By Larry W. Chambers, Madeline Smith
Contrary to popular belief that dementia is inevitable, steps can be taken by individuals and societies to reduce the risk of dementia and, simultaneously, increase brainability.
Research published in the last decade has turned upside down what has long been taught on this subject – making it more important than ever for us to review what is known about the brain and how it changes as we live longer.
Doctors who graduated before 2000 were taught that the brain only developed during childhood, but that after age of 20 all that happened was that brain cells died off. This was the theory that won Professor Santiago Ramon y Cajal the Nobel Prize in 1906; however, we now know he was wrong. There is continued debate over whether we can renew brain cells in adult life as mice do, or as our own kidney and liver cells renew, but we do know that we can develop new brain circuits. This is called neuroplasticity, and there is evidence now that new circuits can be formed at any age if the brain is asked to do so, either by external stimulation or by physical activity.
Dementia is not a disease like rheumatoid arthritis that can be confirmed with a blood test. It is better described as a condition which can be observed by people, including people without a medical degree. There are four changes that indicate that dementia is becoming more conspicuous and which need to be taken seriously. These include:
· failures of self-care, for example failure to wash or get to the toilet in time with apparent disregard for the consequences;
· failure to look after one’s home properly, such as leaving the gas or water on;
· problems with driving, and problems with money.
These signs of dementia are different from normal aging. It is unhelpful to talk about pre-dementia or MCI (mild cognitive impairment) although people, including respected academics, do use these terms. Instead, the emphasis should be on the fact that dementia is different from normal aging.
Some changes occur in the brain as a result of the normal aging process, but these do not cause major problems. For example, people notice memory slips as they live longer — an inability to remember where they put their keys or the name of someone they met yesterday or the name of a book that had an influence 20 years ago — but these memory slips are not signs of early dementia, they are problems with filing and recovering pieces of knowledge.
Aging is too often blamed for the changes taking place in our bodies and minds when, in actuality, the normal biological process of aging does not have a substantial effect on the brain. We now know that three other processes are important in determining what happens to us and how quickly we decline. First, there are changes in the way the brain works due to loss of what could be called brain fitness. As we live longer, our brain is often challenged less. For example, if we retire from a challenging job and do not substitute that challenge with other challenging activities, our brain becomes less fit. There are now techniques for examining how the brain works, and these are revealing how new circuits form when the brain is asked to perform a new task. The task may be physical, such as dancing, or cognitive, such as learning a language, or a combination of cognitive and emotional, for example chairing the committee of a voluntary organization. This runs contrary to ageist assumptions that as people live longer, they need less stimulation and are less capable of responding to stimulation.
Second, Alzheimer’s diseases are only one cause of dementia. Many diseases affect the brain other than Alzheimer’s disease, secondary cancers in the brain, for example. Recent research highlights the contribution of vascular causes of dementia, namely dementia due to impairment of the blood and oxygen supply to the brain. Risk of vascular dementia and other causes of dementia can be changed so the risk of dementia can be reduced, by at least a third.
Aging, fitness and disease are well understood. So too are the factors that affect the mind, the way we think and feel. This is affected not so much by aging as by the attitudes and behaviours of other people, particularly what could be called ageism – consistent under-expectation of what people in their 60s, 70s, 80s and 90s can achieve based on incorrect beliefs, for example, that all intellectual functions deteriorate with age, whereas some improve. New research shows that problems formerly considered to be entirely due to the aging process, such as memory loss, hearing decline, and cardiovascular events, are instead influenced by the negative age beliefs that dominate our society.
What we need is a cultural revolution to rethink aging, and to find out how we can increase our brainability whatever our age, and how we can reduce our risk of dementia. There is no guarantee, of course, because Alzheimer’s disease remains the single most common cause of dementia and we do not know yet how to prevent or treat Alzheimer’s disease, but there are many other causes, and therefore many other actions, that can be taken by individuals and society at large.
What can individuals do? Find a friend and explain to them the difference between dementia and normal aging.
What can the community do? Society needs to educate all members about the difference between dementia and normal aging, the cause of dementia, and the fact that, in the words of The Lancet, “… it is never too early and never too late to reduce the risk of dementia.”
This article is a summary of Larry and Madeleine’s December 2021 presentation on “How to Reduce your Risk of Dementia” for the Learn and Live Program series held at the Niagara-on-the-Lake Library. Larry W. Chambers has authored 200 articles and books concerning disease prevention (e.g. dementia), quality improvement in long-term care homes and innovative approaches for continuing professional development. He is research director of the Niagara Regional Campus, Michael G. DeGroote School of Medicine, McMaster University. Madeleine Smith is a medical student at the Niagara Regional Campus, Michael G. DeGroote School of Medicine, McMaster University.