French adults' cognitive performance after daily supplementation with antioxidant vitamins and minerals at nutritional doses: a post hoc analysis of the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) trial
ABSTRACT Antioxidant properties of some vitamins and trace elements may help to prevent cognitive decline.
The aim of the current study was to estimate the long-term effects of antioxidant nutrient supplementation on the cognitive performance of participants in the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) study 6 y after the end of the trial.
This study included 4447 French participants aged 45-60 y who were enrolled in the SU.VI.MAX study (1994-2002), which was a double-blind, placebo-controlled, randomized trial. From 1994 to 2002, participants received daily vitamin C (120 mg), β-carotene (6 mg), vitamin E (30 mg), selenium (100 μg), and zinc (20 mg) in combination or as a placebo. In 2007-2009, the cognitive performance of participants was assessed with 4 neuropsychological tests (6 tasks). Principal components analysis (PCA) was performed to identify cognitive-function summary scores. Associations between antioxidant supplementation and cognitive functions, in the full sample and by subgroups, were estimated through ANOVA and expressed as mean differences and 95% CIs. Subgroup analyses were performed according to baseline characteristics.
Subjects receiving active antioxidant supplementation had better episodic memory scores (mean difference: 0.61; 95% CI: 0.02, 1.20). PCA indicated 2 factors that were interpreted as showing verbal memory and executive functioning. Verbal memory was improved by antioxidant supplementation only in subjects who were nonsmokers or who had low serum vitamin C concentrations at baseline.
This study supports the role of an adequate antioxidant nutrient status in the preservation of verbal memory under certain conditions. This trial was registered at clinicaltrials.gov as NCT00272428.
Article: Nutrition et maladie d’Alzheimer[Show abstract] [Hide abstract]
ABSTRACT: Deterioration of memory function and ultimately establishment of Alzheimer's disease (AD) severely debilitates the affected individual, uncompromisingly decreasing the quality of life of both patients and their caregivers. The global prevalence of cognitive impairment and dementia including Alzheimer's disease is expected to rise significantly in proportion to increased life expectancy. Weight loss is a common problem among patients with AD and is associated with mortality, morbidity, disease progression, and poor quality of life. The aim of this article is: (1) to emphasize the importance of malnutrition in Alzheimer's disease and (2) to review published evidences for the role of nutrition as a risk factor of the disease.Nutrition Clinique et Métabolisme 12/2011; DOI:10.1016/j.nupar.2011.09.004
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ABSTRACT: BACKGROUND: Vitamin E is a dietary compound that functions as an antioxidant scavenging toxic free radicals. Evidence that free radicals may contribute to the pathological processes of cognitive impairment including Alzheimer's disease has led to interest in the use of vitamin E in the treatment of mild cognitive impairment (MCI) and Alzheimer's dementia (AD). OBJECTIVES: To assess the efficacy of vitamin E in the treatment of AD and prevention of progression of MCI to dementia. SEARCH METHODS: 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 were searched on 25 June 2012 using the terms: "Vitamin E", vitamin-E, alpha-tocopherol. SELECTION CRITERIA: All unconfounded, double-blind, randomised trials in which treatment with vitamin E at any dose was compared with placebo for patients with AD and MCI. DATA COLLECTION AND ANALYSIS: Two review authors independently applied the selection criteria and assessed study quality and extracted and analysed the data. For each outcome measure data were sought on every patient randomised. Where such data were not available an analysis of patients who completed treatment was conducted. It was not possible to pool data between studies owing to a lack of comparable outcome measure. MAIN RESULTS: Only three studies met the inclusion criteria: two in an AD population and one in an MCI population. In the first of the AD studies (Sano 1996) the authors reported some benefit from vitamin E (2000 IU/day) with fewer participants reaching an end point of death, institutionalisation, change to a Clinical Dementia Rating (CDR) of three, or loss of two basic activities of daily living within two years. Of patients completing treatment, 58% (45/77) on vitamin E compared with 74% (58/78) on placebo reached one of the end points (odds ratio (OR) 0.49; 95% confidence interval (CI) 0.25 to 0.96). The second AD treatment study (Lloret 2009) explored the effects of vitamin E (800 IU/day) on cognitive progression in relation to oxidative stress levels. Patients whose oxidative stress markers were lowered by vitamin E showed no significant difference in the percentage change in Mini-Mental State Examination (MMSE) score, between baseline and six months, compared to the placebo group. The primary aim of the MCI study (Petersen 2005) was to investigate the effect of vitamin E (2000 IU/day) on the time to progression from MCI to possible or probable AD. A total of 214 of the 769 participants progressed to dementia, with 212 being classified as having possible or probable AD. There was no significant difference in the probability of progression from MCI to AD between the vitamin E group and the placebo group (hazard ratio 1.02; 95% CI 0.74 to 1.41; P = 0.91). AUTHORS' CONCLUSIONS: No convincing evidence that vitamin E is of benefit in the treatment of AD or MCI. Future trials assessing vitamin E treatment in AD should not be restricted to alpha-tocopherol.Cochrane database of systematic reviews (Online) 01/2012; 11(11):CD002854. DOI:10.1002/14651858.CD002854.pub3
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ABSTRACT: Changes in the intracellular and extracellular redox balance have been correlated with cell fate decisions in terms of proliferation versus differentiation, entering versus existing cell cycle and survival versus cell death. Adult hippocampal neurogenesis has been correlated with neuronal plasticity of learning and memory; however, the process is exquisitely sensitive to changes in redox balance. Cranial irradiation is an effective modality in treating brain tumours but often leads to deficits in hippocampus-related learning and memory, which is most likely due to sustained elevation of oxygen free radical production and suppression of hippocampal neurogenesis. The subcellular redox environment affecting hippocampal neurogenesis is largely unknown. Using mutant mice deficient in each one of the three superoxide dismutase (SOD, EC 18.104.22.168) isoforms, we have begun to determine the consequences of SOD deficiency in hippocampal neurogenesis and the related functions of learning and memory under normal condition and following cranial irradiation.Free Radical Research 02/2012; 46(8):951-8. DOI:10.3109/10715762.2012.664770