B-vitamin therapy looks promising for staving off Alzheimer’s disease

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Last year, I reported on research which found that supplementation with the vitamins B6, B12 and folic acid had been found to reduce the brain shrinkage (brain atrophy) in individuals suffering from ‘mild cognitive impairment’ (impaired brain function not severe enough to be labelled ‘dementia’) [1]. Subsequent research found that this treatment regime actually improved brain functioning [2].

The presumed mechanism involved here concerns the amino acid homocysteine – raised levels of which are associated with an increased risk of dementia. Vitamin B6 and B12 and folic acid have the capacity to lower homocysteine levels in the body. Interestingly, the previous research found that supplementation benefitted those who, prior to the study, had elevated levels of homocysteine, but not those with normal levels. This finding does support the idea that elevated levels of homocysteine can damage the brain, and that bringing levels down helps preserve brain functioning.

This week saw the publication of another follow-up study regarding this research. In this study, the impact of supplementation on the brain areas particularly affected by Alzheimer’s disease including the grey matter (outermost part of the brain) in a part of the brain known as the medial temporal lobe [3]. Compared to people taking placebo (inactive pills), atrophy here in those taking B vitamins was reduced by 90 per cent.

In summary, the research shows:

  • B12, B6 and folic acid found to reduce brain atrophy in those with elevated levels of homocysteine
  • In these people, B12, B6 and folic acid supplementation was found to improve brain function
  • In these people, B12, B6 and folic acid supplementation was found to dramatically reduce brain shrinkage in the part of the brain most affected in Alzheimer’s disease

Lead researcher in this work, Professor David Smith, is listed as an inventor on patents held by Oxford University for B vitamin formulations to treat mild cognitive impairment and Alzheimer’s disease. However, taking the research at face value, what we have here is evidence that B-vitamin supplementation is a legitimate strategy for those suffering with mild cognitive impairment and raised homocysteine levels (the level of homocysteine used as the threshold for ‘raised’ homocysteine in these studies was 11 µmol/L).

What is strange about this research, I think, is how little impact it has had in some quarters of the medical and scientific communities. UK journalist Jerome Burne has been following the story throughout, and wrote this week about this latest study on his blog. Jerome, in his post, also examines some of the political reasons which might explain why the reaction to this research which has enormous implications has been somewhat lukewarm. You can read Jerome’s post here.


1. Smith AD, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial. PLoS One 2010;5(9):e12244.

2. de Jager CA, et al. Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial. Int J Geriatr Psychiatry. 2012;27(6):592-600

3. Douaud G, et al. Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment. PNAS published 20 May 2013 [hr]

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