Prof. Carol Brayne
Carol Brayne 教授
We all hope to have prevention. Medical practitioners treat people, and we deal with diseases and disorders when they're present, but most people understand that it's better to think about prevention.
Well, what do we mean by prevention? We mean trying to stop something, a disease, happening at all, and in ageing we know that dementia becomes very much more common and there's a sense that it might be inevitable, but there's also evidence that it might not be as inevitable as we had thought. So although the increase in dementia is very related to age in our populations, there is some evidence that we can reduce our risks of developing dementia, so in some terms that could be viewed as prevention.
So we understand that dementia, particularly in the oldest old where it's most common, is a mixture of classical Alzheimer's type, which most people have heard of, but also of vascular changes. And that's related to earlier life, what we call non-communicable diseases, which includes things like heart disease and diabetes. Now we've got very good understanding of how to prevent those disorders in the population and those relate to both individually-based prevention but also predominantly to societally-based activities or interventions, such as the smoking bans and trying to reduce excessive alcohol and so on. So these are all factors which can improve health earlier in life and reduce the risk of the risk factors for dementia, and so we have pretty good evidence on those.
I've been working in the field of dementia research for 30 years and for decades I thought that we could not reduce our risk of dementia because it was so closely associated with age. But, when we did the research that suggested that - well, which showed that dementia prevalence, that is the proportion of people who had dementia at any given age, has gone down, I realised that we do have the potential to reduce our risk. It does not mean that we will eradicate dementia because what it means is that we still have a lot of dementia in the oldest old because age is such a powerful risk factor. Because we're living longer, we have more people in the oldest age groups. So we can't prevent all dementia but we might reduce our risk at particular ages.
Researchers for decades have been looking at the risk factors for dementia in a variety of different ways. A lot of these have been what we call cohort studies, which is following people over time who start out without dementia and then, having examined what their risk factors, or what might be risk factors, are at baseline, we then follow them up over time and identify who gets dementia or who meets diagnostic criteria for dementia over time and who doesn't.
Those studies have looked at risk factors close to the expression of dementia and have looked at midlife risk factors as well, and also life course risk factors. Putting all of that together requires systematic reviewing and there have been several exercises in systematic reviewing of the risk factors for dementia in the last decade. One of those identified seven risk factors and it was a very rigorous look at the world literature and it came up with seven, and they included things from across the life course, such as low educational attainment, midlife obesity and hypertension, and then depression and diabetes, and so-called lifestyle behaviours such as smoking.
That exercise has been done in the US as well, as well as the Lancet Commission, and the exact risk factors have been sort of changed a little bit, so there's the addition recently of midlife hearing loss in particular.
If you put all of those risk factors together and try to understand how they operate in different populations, looking at the exposure of the population to the particular risk factors, you can calculate what proportion of people might - what proportion of dementia might be attributed to that risk factor or those risk factors. Now the risk factors cluster. Once you take that clustering into account, all of the different exercises come up with roughly a third of dementia that might be prevented if we assume a causal relationship between the risk factors and dementia. So the ultimate message from those analyses is that, if we pay attention to those risk factors across the life course, we might reduce dementia by about a third over time.
Speaking from a public health perspective, the idea of removal of one risk factor doesn't work terribly well in populations. What we need to do is look at the clustering of the risk factors and see which sectors of the population are at risk with different profiles of those risks, and what is our knowledge about how to address those risks in those populations and in the population at large. So, for example, smoking has reduced enormously and perhaps that is a single risk factor example where we have had a huge effect, but that has been done through legislation and whole-society action. But something as complicated as midlife obesity, midlife hypertension and consequently stroke and so on are much more complicated. So unless we create environments in which we can be healthy and optimise our ageing and our brain health, we're unlikely to be able to affect those particular risks in a big way for the populations.
Not only are risks very complicated in the way that they interact with each other and the behaviour - so we have behaviours, we have disorders and diseases which all interact and they're all our individual profile of risk, but also, when we look at people who have dementia, and it's most common in people aged 80 and over, so if we look in the brains of people who have died with dementia as well as the people who haven't died with dementia, we see that everybody, by the age of 85, 90, has got a mixture of pathologies and changes in their brain, which include atrophy and vascular changes and changes which could be associated with Parkinson's disease as well as the Alzheimer's disease changes, and it's rare to find somebody with a brain at the age of 100 who doesn't have at least some of these pathologies, and the relationship of those with the expression of dementia, with whether the person had dementia, becomes more complicated in the oldest age group.
There is very good evidence now from a variety of different studies, from animal studies through to human studies through to population studies, that there are factors that protect us from dementia, even when we have, say, the neuropathologies that are thought to be classically associated with dementia. So there is good evidence that we can protect the population and protect individuals to some extent, or reduce their likelihood of experiencing dementia during their lives, and these factors probably need to be addressed at different times in the life course.
So we have evidence from early life, from midlife and from later life of the kinds of things that appear to protect us from dementia. We can improve aging, we can improve brain aging and we can probably reduce the amount of dementia at any given age and we can reduce that frailty right at the end of life that is almost inevitable for all of us, but maybe reduce the time that we have to experience that through population health activities and a balance of individual and public health, if you like, actions.