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Current Understanding of Alzheimer's Disease and Other Neurodegenerative Diseases, and the Potential Role of Diet and Lifestyle in Reducing the Risks of Alzheimer's Disease and Cognitive Decline
Charles S. Brennan1,2,3,4, Margaret A. Brennan1,2,4, W.M.A.D. Binosha Fernando5,9 and Ralph N. Martins5,6,7,9
1 Department of Wine, Food and Molecular Biosciences, Centre for Food Research and Innovation, Lincoln University, PO Box 85084, Lincoln, Christchurch, New Zealand
2 School of Food Science, South China University of Technology, Guangzhou, China
3 Riddet Institute, Palmerston North, New Zealand
4 School of Food Science, Tianjin University of Commerce, Tianjin, China
5 School of Medical and Health Sciences, Centre of Excellence for Alzheimer's Disease Research and Care, Edith Cowan University, Joondalup, WA, Australia
6 Department of Biomedical Sciences, Macquarie University, Sydney, NSW, Australia
7 School of Psychiatry and Clinical Neurosciences, University of Western Australia, Perth, WA, Australia
8 KaRa Institute of Neurological Diseases, Sydney, NSW, Australia
9 Australian Alzheimer's Research Foundation, Ralph and Patricia Sarich Neuroscience Research Institute, Nedlands, WA, Australia
This book is intended to give an upâtoâdate overview of what is currently known about neurodegenerative diseases, focusing particularly on Alzheimer's disease (AD). Current and developing diagnostic tests are described, and the pathological relationships between AD and other conditions now believed to be risk factors for AD are also described. In particular, we discuss cardiovascular disease, obesity, insulin resistance and type 2 diabetes, focusing on abnormal lipid and sugar metabolism linked to these conditions, and how this is related to AD risk. We provide evidence that improved diet and exercise may reduce AD risk, not just the risk of the other conditions mentioned above. Hopefully this book will provide some food for thought concerning easily adoptable nonâpharmacological methods to reduce AD risk, which would need to be adopted at early preâclinical stages of the disease.
Diet and health are intrinsically linked, and the effect of dietary intakes on our health has been researched and documented for millennia. The consumption of protein, fat, carbohydrates, vitamins and minerals is required for our physiological function. Certain foodâbased chemicals â bioactive compounds â yield health benefits beyond their mere chemical constituents, and can modify the biological functionality and health of our cells. These bioactive compounds may help enhance repair of our bodies from injuries, mediate the risk of certain diseases (cancer, coronary heart disease) through altering the physiological functions of our cells and organs. There is strong public awareness in terms of the old adage âyou are what you eatâ, however the information available to the public ranges from scientifically based research, to traditional dietary remedies, to dangerous fad diets. There is also a plethora of food products that have been designed by the food industry to provide consumers with foods or supplements designed to combat all sorts of illnesses and disorders.
We have long known that there is a connection between the overâconsumption of calories and weight gain, particularly fats and carbohydrates. For example, an excess of refined carbohydrates has been associated with overweight, obesity, type 2 diabetes and a number of metabolic disorders and now also, as described in this book, neurodegenerative diseases such as AD and cerebrovascular disease. However, despite this knowledge, and despite the introduction of numerous public health intervention programmes by governments and medical bodies, the percentage of the population which can be classified as overweight or obese continues to rise. Though there is research evidence that some genetic traits predispose certain people to easier weight gain, leading to obesity, this rise in obesity is believed by most to be mainly a result of increased calorie intake and reduced calorie expenditure.
Recently there has been an increased interest in the role the food industry has played in the production of modern food materials. Researchers and popular writers alike are keen to blame the food industry for today's nutritional problems by suggesting that modern food processing techniques produce what some people call highâcalorie, energyâdense, nutrientâpoor foods, and it would be foolish to ignore the fact that the food industry has played a part in the situation we find ourselves in. If we are consuming more calories as a population than we were 20 or 50 or 70 years ago, and if many of the foods consumed are highly processed, then this has a double impact on our nutritional status. Combine this with the fact that most of us are becoming more sedentary in our work and social lives, then the balance would be that we will be prone to storing excess calories. As described in this book, overweight and obesity as well as high consumption of refined carbohydrates lead to insulin resistance, type 2 diabetes and cardiovascular disease, which are in epidemic proportions in western countries. There is a train of thought that suggests that this overconsumption of calories is a âwesternâ problem; however, the situation is manifesting itself to be a global problem, with dramatic increases in Asian countries in recent years (for instance, rapid rises in obesity and diabetes levels in China, Malaysia, Singapore and Taiwan, to name a few).
Fat and lipid metabolism has been studied at length in relation to cardiovascular health, and more recently this topic has become important in AD studies. A few decades ago, all fats were regarded as unhealthy, and a high fat intake, particularly cholesterol, was considered to be the main dietary problem when taking into account the increasing rate of obesity, hypertension and cardiovascular disease in western countries. This led to the food industry generating products that were low in fat. However, to compensate on flavour, these foods often contained higher sugar and salt levels than previously. More recent research indicates that cholesterol is not the main problem, that longâchain saturated fat is a greater problem than cholesterol, and that high sugar intake from carbonated drinks, confectionery and processed foods has only exacerbated the increasing obesity level. Furthermore, lifestyle changes [1] have created a demand for more convenience foods, and foods with a long shelf life. These foods are generally more highly processed than those which were available 30â70 years ago. There is also scientific research which indicates that food processing affects the structure of the protein, fat and carbohydrate components (including sugar in the carbohydrate fraction) in foods. These changes may have led to longer shelfâlife, or made the foods more desirable, however many have a high salt or high sugar content, and may contain undesirable fats such as transâfatty acids. In addition, our intake of essential fatty acids has changed with the advent of processed foods and other western dietary changes. The intake of essential polyunsaturated fatty acids, in particular the omegaâ3 and omegaâ6 fatty acids, has considerable influence on our brain health, levels of inflammation and brain function, yet our intake, and the ratio of omegaâ6 : omegaâ3 fatty acids has changed over the millennia. There is evidence that we evolved on a diet with a ratio of omegaâ6 : omegaâ3 fats of approximately 1 : 1, yet a western diet has a ratio of approximately 15 : 1, and omegaâ6 fatty acids are linked to increased brain inflammation, as discussed in this book.
Several chapters in this book describe how excess refined carbohydrate intake disrupts the metabolic functions of the body. Once these are compromised, the body is subjected to stress. This stress is in the form of chronic inflammation and oxidative stress [2], which then negatively influences cellular functionality, cellular signalling and in the brain â neurological function. These are some of the findings of studies illustrating that obesity and type 2 diabetes are significant risk factors for the development of neurological disorders including AD [3].
Two chapters of the book discuss the various common causes and symptoms of dementia, differential diagnosis, AD diagnostic tests, and current treatments. AD is characterised by gradual cognitive impairment, and the risk of developing this condition increases with age, such that, past the age of 65, the risk doubles every five years. Pathologically, the disease is characterised by the death of neurons in the cerebral cortex, hippocampus and forebrain, which is associated with the formation of extracellular amyloid deposits, intracellular neurofibrillary tangles consisting of hyperâphosphorylated tau protein, as well as inflammation [4]. Although medications are available for the treatment of AD, these medications only serve to reduce the cognitive symptoms of some people with AD and then only for a relatively short period. There are also medications that can reduce other symptoms of Alzheimer's, such as anxiety and sleeplessness, and these are all discussed in this book. However, there are currently no medications that can stop the eventual continuing neurological degeneration and resultant cognitive degeneration of Alzheimer's. As mentioned earlier, one of the main messages of this book is that, if we can manipulate our diet and lifestyle at midâlife, and reduce our risks associated with excess calorie intake, overweight, obesity and type 2 diabetes, we may be able to achieve longâterm prevention or delay of the disorder.
We should be concerned about food consumption and obesity. This could be discussed in terms of a change in lifestyle opportunities, or selfâesteem or peer perception. The way weight issues contribute to psychological and personal wellâbeing has been studied extensively in the past. More importantly, there is a health cost associated with ...
