The Latin word, dementia, chronic loss of memory often accompanied by emotional changes, has been in use in English since the late 17th century but has probably come into general consciousness in the last 100 years, over which period many more have lived long enough to develop it. In the late 1930s, average life expectancy was 58 for men and 65 for women, so initially dementia appeared more commonly among women. However, the condition is now common enough in both sexes for most people in the UK to know of a family member who developed it. And with increasing awareness of the condition comes increased curiosity about its causes. Why has it become so common? Can we stop it happening to us?
To put complex matters at their simplest, there are only two causes of disease: genetic and environmental. Humans have recognised this since we became, well, humans with our cognitive abilities. In earlier times we thought of genetics as imbalance of the humours – born with too much blood, bile or phlegm, often inherited and giving us sanguine, choleric, melancholic or phlegmatic characteristics. Not as daft as it sounds, and sooner or later specific combinations of genes will be discovered that can be substituted for these archaic terms.
Along with this theory, an early concept of the environment was that demons lurked there to attack us and cause us to fall ill – influenza got its name from the belief that it came from the influence of the heavenly bodies. Miasma was the name given to something sinister in the air that caused infection (malaria got its name from this concept) and then water-borne disease was proved in the case of cholera and typhoid fever in the mid-19th century. Then came the discovery of microscopic living creatures and the work of Louis Pasteur and Robert Koch showing the disease-causing role of micro-organisms more generally in the environment in the 1880s.
I used to play a little game with medical students called 'spot the hazard' as we walked through a workplace, with the intention of showing how to detect things that could harm health. I explained that hazards could be chemical, physical, biological and psychological and that, having identified them, we could try to estimate the risk to us or to our patients that they might entail. Try it as you go to work and spend your day, at home or elsewhere. Imagine how those risks would change were you a lively teenager, disabled or a doddery old person. It gave us plenty to discuss and for some it must have been a pleasant break from learning about genetic mutations.
I don't want to make you over-cautious or neurotic and, unless you are a young adventure seeker or inclined to drink too much, most risks (like crossing a road) turn out to be small and worth taking if the benefits are clear. But for me, this way of thinking led me to ask what environmental factors might influence the risks of dementia at a time when most serious research in the subject seemed to be looking for genetic factors that change brain biology. Unfortunately, we can't do much to change our genetic make-up, but we can do a lot to reduce environmental risks. Could the environment affect the brain? Of course, we already knew it could.
As a young doctor, I had worked in a neurology clinic and saw ex-boxers with dementia – we called it punch-drunk syndrome or dementia pugilistica. You will have heard of the recent death of Ken Buchanan, perhaps the most celebrated Scottish boxer and, some 20 year ago, of Billy Liddell, probably our most famous footballer, famed for the power of his header. Both sadly died with dementia.
The branch of medicine that investigates environmental risk factors for disease is called epidemiology. It seems rather unglamorous compared to genetics or neuroscience, the main ways of studying the brain, since it relies on asking large numbers of people lots of questions and analysing the answers in a computer. But those answers can give very important clues about possible causes of diseases and lead to understanding how to prevent them, to reduce people's risks.
About 20 years after I first saw those poor punch-drunk boxers, I decided to take an interest in neurology, having been busy trying to understand lung diseases previously. It started with being asked to see a patient who believed, rightly as it turned out, that his nervous disorder had been caused by paint fumes, from organic solvents. With my colleagues we started to look at the long-term effects of solvents and found lots of interest, but one quite incidental finding was that being knocked unconscious significantly increased the risk of Parkinson's disease.
Looking at research by others, it became apparent that heavy solvent exposures had also been associated with increase in risks of the three other most important and ultimately fatal neurological diseases: motor neurone disease, multiple sclerosis and dementia. And also repeated head injury has been associated with them all. It seems there is some common factor across these very different diseases and different environmental factors, so now we enter the exciting world of speculation and the formulation of hypotheses.
Although those four diseases are very different and affect different parts of the central nervous system, they share environmental risk factors. This suggests that while genetic factors alter one's susceptibility, the environment may trigger the disease. This is now established in multiple sclerosis, for which certain gene combinations substantially increase the risk from solvent exposure and from smoking. What about dementia? Do we know enough about environmental risk factors to prevent some of it or to reduce our own risks?
The most obvious risk is from head injury, so any sport in which head trauma is common should be avoided. In boxing, the whole purpose is to cause brain injury and it is sheer folly to encourage young people to take part in it. Heading of a football is also a form of head trauma and is slowly being discouraged at junior level, but the brain can be damaged by repetitive trauma at any age and professional footballers must accept an increased risk of dementia until heading is banned.
Rugby at professional level will I fear soon be recognised as an important and increasing risk factor – even at the lowly level I played, I was knocked out twice, and since then the changed laws on tackling have facilitated high impact head trauma. The attention given to players after the injury may help a bit but the laws must be changed to prevent the impact in the first place. In my day, tackling above the waist was forbidden and clashes of heads were rare.
Most of you will not play dangerous games and if you did there is no point regretting it. There are other less well-known risk factors for dementia to avoid, and some may surprise you. Obesity, diabetes, high blood pressure, smoking – they sound familiar, as they are also risk factors for heart attacks and they are often combined in the same person. Strangely, exposure to high levels of air pollution, such as we were in the 1950s and others still are in developing economies, is now recognised to increase risks. Depressive illness and episodes of delirium in infectious disease, repeated exposure to solvents or pesticides, and high alcohol intake are also likely risk factors for dementia. Dealing with these is partly up to us and partly dependent on good medical care, early detection and so good care of diabetes, high blood pressure and depression are important.
On a personal basis, a Mediterranean diet, avoiding smoking, and regular physical and mental exercise have been shown to reduce risks. Some things are useful to know if you are bringing up children – a good diet aside, regular physical exercise, education beyond age 16 and learning a second language also reduce their future risks.
All this advice is based on epidemiological studies that have shown statistically significant effects in populations, but the influence of each in an individual may be quite small. Some of them provide opportunities for doctors to reduce the burden of dementia on society, for example by careful management of febrile illness, diabetes, depression and hypertension. Some provide further incentive to sensible people to modify their bad habits and lead healthier lives. But all provide intriguing clues to the answer to the question: what other than genetic risk causes dementia?
It has been the popular medical view that, aside from some rare strongly genetic types of dementia, there are two common forms: Alzheimer's disease and vascular dementia. The first of these is thought to be due, in simple terms, to accumulation of a toxic chemical, amyloid in the brain, the second to narrowing of blood vessels leading to the brain. But the risk factors for both types seem to be the same, so researchers are beginning to consider if both may be a consequence of effects of inflammation on blood vessels, in one case the larger arteries and in the other the smallest vessels at the level they actually come into close contact with the brain cells, the blood-brain barrier. Perhaps the accumulation of amyloid is secondary to this inflammation? We don't know but, intriguingly, statins, which many of us who have suffered heart problems are taking regularly, have been shown to be associated with reduction in the risks of dementia.
If this positive epidemiological evidence accumulates, widespread prescription of statins may prove to be a cheap and effective public health measure to prevent dementia, as they are for heart attack.
I remember the moment, as a final year student in 1956, that I became fascinated by human ecology. It was a time of hope, following the development of the NHS and Welfare State, that we would repair our war-ravaged ecology and life would get better. It did, until sadly much started to unravel with the political changes of Thatcher and Lawson. Now we see an increased gap between rich and poor, decreasing life expectancy among an important sector of the population, and growing dissatisfaction with professional politicians who don't understand their powerful influence on the ecology and concern themselves with self-perpetuation rather than their first duty, the welfare of the people.
Anthony Seaton is Emeritus Professor of Environmental and Occupational Medicine at Aberdeen University and Senior Consultant to the Edinburgh Institute of Occupational Medicine. The views expressed are his own
