‘You are what you eat’ the saying goes, and indeed, much government health advice these days centres around what we eat, how much we eat and how we ‘should’ be eating. Diet related ill-health is now believed to be the leading cause of chronic disease around the world.1 It may appear surprising then that comparatively little research has been done on the effects of diet on dementia and the risks of dementia.
Just as our bones and muscles need to be fed properly in order to function correctly, so too do our brains if they are to work at the optimal level. The physical body and the brain are both composed of body cells. The food used by the brain is glucose, of which more below.
The brain is composed of many different types of cells, but the primary functional unit is a cell called a neuron. All sensations, movements, thoughts, memories and feelings are the result of signals that pass through neurons. Neurons have a cell body which contains: the nucleus; dendrites. which extend out from the cell body like the branches of a tree and receive messages from other nerve cells; and axons, down which signals travel away from the cell body, to another neuron, or a muscle cell, or cells in some other organ. Some particular kinds of cells are wrapped around the axon to form an insulating sheath. This sheath can include a fatty molecule called myelin, which provides insulation for the axon and helps nerve signals travel faster and farther.
The place where a signal passes from the neuron to another cell is called the synapse. It is a minute gap; neurons do not actually quite touch each other. When the signal reaches the end of the axon of a neuron it stimulates tiny sacs in that neuron to release chemicals known as neurotransmitters into the synapse. The neurotransmitters cross the synapse and attach themselves to receptors on a nearby cell. If the receiving cell is also a neuron, the signal can continue the transmission to the next cell.
One neurotransmitter, acetylcholine, is classified as an ‘excitatory’ neurotransmitter because it generally makes cells more able to work. It governs muscle contractions and causes glands to secrete hormones. Alzheimer’s disease is associated with a shortage of acetylcholine. This shortage means that signals are transmitted less easily between neurons.
The sole food of the brain is glucose (although the brain cannot store glucose), and it makes use of almost a quarter of the glucose and oxygen which the body takes in. Because the brain uses glucose as its main source of energy, it might be thought that a high level of glucose in the blood would be good, encouraging it to work better. In actual fact, fluctuations in blood glucose level, such as are caused by a diet high in carbohydrate and fructose (a type of sugar found particularly in fruit), are detrimental. The brain needs a sustained and balanced supply of glucose and this is best obtained from eating foods which cause blood glucose levels to rise more slowly and to be sustained for longer.
So, because the brain needs a sustained and balanced supply of glucose, our diet should consist of foods which will give a steady supply (see below) and not cause high peaks in blood glucose. High peaks in blood glucose level are inevitably followed by low troughs. People who are sensitive to blood sugar fluctuations (e.g. those who suffer from hypoglycaemia) know very well the feelings of edginess, irritability, shakiness and sometimes even nausea which extreme hunger can cause. People with diabetes may suffer from these symptoms if they do not control their blood sugar levels. Diabetics are taught to carry sweets or chocolate or sugar with them to avoid suffering from a ‘hypo’. These sweet items will cause a swift rise in blood sugar levels, which may be beneficial in an emergency. However, it is better for everyone to eat a diet which avoids these highs and lows. We should all aim for a slow and sustained release of glucose into the blood.
Many of us were taught at school about the body’s basic dietary requirements for protein, fats and carbohydrates.
Proteins: Put simply, proteins are required for bodily growth and repair of tissues, as, for example, during recovery from injury. We need proteins every day to remain healthy as our bodies cannot store them in any quantity. Proteins are made up of chains of ‘amino acids’. There are eight amino acids which are essential to the body and have to be obtained from food as our bodies cannot make them. Meat, fish, eggs and dairy produce all contain the eight essential amino acids in the proportions needed by the body. Other foods, such as nuts, legumes (peas, beans and lentils) and seeds contain some of the essential amino acids and can be eaten in combination to provide the body with the right amino acid mixture. Strict vegetarians have to be careful to eat both adequate amounts and an adequate variety of protein-containing foods to ensure a sufficient supply of essential amino acids.
Fats provide energy for the growth and maintenance of body tissues and help to maintain body temperature. They also provide fat-soluble vitamins (vitamins A, D and E). A sufficient amount of fat in our diet causes us to feel full and prevents us overeating, while an excess will cause us to feel sick – it is difficult to overeat fats, unlike sugars and carbohydrates. When digested, fats break down into ‘fatty acids’. To supply the fatty acids essential for proper functioning of the brain, you need to eat at least 15 grams of these each day. As well as the obvious fat on meat and in butter and cooking fats, fat is found in oily fish, milk, cheese, eggs and condiments such as mayonnaise. Some foods such as nuts have quite a high fat content, although this may not be obvious. Do not be misled by the simple (and erroneous) statement commonly read in popular literature that ‘eating fat makes you fat’. When fat is digested it is oxidised by the body to provide energy for tissue activity and for the maintenance of body temperature. Deposits of fat around the vital organs of the body hold these organs in position and protect them from damage. Fat is particularly important in the structure of the brain and nervous tissue. We need a steady intake of fat for it to function properly and fats make up 60 per cent of the brain and the nerves that run every system in the body. The body needs two kinds of fat to manufacture healthy brain cells and prostaglandins. These fats are omega-6 (linoleic acid) and omega-3 (alpha linolenic) and are often known as essential fatty acids. Cholesterol is a fatty substance known as a ‘lipid’ and is vital for the normal functioning of the body. It is mainly made by the liver, but can also be found in many foods that we eat. Cholesterol is needed everywhere in the brain as an antioxidant and to manufacture the neurotransmitters, such as acetylcholine, which we have seen are the means by which nerve cells communicate.
Carbohydrates also provide energy. Most people think of things like bread and potatoes when they consider the word carbohydrates, but it is important to remember that all sugars and starches are actually carbohydrates. This includes sucrose (table sugar) and fructose, which is the sugar found in fruit. After absorption in the intestines the products of carbohydrates (sugars) are utilised to produce energy. Excess sugars are converted into fat. If insufficient carbohydrate is taken in the diet to produce the required glucose, then the body can convert fat into glucose to produce energy, and if there is not enough fat, then protein can be diverted to produce energy. It is clear that the availability of glucose is an essential for life.
Other essentials: The body also requires a supply of vitamins, minerals and trace elements to function correctly. Generally, if the diet is adequate in respect of protein, fats and carbohydrates, then a sufficient supply of vitamins, minerals and trace elements will be taken in.
In order to produce the slow and sustained release of glucose mentioned previously, our diet should not be too high in carbohydrates which tend to produce a ‘spike’ in blood sugar levels. Every meal should contain protein, fat and a limited amount of carbohydrate, and meals should be eaten at regular intervals. If they are properly balanced and eaten regularly, then additional snacks should not be necessary or even desired. This doesn’t mean that you should not treat yourself to the odd slice of cake with your afternoon tea. It means that if you actually need that slice of cake in order to last out until the next meal, then either your diet is not properly balanced or your meals are too far apart from each other.
Standard current dietary advice is based around what is considered to be ‘good’ for the health of our heart and cardiac system. Broadly, the advice is to base our diet around carbohydrates, to reduce our intake of fats, increase our intake of fruit and vegetables and to keep cholesterol levels low. Whilst this diet is popularly considered to be a ‘healthy heart diet’ for those in mid-life, some specific research shows that in adopting this way of eating we are no longer giving our brain the optimum diet. As explained above, in order to work properly the brain needs dietary fat, cholesterol and a steady intake of glucose.
What is becoming clear from research is that there is a definite link between excess dietary carbohydrates (particularly refined carbohydrates and, above all, the sugar called fructose) along with a deficiency in dietary fats and cholesterol which may lead to the development of Alzheimer’s disease.
One paper, published in the Journal of Neurochemistry in 2008, points out that in trials, a reduced carbohydrate intake prevented Alzheimer’s disease-type amyloidosis (a condition where proteins are abnormally deposited in organs or tissues and cause harm). This paper mentions the term ‘metabolic syndrome’ which is used to describe a group of risk factors that occur together and are thought to increase the risk for coronary artery disease, stroke and type 2 diabetes. The suggestion is that this syndrome also increases the risk for Alzheimer’s disease and the syndrome is linked to high calorie intake and diets high in sugar and refined flour. The authors recommend that those at risk of Alzheimer’s disease eat whole and unrefined foods with natural fats, especially fish, nuts and seeds, olives and olive oil, and reduce the intake of foods that disrupt insulin and the blood sugar balance.2
A 2011 paper published in the European Journal of Internal Medicine points out that the cerebrospinal fluid in the brains of people with Alzheimer’s disease is deficient in fats and cholesterol and suggests that Alzheimer’s disease may be caused by a deficiency in the supply chain of cholesterol, fats and antioxidants to the brain. This paper suggests that a diet high in high-glycaemic carbohydrates (especially fructose) and low in cholesterol and fats begins the process that leads to neuronal failure. The authors propose that dietary modifications resulting in fewer highly processed carbohydrates and more fats and cholesterol are a protective measure against Alzheimer’s disease. We have seen that neurons are involved in the transmission of signals in the brain. Astrocytes are the cells that supply cholesterol and fats to the neurons. It is believed that excess exposure to glucose and to oxidising agents can lead to damage in the astrocytes. This, say the authors of the paper, leads to defects in the transmission of neural signals.3
Recent animal-based research has suggested that cutting calories overall may halt or even reverse the symptoms of Alzheimer’s disease. Published in the Journal of Alzheimer’s Disease, this study involved a team of researchers from the Mount Sinai School of Medicine in New York City maintaining a group of squirrel monkeys on either calorie-restrictive or normal diets throughout their lifespan. Compared to those on a normal diet, the monkeys that were fed the reduced-calorie diet were less likely to have Alzheimer’s disease-type changes in their brain.4
The reduced-calorie diet was also associated with increased longevity of a protein known as SIRT1, which influences a variety of functions, including age-related diseases. The significance of this research is reflected in the further studies around ketones (see below).
However, when considering a reduced-calorie diet it is also important to remember that many elderly people may be in a poor nutritional state due to increasing frailty, lack of exposure to sunlight and inability to shop for food and prepare meals because of cognitive impairment or physical disability. If someone is already suffering from under-nutrition it would be quite inappropriate to suggest a reduction in calories. Instead, action to enrich the diet should be taken in accordance with the suggestions given at the end of this chapter.
Research has already indicated a clear link between Alzheimer’s disease and diabetes (see chapter 8 on physical disease). A diet high in processed carbohydrates like white bread, breakfast cereals and fruit juices, particularly if this diet is also low in fats, results in a rapid rise in blood glucose levels after meals. Over time it is believed that this may lead to insulin resistance and diabetes.
One of the most interesting links between nutrition and the risk of dementia was the subject of a piece of research which showed a link between the nutritional status of mothers in pregnancy and the development of dementia in their children in later life. At the end of World War II a severe famine occurred in cities in the western part of the Netherlands. At one stage the rations were as low as 400 calories per day. This study found that in late middle life (age 56-59 years) people exposed to famine during the early stage of gestation performed worse than expected on selective attention tasks.5
Eating a well-balanced diet will give a controlled release of glucose, ensure we have the nutrients we need to stay healthy and help to protect against dementia. But what truly is a well-balanced diet? Research information indicates that not all current ‘accepted’ advice about low-fat/high-carbohydrate diets and restricted cholesterol should necessarily apply to older people wishing to protect themselves against dementia. It appears that simple dietary modification towards fewer highly processed carbohydrates and relatively more fats and cholesterol is likely to be a protective measure against Alzheimer’s disease.
As was mentioned earlier in this chapter, omega-6 and omega-3 are often known as essential fatty acids as they must be obtained from our food; we cannot make them ourselves. There are three types of omega-3: alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). ALA is thought to help reduce heart disease and EPA and DHA help maintain the tissues of the eye and brain.
Omega-6 has two types: linoleic acid (LA) and arachidonic acid (AA). These are the prime structural components of brain cell membranes and are also an important part of the enzymes within cell membranes that allow the transport of valuable nutrients in and out of the cells.
Omega-6 is found in a variety of foods, including meat and animal products such as eggs, and it is believed that a shortage of this fat is rare in most western diets. Omega-3 is found generally in oily fish as well as in some oils, nuts and seeds. Most current advice centres around the suggestion that we increase our intake of omega-3 in order to balance our intake of omega-6. However, the simple fact is that there is very little consensus among nutritionists about how much omega-3 and omega-6 oils are needed in total for optimum health and about the ideal ratio between the two. While there is a theory that omega-3 fatty acids are better for our health than omega-6 fatty acids, this is not necessarily supported by the latest evidence.
As far as there is any consensus, it seems to centre on the suggestion that for the health of our hearts and our brains we should all be eating more oily fish. A research paper looking at fish consumption and cognitive function in people without dementia showed that: ‘there were significant positive associations between reported fish consumption and the CVLT (Californian Verbal Learning Test) scores.’ It concluded: ‘we have demonstrated a positive association between reported fish consumption and cognitive function in a large sample of healthy older people in the UK.’6
The usual recommendation is two servings of oily fish per week. The word ‘oily’ seems to put many people off, but in fact this term includes a number of different species which makes it easier to include these in the diet: mackerel, herring, salmon, whitebait, sardines, trout, pilchards, kippers, eels, fresh tuna, anchovies, swordfish and sprats. Tinned tuna is not included in this list because the canning process is thought to negate the omega-3 content. However, high-quality brands canned in water rather than oil can in fact contain significant amounts. You need to read the label.
Vegetarians can get omega-3 from flax-seed, hemp-seed, nuts and (if eaten) eggs. Given such a comprehensive list you may begin to think that increasing our omega-3 intake is not really very difficult.
An interesting piece of information and anecdotal evidence has come from the USA. A Florida doctor, Dr Mary Newport, who is married to someone who has dementia, read some information about coconut oil and begun dosing her husband with this. She claims that he has shown a remarkable improvement on this regime and has submitted some of his test results to bear out his recovery.7 The improvements in her husband’s cognition have not all been maintained and this type of initial promise followed by a disappointing follow-up is common to many of the ‘exciting break-though’ research headlines in the popular press. No serious research has been done on the benefits of coconut oil in the UK, but the theoretical reasoning behind this supplement is borne out by nutritional knowledge which indicates that the brain can use ketones for nourishment when glucose is unavailable. The first placebo-controlled trial of coconut oil is just beginning in Florida USA and many will await the results with interest.
Research has been done which involves using mice to test the effect of a high-fat/low-carbohydrate diet. The conclusion of this research states: ‘Here we demonstrate that a diet rich in saturated fats and low in carbohydrates can actually reduce levels of Abeta [amyloid beta]. Therefore, dietary strategies aimed at reducing Abeta [amyloid beta] levels should take into account interactions of dietary components and the metabolic outcomes, in particular, levels of carbohydrates, total calories, and presence of ketone bodies, should be considered.’8 Of course it needs to be remembered that not all animal-based research translates into benefits in humans.
A US-based, 90-day, randomised, double-blind, placebo-controlled, parallel-group study which involved giving people with early to moderate Alzheimer’s disease (AD) an oral ketogenic compound, resulted in significant differences in ADAS-Cog scores between those taking the compound and the placebo group. The authors concluded: ‘Therefore, chronic induction of ketosis may offer a novel strategy for AD that can be used with current therapies’.9
There have been a number of trials of various dietary supplements (other than coconut oil) to test whether they are effective in preventing dementia and whether these supplements improve symptoms in those who already have dementia. A problem with such trials is the fact that any dietary supplementation takes time to show its effects. This means any trials have to be carried out over a long period of time. In addition, trials usually have to be carried out using specific pre-packaged supplements – perhaps in pill form - which make it easy for participants to take part. Trying to ensure that participants in a trial eat particular foods in sufficient quantities is much more difficult. Below is a summary of the current status of some of the trials.
Significant research has been carried out around B vitamins, particularly folic acid. It has been noted that a rise in blood levels of a particular amino acid called homocysteine is associated with an increased risk of Alzheimer’s disease and vascular dementia as well as stroke and heart disease. At this present time it is still not clear whether raised homocysteine levels are a pointer to an increased risk of dementia and heart disease (including stroke) or whether raised levels are caused by heart disease and dementia. Supplements of folic acid (also called vitamin B9) can be shown to lower the levels of homocysteine in the blood and for a while this line of research appeared very exciting. However, trials have shown that even when homocysteine levels are reduced, this does not restore cognitive function in those people with early stage dementia, nor does it appear to improve the prognosis for those with cardiac problems. Further research into the efficacy of vitamin B is ongoing, and this still looks like a promising area. It needs to be noted that the levels of B vitamins used in the trials were much higher than can usually be obtained in our diets or by taking supplements. Therefore no causal effect of (for example) a low level of B vitamins in those who develop dementia is suggested at this stage.
Some research has been carried out into the connection between low levels of vitamin D and dementia. Levels of this vitamin are often low in older people and are also lower in the general population than a generation ago. The reason seems to be that the main source of vitamin D for the body is from the action of sunlight on the skin. Many older people, especially those living in residential care homes, may not go out into the sun very much. In addition a great deal of publicity has been given to the connection between skin cancer and sunlight-damage to the skin, and the use of sunscreen cream is much higher than it used to be. The American Journal of Alzheimer’s Disease and Other Dementias reported in a paper published in 1997 that: ‘Patients with Alzheimer’s disease in particular have a high prevalence of vitamin D deficiency, which is also associated with low mood and impaired cognitive performance in older people.’ The authors noted that: ‘Vitamin D clearly has a beneficial role in AD [Alzheimer’s disease] and improves cognitive function in some patients with AD.’10
Given that current advice is to apply high-factor sunscreen and to avoid direct sunlight in the middle of the day (the time when the action of sun on the skin is most effective at producing vitamin D) this research finding is clearly very interesting, if, perhaps, controversial.
Vitamin E is an ‘antioxidant’ – that is, a substance that scientists believe may protect brain cells and other body tissues from certain kinds of chemical wear and tear. A 1997 study showed that high doses of vitamin E delayed loss of ability to carry out daily activities and placement in residential care by several months.11 However, since the study was carried out, scientists have found evidence in other studies that high-dose vitamin E may slightly increase the risk of death, especially for those with coronary artery disease. Vitamin E in high doses can interact with other medications, including those prescribed to keep blood from clotting or to lower cholesterol. Therefore, vitamin E supplements should be taken with caution and only after checking with your doctor.
Ginkgo biloba is a herbal supplement which has a reputation for improving learning and memory. Initial research published in 2002 seemed to show promise for application of its properties to help those diagnosed with dementia.12 This fitted with the reputation of the herb, and its use by herbalists for the improvement of memory in students studying for examinations. However, in a later study published in the Journal of the American Medical Association, 240 milligrams per day was found to be ineffective in reducing the development of dementia in general, and Alzheimer’s disease in particular, in older people. This study, known as the ‘GEM’ (Ginkgo Evaluation of Memory) study, led by Steven T. DeKosky, MD, is the largest clinical trial ever to evaluate ginkgo’s effect on the occurrence of dementia.13 Some medical herbalists have claimed that the dose used was insufficient to achieve effective improvement. The fact is that, unfortunately, clinical trials have not shown consistently that ginkgo helps to prevent cognitive loss in normal elderly subjects, or to improve cognitive function in patients already diagnosed with Alzheimer’s disease. Doctors are therefore not convinced of any benefit from this supplement.
Aluminium is not regarded as a food supplement but I am discussing its possible link with dementia here because it can be absorbed by the body via the food chain.
As was described in chapter 1, people with Alzheimer’s disease have typical changes in brain organisation that are called ‘neurofibrillary tangles’. Beginning in the 1960s, various studies have found high concentrations of aluminium at autopsy in the brains of people suffering from Alzheimer’s disease – and almost always in the characteristic neurofibrillary tangles in the brain. However, other studies have found no difference between the overall amount of aluminium in the brains of people with Alzheimer’s and the amount in normal brains. It seems the neurofibrillary tangles are very ‘sticky’ and absorb aluminium.
When patients with chronic kidney failure began to be routinely treated with a new technique called ‘dialysis’, this technique used hundreds of litres of water each day to purify the blood. Unfortunately, the aluminium naturally present in the water entered the blood, and couldn’t be removed – because the kidneys of those with kidney failure were not working. As the blood levels of aluminium soared to thousands of times higher than normal, the patients became confused and demented. We now know that this ‘dialysis encephalopathy’ can be rectified by removing any aluminium from the water used for dialysis.
Although aluminium seemed to be implicated as a cause of dementia, the findings described above have led to the conclusion that it is not the main causal factor in Alzheimer’s disease, or other forms of dementia. None of the evidence so far has proved that aluminium contributes to the degenerative changes which cause Alzheimer’s disease and the risk from increased exposure is considered to be small in general terms. However, there is little doubt that aluminium is neurotoxic (poisonous to brain cells) and excessive intake should be avoided. If you are worried about the risk, you can avoid cooking acidic foods in aluminium pans, reduce your intake of antacids (which usually contain aluminium), avoid the food additive E173 and filter your drinking water.
If you have been diagnosed with dementia, or if you are caring for someone with this diagnosis, you can make useful changes to the diet. You can switch to using full-fat milk and include plenty of eggs, cheese and butter in the diet. You can also include oily fish several times per week. (Some people prefer a fish-oil supplement.) You can ensure that you or the person you care for eats more unprocessed foods (for example, brown rice and wholemeal bread) and reduces consumption of processed carbohydrates and hydrogenated fat.
Although research so far has not shown food supplements to be the magic answer to dementia, there is no reason why you should not include supplements in the diet provided you follow recommended guidelines. So, for example, if you want to include a multi-vitamin or coconut oil or ginkgo biloba in the diet, this is unlikely to be harmful.
Above all, keep the consumption of refined sugar to a minimum. People with dementia often seem to crave sweet things (this may be connected with the brain’s loss of ability to process glucose efficiently), including alcohol. Alcohol consumption needs to be supervised, if only for the simple reason that someone with dementia may forget how much alcohol they have consumed and may unwittingly drink to excess. It should also be remembered that, where the action of the brain is already impaired, alcoholic drinks will be likely to make the brain processes even slower.
In some people with dementia, the sense of taste changes so that appetite may decrease. Where people with dementia live alone, their diet is often poor. They may forget to eat regularly; they may lose the skills of cooking and revert to eating easily prepared food such as biscuits and cake. Agency helpers employed to prepare meals may (due to a shortage of time) deliver only cook-chill foods of limited nutritive content. Well-meaning family members may also see such meals as useful due to the fact that they can be quickly prepared and need little cooking skill. Often relatives and carers fall back on fortified meal replacement drinks which are frequently rich in sugar. Of course, any food is better than none and all these options help to prevent starvation. However, someone suffering from a progressive and terminal disease (which is what dementia is) deserves the best nutrition available.
People in the later stages of dementia often lose weight so it is then even more important to ensure that whatever they eat is nutrient rich. This is the reason for the advice above on giving full fat milk, plenty of eggs and cheese. If weight loss is significant, food can be fortified and advice on the best way to manage this can be obtained from the Community Mental Health Team or a dementia support worker.
1. WHO Global status report on non-communicable disease 2010.2011. www.who.int/nmh/publications/ncd_report_full_en.pdf
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