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Taking B vitamins won't prevent Alzheimer's disease
Myriam
Posted: Tuesday, July 15, 2014 2:07 PM
Joined: 12/6/2011
Posts: 3326


Taking B vitamins doesn't slow mental decline as we age, nor is it likely to prevent Alzheimer's disease, conclude Oxford University researchers who have assembled all the best clinical trial data involving 22,000 people to offer a final answer on this debate. 

 

High levels in the blood of a compound called homocysteine have been found in people with Alzheimer's disease, and people with higher levels of homocysteine have been shown to be at increased risk of Alzheimer's disease. Taking folic acid and vitamin B-12 are known to lower levels of homocysteine in the body, so this gave rise to the 'homocysteine hypothesis' that taking B vitamins could reduce the risk of Alzheimer's disease. 

 

The new analysis was carried out by the B-Vitamin Treatment Trialists' Collaboration, an international group of researchers led by the Clinical Trial Service Unit at the University of Oxford. The researchers brought together data from 11 randomized clinical trials involving 22,000 people which compared the effect of B vitamins on cognitive function in older people against placebo. Participants receiving B vitamins did see a reduction in the levels of homocysteine in their blood by around a quarter. However, this had no effect on their mental abilities. 

 

When looking at measures of global cognitive function -- or scores for specific mental processes such as memory, speed or executive function -- there was no difference between those on B vitamins and those receiving placebo to a high degree of accuracy. 

 

'It would have been very nice to have found something different,' says Dr Robert Clarke of Oxford University, who led the work. 'Our study draws a line under the debate: B vitamins don't reduce cognitive decline as we age. Taking folic acid and vitamin B-12 is sadly not going to prevent Alzheimer's disease.' 

 

The study was funded by the British Heart Foundation, the UK Medical Research Council (MRC), Cancer Research UK, the UK Food Standards Agency and the Department of Health. The findings are published in the American Journal of Clinical Nutrition. 

 

'Taking supplements like B vitamins doesn't prevent heart disease, stroke or cognitive decline,' says Professor Clarke. 'About 25% of the adult population take multi-vitamins, often with the idea that they are also good for the heart or the brain, but the evidence just isn't there. Much better is to eat more fruit and vegetables, avoid too much red meat and too many calories, and have a balanced diet.' 

 

Maternal folic acid intake before and during early pregnancy reduces a woman's risk of having a neural tube defect birth defect and those thinking of having a baby are routinely advised to take folic acid supplements. Countries that have adopted mandatory population-wide folic acid fortification programmes have also demonstrated reductions in neural-tube defect associated pregnancies without any adverse effects. 

 

Dr Simon Ridley, Head of Research at Alzheimer's Research UK, said: 

'Although one trial in 2010 showed that for people with high homocysteine, B vitamins had some beneficial effect on the rate of brain shrinkage, this comprehensive review of several trials shows that B vitamins have not been able to slow mental decline as we age, nor are they likely to prevent Alzheimer's. While the outcome of this new and far reaching analysis is not what we hoped for, it does underline the need for larger studies to improve certainty around the effects of any treatment. 

 

'Alzheimer's is feared by many and it's natural that people want to take action to try to prevent the disease, but people should always speak to their GP before changing their diet to include vitamin supplements. Research to understand how to prevent Alzheimer's must continue, and in the meantime evidence shows that a number of simple lifestyle changes can help reduce the risk of the disease. Eating a healthy, balanced diet, taking regular exercise and keeping blood pressure and weight in check can all help lower the risk of Alzheimer's.' 

 

Dr James Pickett, Head of Research at Alzheimer's Society said: 

'Given that many previous studies have shown that vitamin B doesn't slow the progression of dementia or reduce risk, it's not a huge surprise that a review of all of the evidence finds much the same. While taking B vitamins may not help everyone, they may have some benefits in specific groups of people with dementia. However, this study suggests that we need much more work to establish more evidence for this. 

 

'One in three people over the age of 65 will develop dementia and yet research funding lags behind other conditions and we haven't seen a new treatment made available in a decade. We need to see significantly more investment and recruit the next generation of leaders in research in order to deliver breakthroughs that could prove so vital to those affected by the condition.' 

 

Hugh Perry, chair of the MRC Neurosciences and Mental Health Board, said: 

'Science progresses through testing and re-testing previous research and sometimes overturning existing theories. Health advice always needs to be based on the best available data from the largest possible studies and this is even more important when the findings have implications for what we do or don't eat and drink.' 

 

  1. R. Clarke, D. Bennett, S. Parish, S. Lewington, M. Skeaff, S. J. Eussen, C. Lewerin, D. J. Stott, J. Armitage, G. J. Hankey, E. Lonn, D. Spence, P. Galan, L. C. de Groot, J. Halsey, A. D. Dangour, R. Collins, F. Grodstein. Effects of homocysteine lowering with B vitamins on cognitive aging: meta-analysis of 11 trials with cognitive data on 22,000 individuals. American Journal of Clinical Nutrition, 2014; DOI: 10.3945/%u200Bajcn.113.076349 
 

Serenoa
Posted: Tuesday, October 4, 2016 5:54 AM
Joined: 4/24/2012
Posts: 484


Not so fast. It looks like this study examined participants taking vitamin B compared to those taking a plecebo. And, it seems they already had dementia before the vitamin B intervention. The following study found that it took FOUR YEARS before and association between high homocystene and onset of demetia, so the benefits were derived by taking vitiamin B before the onset of dementia.

Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer's Disease

 "In our study population, an elevated homocysteine level at base line was related to a decline in the scores on the Mini–Mental State Examination, but only after a follow-up period of at least four years"

"The observed association appeared to be independent of age, sex, APOE genotype, plasma vitamin levels, and other putative risk factors for dementia and Alzheimer's disease. The prospective nature of this study and the strong association between newly diagnosed dementia and Alzheimer's disease and plasma homocysteine levels measured eight years before base line suggest that the elevation in the homocysteine level preceded the onset of dementia. Finally, subjects with a sustained elevation of plasma homocysteine had the greatest risk of dementia."

"plasma homocysteine levels are associated with carotid atherosclerosis and an increased risk of stroke.8,10 Atherosclerosis and stroke, in turn, increase the risk of clinical Alzheimer's disease.2,4 Hyperhomocysteinemia has been related to cerebral microangiopathy,44 endothelial dysfunction,45 impaired nitric oxide activity,46 and increased oxidative stress47 — all factors associated with the aging of the brain.48,49 Increased concentrations of homocysteic acid, an N-methyl-D-aspartate receptor agonist and a metabolite of homocysteine, may result in excitotoxic damage to neurons.50 Homocysteine promotes copper-mediated and beta-amyloid-peptide–mediated toxic effects in neuronal cell cultures51 and induces apoptosis in hippocampal neurons in rats."

 

 


Lane Simonian
Posted: Wednesday, October 5, 2016 10:16 AM
Joined: 12/12/2011
Posts: 5161


This is a really good find in terms of mechanism and the need to use certain antioxidants before the start of dementia (and to correct the record). 

The argument for combination rather than single antioxidant therapies appears to be a good one.

Abstract: Pauling suggested that responses to high-dose vitamin therapy were due primarily to small increases in response due to lack of complete saturation of enzyme targets. He also suggested that they may be due, in part to “local vitamin deficiencies” although the origin of such deficiencies were unclear. Ames suggested that such therapy might be explained by enzyme polymorphisms involving mutants with lowered Michaelis constants, and while this is an explanation in some cases, this mechanism does not explain any effectiveness of in the broader population of diseased patients. Responses to four vitamins advocated by Pauling can be best explained by the effects of these vitamins on lowering the nitric oxide (NO)/peroxynitrite (ONOO-) cycle, a possible generic mechanism for many different chronic inflammatory diseases. Ascorbate lowers three aspects of the central couplet of the cycle, acting as a peroxynitrite scavenger, restoring tetrahydrobiopterin (BH4) by reducing an oxidized form and inducing increased de novo BH4 synthesis. "e nicotinamide form of niacin inhibits poly adenosine diphosphate-ribosylation, thus sparing nicotine adenine dinucleotide (NAD), as well as supplying niacin for synthesis of NAD/NADH, thus helping restore mitochondrial function in NO/ONOOcycle diseases. Folate in the form of 5-methyltetrahydrofolate is a potent peroxynitrite scavenger, thus lowering the NO/ONOO- cycle in that way. Vitamin B12 as hydroxocobalamin lowers the cycle by acting as a nitric oxide scavenger. Each of these responses involve mechanisms that are distinct from the classic functions of these vitamins and they all require supraphysiological levels in order to be effective. Thus they provide explanations for each of the four high-dose therapy vitamins that Pauling suggested and for Hoffer’s responses to niacin therapy.

Pages 895-903
Fumihiko Yasuno, Satoshi Tanimukai, Megumi Sasaki, Chiaki Ikejima, Fumio Yamashita, Chiine Kodama, Katsuyoshi Mizukami, Takashi Asada 
Combination of antioxidant supplements improved cognitive function in the elderly
Abstract: Although nutrients or agents with antioxidant properties were reported to show a preventive effect on cognitive decline in animal studies, epidemiologic data on select antioxidants have shown conflicting results. We investigated whether a combination of antioxidants from supplements is effective for the improvement of cognitive function of elderly. Forty-one subjects from a community dwelling aged 65 years and older took supplements containing n-3 polyunsaturated fatty acids (n-3 PUFA), lycopene, and Ginkgo biloba extracts (GE) daily for 3 years. The data of 622 subjects without supplement intake were used as control. We investigated the changes in cognitive function during a 3-year follow-up. We also investigated the influence of apolipoprotein E (APOE) genotype on the effect of antioxidants. We found that a combination of antioxidants improved cognitive function of aged persons after 3 years. Our present study also indicated this improvement in cognitive function with supplement intake in both APOE4 non-carrier (E4-) and APOE4 carrier (E4+) groups. Especially, in E4+, we found a large effect size of the improvement of cognition. When multiple antioxidants are used in combination, they protect against vulnerability to other agents and synergistically potentiate their antioxidant properties. These synergistically potentiated antioxidant effects of agents contribute to the improvement of cognitive function.

http://www.j-alz.com/issues/32/vol32-4.html (there are a couple of other interesting abstracts here).

Certain antioxidants may delay or prevent the onset of Alzheimer's disease and improve cognitive function in people with mild cognitive impairment.  Others may slow down the progression of Alzheimer's disease or partially reverse certain aspects of cognitive decline in individuals with Alzheimer's disease (object recognition, location memory--remembering home, repetitive memory, for instance).