One fear that nags us all – that we will lose our mind as we get older – became more real earlier year. Until then, the danger date had generally been agreed to be post-65, but a new study revealed that the decline could be spotted as early as 45.
Is there anything we can do about it? A large study of British civil servants, reported in the British Medical Journal, found that the reasoning powers of both males and females aged 45 to 49 dropped by 3.6 per cent over the next ten years.
The good news, according to the authors, was that there is something you can do about it.
Unfortunately their recommendation was remarkably unhelpful and showed up a serious problem with the mainstream approach to Alzheimer’s. There is emerging evidence, they said, that “what is good for our hearts is also good for our heads”; that a healthy lifestyle, particularly cardiovascular health, could cut your risk of a failing memory.
This sounds sensible: eat well, exercise, don’t smoke. But it is misleading in several important ways. It is so general and bland as to be useless. It completely ignores the one specific lifestyle option that is backed up by better evidence than anything else, and it gives no indication that some experts believe that all lifestyle options are a waste of time. Welcome to the complicated world of dementia.
Normal brain shrinkage
First, a clarification. A slight decline in cognitive abilities is normal as we age, along with poorer eyesight, lower hormone levels, weaker bones and so on. But this is not the same as Alzheimer’s or dementia, which are far more savage and have subtly different patterns of brain damage.
Normally, older brains shrink by an average of 0.5 per cent a year; a bit faster than those Whitehall youngsters but far slower than the 2.5 per cent of an Alzheimer’s patient. Mild cognitive impairment (MCI) is an in-between state, with shrinkage of around one per cent. On average, half of those with MCI go on to develop full-blown Alzheimer’s.
So can a healthy heart stop your brain shrinking? A recent study in the American Journal of Nutrition found that the more closely you follow a healthy Mediterranean diet (lots of fruit and vegetables, healthy fats, wine, fish, nuts and beans), the lower your Alzheimer’s risk.
A recent article in Nature concluded that regular dancing, with its combination of exercise, having to think fast and social interaction, was as good a way of keeping your brain in shape as any. Both of these pieces of advice are far more specific than the Whitehall study.
They are contradicted by the National Institutes of Health in America. In 2010, it analyzed the evidence for the lifestyle approach and concluded that there was no strong scientific evidence that any of it worked.
Bizarrely, what is ignored by both these is the one study involving diet that has better evidence than any other. It was run by Professor David Smith at Oxford, and ticked all the evidence boxes: it was randomized, placebo controlled, followed 270 patients diagnosed with mild cognitive impairment (MCI), and was conducted over two years. (See: Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment.)
Brain size at the beginning and end of the study was measured with a brain scan. The results were remarkable. Brain shrinkage of some of the treated patients more than halved compared with the placebo group: a drop of 53 per cent, down to almost normal levels for healthy ageing.
So why on earth do we hear almost nothing about this result? A plausible explanation is that it doesn’t involve a drug that could earn billions for pharmaceutical companies. The patients were treated with three B vitamins – folic acid, B12 and B6 – which cost only pennies a day. In addition, they were given very high doses (several hundred times above the recommended daily amount, in the case of B12). This challenges the standard advice that you can get all the vitamins you need from a healthy balanced diet.
The test for risk
The reason B vitamins seem to work is that they reduce the level in the body of an amino acid called homocysteine, high levels of which are linked with a raised risk of both Alzheimer’s and heart disease. Importantly, the only people who benefitted were those whose homocysteine level was more than 13. This gives much greater confidence that we are dealing with a real effect rather than with statins, where the claim is that, whatever your level of cholesterol, bringing it down is beneficial.
It also provides a useful marker for who is at risk: have a homocysteine test and, if your level is more than 13, B vitamins will not only cut your risk of Alzheimer’s but most likely of heart disease too. So here we have something that is both a marker for risk – something all Alzheimer’s researchers say they are desperately searching for – and a treatment, which is also desperately needed.
Yet it is effectively ignored because there are no drugs that lower homocysteine. This suggests that relying on drugs to deal with all our health problems is not in the consumers’ interests.
Of course, the study needs to be repeated. And it doesn’t prove that it will stop people developing Alzheimer’s, only that it slows actual shrinkage among half of the people who will go on to develop it.
But who benefits from ignoring it? And how long should you or I wait for more evidence of a cheap treatment with little risk of damaging side effects? Let us decide before our brains shrink too much to allow us to do so rationally.