognitive impairment (MCI). A systematic literature review was conducted in EMBASE, MEDLINE ® , PsycINFO, and Cochrane Central Register of Controlled Trials. The research question was formulated using the Population, Intervention, Comparison, and Outcome (PICO) framework: in patients with MCI (P); what is the efficacy of vitamins B 6 , B 12 , and/or folic acid intake (I); compared with baseline values, and/or compared with controls (C); in reducing homocysteine levels from baseline (O). A total of eight primary studies with a total of 1,140 participants were included in the review. Four were randomized controlled trials, one was a quasi-controlled trial, and three were observational studies. All studies included folic acid in their intervention, seven vitamin B 12 , and four vitamin B 6 . Mean (SD) length of the intervention period was 18.8 (19.

Dietary Flavonoids and Human Cognition: A Meta‐Analysis

“…Vitamin B is thought to reduce homocysteine levels, beyond which multiple biological mechanisms of action could explain the connection it has with improved cognitive performance, including vascular mechanisms, prevention of neuronal apoptosis, and epi‐genetic modifications. [ 117 ] Similarly, a range of vascular, metabolic, and neurochemical mechanisms of action have been proposed for flavonoids and their benefits to cognition.…”

Neurological Implications of Vitamin B12 Deficiency in Diet: A Systematic Review and Meta-Analysis

“…The trial participants in our review were generally healthy, so it is possible that the findings do not apply to the entirety of the elderly population. Additionally, the course of treatment might have been too brief, and any effects of Vitamin B12 supplementation might not have been seen until years later or during follow-up [ 39 ]. To our knowledge, no relevant experiment using Vitamin B12 supplementation for a duration longer than two years has been carried out [ 39 ].…”

“…Additionally, the course of treatment might have been too brief, and any effects of Vitamin B12 supplementation might not have been seen until years later or during follow-up [ 39 ]. To our knowledge, no relevant experiment using Vitamin B12 supplementation for a duration longer than two years has been carried out [ 39 ]. Direct links between nerve conduction and Vitamin B12 levels have been observed in observational studies [ 40 ], although this finding has not always been the case [ 40 , 41 ].…”

“…No prior randomised controlled trial has, to our knowledge, examined the effect of Vitamin B12 supplementation on neurologic function in elderly individuals. Prior studies examining the impact of Vitamin B12 supplementation on cognitive performance mostly failed to demonstrate any positive effects, although they were of inconsistent quality, small scale, and short duration [ 39 , 42 ]. Recently, there has been some indication of the benefit of taking numerous B Vitamins, particularly in subgroups of people with worse biochemical state when randomly assigned at baseline [ 43 ].…”

Effects of Supplementation with Folic Acid and Its Combinations with Other Nutrients on Cognitive Impairment and Alzheimer’s Disease: A Narrative Review

“…Therefore, preventive strategies that protect individuals from neurological decline and minimize the development of related adverse effects are urgently needed [4,5]. Emerging evidence shows that early improvement of MCI decreases the prevalence of AD [6] and, in this regard, nutritional strategies are of special relevance [7,8]. Pathogenesis and progression of AD, the first cause of dementia, as previously stated, are linked to different inflammatory processes [9].…”