Research: FARINA and COLLEAGUES,

Listed in Issue 254

Abstract

FARINA and COLLEAGUES, 1. Centre for Dementia Studies, Brighton and Sussex Medical School, Brighton, UK, BN1 9QH; 2. Medical School, University of Exeter, Exeter, UK, +44 (0) 1392 726018; 3. Old Age Psychiatry, Sussex Partnership NHS Foundation Trust, Master's House, Compton Place Road, Eastbourne, East Sussex, UK, BN20 8BJ proceeded to update a Cochrane Review from 2000, and updated in 2006 and 2012 to assess the efficacy of vitamin E in the treatment of mild cognitive impairment (MCI) and dementia due to Alzheimer's disease (AD).

Background

Vitamin E occurs naturally in the diet. It has several biological activities, including functioning as an antioxidant to scavenge toxic free radicals. Evidence that free radicals may contribute to the pathological processes behind cognitive impairment has led to interest in the use of vitamin E supplements to treat mild cognitive impairment (MCI) and Alzheimer's disease (AD). This is an update of a Cochrane Review first published in 2000, and previously updated in 2006 and 2012.

Methodology

Objectives: To assess the efficacy of vitamin E in the treatment of MCI and dementia due to AD. Search Methods: The authors searched the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (ALOIS), the Cochrane Library, MEDLINE, Embase, PsycINFO, CINAHL, LILACS as well as many trials databases and grey literature sources on 22 April 2016 using the terms: "Vitamin E", vitamin-E, alpha-tocopherol. Selection Criteria: The authors included all double-blind, randomized trials in which treatment with any dose of vitamin E was compared with placebo in people with AD or MCI. Data Collection And Analysis: The authors used standard methodological procedures according to the Cochrane Handbook for Systematic Reviews of Interventions and rated the quality of the evidence using the GRADE approach. Where appropriate they attempted to contact authors to obtain missing information.

Results

Four trials met the inclusion criteria, but the authors could only extract outcome data in accordance with our protocol from two trials, one in an AD population (n = 304) and one in an MCI population (n = 516). Both trials had an overall low to unclear risk of bias. It was not possible to pool data across studies owing to a lack of comparable outcome measures. In people with AD, we found no evidence of any clinically important effect of vitamin E on cognition, measured with change from baseline in the Alzheimer's Disease Assessment Scale - Cognitive subscale (ADAS-Cog) over six to 48 months (mean difference (MD) -1.81, 95% confidence interval (CI) -3.75 to 0.13, P = 0.07, 1 study, n = 272; moderate quality evidence). There was no evidence of a difference between vitamin E and placebo groups in the risk of experiencing at least one serious adverse event over six to 48 months (risk ratio (RR) 0.86, 95% CI 0.71 to 1.05, P = 0.13, 1 study, n = 304; moderate quality evidence), or in the risk of death (RR 0.84, 95% CI 0.52 to 1.34, P = 0.46, 1 study, n = 304; moderate quality evidence). People with AD receiving vitamin E showed less functional decline on the Alzheimer's Disease Cooperative Study/Activities of Daily Living Inventory than people receiving placebo at six to 48 months (mean difference (MD) 3.15, 95% CI 0.07 to 6.23, P = 0.04, 1 study, n = 280; moderate quality evidence). There was no evidence of any clinically important effect on neuropsychiatric symptoms measured with the Neuropsychiatric Inventory (MD -1.47, 95% CI -4.26 to 1.32, P = 0.30, 1 study, n = 280; moderate quality evidence). The authors found no evidence that vitamin E affected the probability of progression from MCI to probable dementia due to AD over 36 months (RR 1.03, 95% CI 0.79 to 1.35, P = 0.81, 1 study, n = 516; moderate quality evidence). Five deaths occurred in each of the vitamin E and placebo groups over the 36 months (RR 1.01, 95% CI 0.30 to 3.44, P = 0.99, 1 study, n = 516; moderate quality evidence). The authors were unable to extract data in accordance with the review protocol for other outcomes. However, the study authors found no evidence that vitamin E differed from placebo in its effect on cognitive function, global severity or activities of daily living . There was also no evidence of a difference between groups in the more commonly reported adverse events.

Conclusion

The authors found no evidence that the alpha-tocopherol form of vitamin E given to people with MCI prevents progression to dementia, or that it improves cognitive function in people with MCI or dementia due to AD. However, there is moderate quality evidence from a single study that it may slow functional decline in AD. Vitamin E was not associated with an increased risk of serious adverse events or mortality in the trials in this review. These conclusions have changed since the previous update, however they are still based on small numbers of trials and participants and further research is quite likely to affect the results.

References

Farina N1, Llewellyn D2, Isaac MG3, Tabet N1. Vitamin E for Alzheimer's dementia and mild cognitive impairment. Cochrane Database Syst Rev. 1:CD002854. doi: 10.1002/14651858.CD002854.pub4. Jan 27 2017. Update in Vitamin E for Alzheimer's dementia and mild cognitive impairment. [Cochrane Database Syst Rev. 2017]; Vitamin E for Alzheimer's dementia and mild cognitive impairment. [Cochrane Database Syst Rev. 2012].

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