The BBC story says:
Certain B vitamins - folic acid, vitamin B6 and B12 - control levels of a substance known as homocysteine in the blood. High levels of homocysteine are associated with faster brain shrinkage and Alzheimer's disease.
The study authors believe it was the B vitamins' effect on levels of homocysteine that helped slow the rate of brain shrinkage.And the size of the effect surprised the authors of the paper.
"It's a bigger effect than anyone could have predicted," he said, "and it's telling us something biological.
"These vitamins are doing something to the brain structure - they're protecting it, and that's very important because we need to protect the brain to prevent Alzheimer's."It's nice to see the focus being taken off genes, and put on environmental risk factors that may lead to this devastating disease. This was a small and fairly short-term study, and of course the authors say that more research is needed, but it does sound promising, and perhaps we should all think about taking B vitamins with our cereal.
But hold on.
A paper that seems to have gotten a lot less notice (we wonder why!?) is one that appeared online ahead of print in Neurology on Sept 22. This is a report of another double-blind controlled study of 299 men over 75 given either folic acid and vitamins B6 and B12, or placebo, and who were assessed for signs of dementia initially, at 2 and at 8 years. This study found that treatment had no effect on cognitive function in men, even while lowering homocysteine levels by 22.5%.
They point out that high homocysteine levels (tHcy) have been associated with dementia, and that levels have been shown by other studies to be lowered by 20% or so with B vitamins, as the PLoS paper describes, but that it's not clear whether this link is causal. They also point out that this link has been studied before, but it has not been successfully demonstrated that B vitamins can affect risk of dementia. Why not?
Observational studies have consistently linked high tHcy to cognitive impairment, but the results of randomized trials have thus far failed to show any obvious benefits associated with tHcy-lowering therapy. These conflicting findings may be due to bias and confounding in observational studies, inclusion of prevalent cases of cognitive impairment in some trials, lack of power to measure small but important treatment effects, insufficient treatment duration,and recruitment of excessively healthy volunteers.Ah, our old friends bias and confounding.
And, outcome measures differ between studies, which may affect conclusions. In just these two studies alone, one used a measure of cognitive impairment and the other brain size (though the authors state that they will publish on their cognitive results at a later time). The paper in Neurology concludes by suggesting that "elevated plasma homocysteine is not a risk factor but merely a marker that reflects underlying common processes responsible for both dementia and high tHcy, and that homocysteine-lowering treatment with B-vitamins does not affect the long-term cognitive function of people at risk."
We will certainly be hearing more on this subject. But we wouldn't buy stock in B vitamins yet.