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Monday, November 25, 2013

B-vitamins, brain shrinkage and Alzheimer's disease

Globally, we are approaching a diagnostic rate for Alzheimer’s disease of about I confirmed case per second. This will quadruple by 2040 and by then 70% of all cases will be living in developing and emerging economies. These are average values and although a 100% increase can be expected on average by 2040, this will be as high as 300% in China and India. At present, the costs of Alzheimer’s disease to society in the EU is €160 billion and that would suggest, by extrapolation, a global cost in 2040, of € 1.6 trillion. This, in today’s terms is equivalent to the combined GDP of Ireland, New Zealand, Israel, Singapore, Sweden and Nigeria. That’s a lot of dosh and suffering by any measure.

For many years, researchers in nutrition have been interested in studying the link between Alzheimer’s disease and dietary patters and the two classes of nutrients of interest have been fats, specifically a protective role for omega-3 fats and B-vitamins, specifically a protective role for folic acid and vitamin B12.  The data in this area are strongly supported by epidemiological studies, which use blood markers of these nutrients and the progression on dementia. However, as I pointed out in a previous blog (“Brain food ~ get it early” 18th of June, 2012), when dietary intervention studies are used to verify the associations found between diet and dementia, the outcomes have been extremely disappointing and this, I suggested may be due to a strong link between certain genetic factors, diet and Alzheimer’s disease.

A recent paper published in the Proceedings of the National Academy of Sciences[1]examines the link between B-vitamin supplementation and the destruction of grey matter material from those parts of the brain specifically associated with Alzheimer’s disease. An initial study was carried out over two years with 156 subjects (mean age of 77 years) with mild cognitive impairment. Half the group received a placebo while the other got a B-vitamin supplement (folic acid, vitamin B12 and vitamin B6). The initial study showed that whereas brain size shrank in both groups, B-vitamin group had, overall, a reduction in the rate of shrinkage of grey matter. This paper now moves the same research from total brain shrinkage to the loss of grey matter specifically in those regions of the brain associated with Alzheimer’s disease (AD) In fact, the rate of shrinkage of AD-sensitive grey matter was 3.7% in the placebo group compared to just 0.5% in those receiving the B-vitamin supplement.

Homocysteine is a natural part of our blood biochemistry and high levels of homocysteine have been associated with adverse health outcomes and, classically, low levels of plasma folic acid and vitamin B-12 lead to high level of blood homocysteine. In this study, the authors considered the effect of B-vitamin supplementation on individuals with initially high or low levels of plasma homocysteine. They found that if the levels of homocysteine were elevated at the outset, the effects of B-vitamin supplementation was amplified among individuals with elevated homocysteine (5.2% brain loss in the placebo group with only 0.6% loss in the B-vitamin group).

This paper doesn’t use the usual “soft” end points used to measure cognitive decline. Instead it used structural imaging techniques of those regions of the brain sensitive to AD atrophy as an outcome measure. This is a very interesting finding and even a strong indication that habitual high intakes of certain B-vitamins will reduce the rate of neuro-degeneration from mild cognitive impairment to AD, specifically, in those subjects with high plasma homocysteine levels. However, it isn’t definitive proof of such a link. To begin to build of a supporting body of evidence, one would need to prove that accelerated (rate to be defined) shrinkage (extent to be defined) of AD sensitive regions of the brain are indeed associated with the development of Alzheimer’s disease in subject’s with specific biochemical (such as low homocysteine levels on blood) and genetic (gene SNP’s to be determined) attributes. Then we would have a robust biomarker. With that established then all manner of dietary and drug interventions could be used to study their outcome on the biomarker and, by implication Alzheimer’s disease itself.

One thing is sure. Alzheimer’s disease, like other neurodegenerative diseases, is likely to have a significant nutritional dimension.

[1] Douaud et al (2013) PNAS, 110, 9523-9528

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