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How and why does a bad diet increase the chance of developing dementia?
By Emma Leong
Dementia is a brain disorder. It triggers the loss of brain function. This includes memory loss, confusion, understanding and judgement, and problems with speech. Dementia affects about 800,000 people in the UK. The older one is, the more likely the risk of developing dementia. People aged over 65 years usually develop the condition. 1 in 100 people over 65 years old have dementia. Since people now are beginning to live longer, the number of people with dementia is increasing. By 2021, it is estimated that the number of people in UK with dementia will be 950,000.
Several diseases and conditions cause dementia. As shown in figure 1, the most common type of dementia is Alzheimer’s disease. The chemistry and structure of the brain changes during the development of the Alzheimer’s and eventually leads to the death of brain cells. Initial signs of this disease would be problems with short- term memory. Another is vascular dementia. This develops when the oxygen supply to the brain fails and the brain cells eventually die. Symptoms occur suddenly after a stroke or after a series of small strokes in time. There is also Fronto-temporal dementia (including Pick’s disease), which is when the front part of the brain (i.e. the frontal lobe) is damaged. Symptoms for this dementia are associated with personality and behaviour changes. Dementia with Lewy bodies is another form of dementia and this is when tiny abnormal structures develop inside nerve cells. Because of these abnormal structures, the brain leads to the degeneration of brain tissue. Symptoms of Lewy bodies include disorientation and hallucinations. Lewy bodies also affect planning, reasoning and problem solving in the brain. Lewy bodies have similar characteristics to those with Parkinson’s disease.
Diet is one of many factors that contribute to the risk of many illnesses, including dementia. In order for a person to maintain a normal body weight, this person must have a healthy and balanced diet. This healthy diet will likely reduce the development of high blood pressure which can lead to heart diseases, including myocardial infarction (a heart attack). Heart problems have been shown to increase the chance of developing vascular dementia.
What is vascular dementia?
Vascular dementia is caused by difficulties in the supply of blood to the brain. It is the second most common form of dementia with Alzheimer’s being the first. Vascular dementia tends to begin suddenly, such as, after a stroke. Some symptoms are similar to other types of dementia, such as Alzheimer’s disease. Symptoms include problems with thinking, concentration and communication; stroke or physical weakness; memory problems; depression; seizures; severe confusion; mood swings; hallucinations and misperceptions.
Vascular dementia develops when too much saturated fat in the body narrows the arteries, causing an insufficient supply of blood reaching the brain cells, and so the brain becomes damaged and the cells eventually die. For the brain cells to function properly, they need a good supply of blood. One can develop vascular dementia when blood cannot be delivered as efficiently through the network of blood vessels (i.e. the vascular system). Many conditions can lead to this problem such as diabetes, high cholesterol, heart problems and high blood pressure, which increase the chance of vascular dementia. Therefore, the best solution to this is to identify and treat these conditions as early as possible. Effective treatment could delay or even stop the developing risk of vascular dementia.
There are a few types of vascular dementia, depending on what has caused the damage to the brain, and which part of the brain is affected:
A stroke occurs when blood cannot reach the brain. This interruption causes permanent damage to the brain. The cause of a stroke is usually caused by a bursting blood vessel (haemorrhagic) or a blood clot (ischemic). Symptoms of a stroke depend on which part of the brain has been affected. A person may become paralysed or have problems with speech. Other parts of the brain damaged could cause dementia.
A common type of vascular dementia is multi-infarct dementia. This is caused by a series of small strokes. One may experience temporary symptoms or none at all. Another type is called single-infarct dementia. This is when vascular dementia develops after an obvious stroke.
Sub-cortical vascular dementia (Binswanger’s disease)
Binswanger’s disease is also known as small vessel disease. Sub-cortical vascular dementia is caused by the damage of tiny blood vessels within the brain. Symptoms include walking difficulties, speech difficulties and loss of bladder control. These symptoms are not always present.
Mixed dementia (vascular dementia and Alzheimer’s disease)
Both Alzheimer’s disease and vascular dementia affect the brain. The symptoms of mixed dementia are a combination of the two types of dementia. About 10 per cent of people have mixed dementia.
Factors that increase the risk of vascular dementia are very similar to those that increase the risk of cardiovascular disease (e.g. smoking) because the cardiovascular system is responsible for delivering blood to the brain. Factors include a lack of exercise, drinking excess alcohol, smoking and a bad diet; a medical history (or untreated) of stroke, diabetes, high blood pressure, heart problems, or sleep apnoea; a family history of stroke or cardiovascular disease; and one’s ethnic background.
To diagnose vascular dementia, a specialist may carry out brain scans to help make a diagnosis. Investigations will also identify conditions that contribute to vascular dementia (e.g. high blood pressure). Early diagnosis ensures a better chance of treatment to delay the disease. If sudden symptoms, such as slurred speech) are left untreated, it can lead to permanent damage as these symptoms may cause a permanent interruption in the blood supply within the brain.
Unfortunately, as for treatment, vascular dementia cannot be reversed. However, there are ways of delaying the disease and preventing further damage. These include taking medication for heart and diet conditions; adopting a healthier lifestyle (more exercise, no smoking, good diet, less alcohol) and receiving rehabilitative support to regain lost functions.
What is Alzheimer’s disease?
Alzheimer’s is the most common form of dementia. It affects about 496,000 people in the UK. Alzheimer’s is a neurological disease in the brain that progresses and leads to the permanent loss of neurons. Symptoms for this disease mainly affect the intellectual abilities. This includes memory and reasoning. If the condition is very severe, Alzheimer’s will impede on the social or occupational functions in the brain.
Alzheimer’s disease is progressive; therefore more and more parts of the brain are damaged over time and so symptoms become more severe.
Alzheimer’s disease has biochemical abnormalities that include cell loss. The disease lacks some important chemicals, which involve the transmission of chemicals in the brain. It also causes neurofibrillary tangles, beta-amyloid (βA) deposits and amyloid precursor proteins (APP) in the brain (the primary component of developing Alzheimer’s). This disease also increases the activation of pro-death genes and signalling pathways. It not only causes damage to the energy metabolism, but it also causes DNA damage.
Dr. Alois Alzheimer was a psychiatrist and neuropathologist from Germany. In 1906, he discovered an ‘unusual disease of the cerebral cortex (the outer layer of neural tissue of the cerebrum of the brain)’ which affected a woman called Auguste .D. Her symptoms included memory loss; disorientation; hallucinations, and sadly died at the age of fifty-five. Her brain was analysed after her death and showed various abnormalities in the brain. First of all, the cerebral cortex was thinner than normal. Alzheimer used a stain and identified neurofibrillary tangles. He also noticed during the course that protein ‘plaques’ developed in the structure of the brain and lead to the death of brain cells. These plaques are known now as Beta-amyloid plaques.
Beta-amyloid’s primary component, amyloid precursor protein (APP) is a protein throughout the body. Scientists have thought to believe that there is an error with the processing of amyloid precursor protein in the brain which leads to short fragments of APP produced known as beta-amyloid. The theory is that this sticky protein accumulates and triggers the disruption and destruction of nerve cells, which causes Alzheimer’s disease. Therefore, there is a fault with the over production of beta amyloid and with the mechanism that clears the beta amyloid from the brain.
Beta amyloid is a piece from a larger protein that helps form cell membranes in the brain and other parts of the body. Other important functions include fighting microbes, transporting cholesterol and regulating the activity of certain genes. However, if there is a build up of beta amyloid, it can form into plaques. First described by Dr. Alois Alzheimer in 1906, the beta-amyloid plaques are found in the brain between the spaces of the nerve cells. The plaques are made up of large insoluble deposits of a toxin protein peptide known as, beta-amyloid (βA).
Not only is diet an important factor affecting the development of dementia, but so is aging. The more people age, the more plaques start to develop in their brain tissue. A genetic mutation is also a factor that could increase the production of beta-amyloid and can cause inherited forms of Alzheimer’s disease.
How are Beta-amyloid plaques formed? They first start off as an amyloid precursor protein (APP), which is one of the many proteins associated with the cell membrane. And so, the amyloid precursor protein embeds itself in the membrane. Specific enzymes from a number of cell compartments divide the APP into tiny fragments. These enzymes, identified in 1999 and 2000, are called the alpha-secretase, beta-secretase, and gamma-secretase. Scientists had a major breakthrough as they discovered these enzymes, depending on the enzyme involved and the certain area of the APP the enzyme cleaves, the process of APP can lead to two pathways that potentially lead to two very different consequences for the nerve cell.
The APP, located on chromosome 21, is in fact important for the survival and growth of neurons. This protein also helps the damaged neurons repair themselves after a brain injury. Its primary function and its structure is not yet known, however, it is a precursor in the synapses of the neurons to the beta-amyloid.
Beta (β)-secretase and Gamma (γ)-secretase
The beta amyloid is formed by two enzymes, which cut the APP molecule at two different positions. One is the β-secretase, which ceases the APP outside the cell whereas γ-secretase is cut at a position inside the cell. The cuts of the APP molecule release APP fragments, which could potentially lead to apoptosis (cell death). Aβ40 and Aβ42 are the most prevailing, however Aβ42 is more toxic.
Oligomers (primary pathogenic form of βA) are formed and these are likely to be cleared from the brain, however, an increase in saturated fats (or other factors like age, genetics etc.) can cause the oligomers to clump together with more beta-amyloid peptides. These oligomers also disrupt the communication between neurons. The process continues and the oligomers grow larger. Other proteins and cellular material are added and therefore these become even more insoluble and become plaques: a well-known characteristic to Alzheimer’s disease.
For a while, scientists have assumed that plaques might be the main cause of the damage in neurons seen in brains with Alzheimer’s. However, this concept has evolved throughout the years. Scientists now believe that oligomers may be the major culprit. The plaques may be a late-stage attempt by the brain to remove this harmful beta-amyloid from the neurons.
Beta Amyloid Protein is a peptide consisting of 36-43 amino acids. These are best known to form amyloid plaques in association with Alzheimer’s disease. The primary component for amyloid plaques is the amyloid precursor protein (APP). This peptide is composed in deposits found in the brains of people with Alzheimer’s disease. In abstract, beta amyloid can stop neurons from responding to insulin, which leads to some very serious damage in the brain. However, some activity for beta amyloid is not associated with disease. This includes the activation of kinase enzymes (transfers phosphate groups from high-energy donor molecules, such as ATP), protection against oxidative stress and regulation of cholesterol transport.
Unfortunately, when it is associated with disease, it is the main component of deposits located in the brains of people with Alzheimer’s disease known as amyloid plaques. These plaques also occur in other diseases such as Lewy bodies and inclusion body myositis (a muscle disease). These plaques are made of tangled amyloid fibres. Amyloid plaques build up outside nerve cells/neurons in the brain. Scientists have said, although the proof behind it is yet to be discovered, the protein divides underhandedly producing beta amyloid, which is neurotoxic in the brain. A possibility could be that beta amyloid forms small channels in neuron membranes, accepting excess amounts of calcium. Although calcium is necessary for regular neuronal function, too much can kill a neuron.
Research has shown that beta amyloid proteins play an important role in the development of Alzheimer’s disease. There have been a number of studies linked with genetics, cell biology, biochemistry and animals, which have supported this hypothesis. So many studies have supported this concept, proving that the soluble forms of this peptide are likely to be the causative agents in a person developing Alzheimer’s.
But how and why does a bad diet increase the chance of developing dementia? Does diabetes have anything to do with it? In principle, the more fatty and sugary a person’s diet is, the higher the levels of glucose in the blood, the more likely that person will develop diabetes and therefore, the higher risk of developing dementia. However, how much of an impact does this have on our brain? Modern research has shown how dementia could potentially be ‘Type 3 diabetes’ as there are strong links about insulin resistance between the two problematic disorders to our body in this generation.
The types of diabetes
Diabetes mellitus is a chronic disease known as the high glucose levels in the blood due to a malfunction of the body’s production and use of insulin. The main role for insulin is that the hormone controls glucose levels by transporting glucose from the blood stream into our cells by facilitated diffusion. There are two types of diabetes that the world evidently knows.
Type-1 diabetes, also known as insulin-dependent diabetes mellitus, is known to destroy the pancreatic beta cells (often due to an autoimmune deficiency), which produces most of the insulin in the body. Therefore for someone with type-1 diabetes, the result for him or her is severe insulin deficiency. There is no prevention and no cure for this disease. Diet must be controlled and must be regularly injected with insulin, as since there is a lack of insulin produced from the pancreas, the glucose sugars cannot be absorbed into the body’s cells without the help of the injected insulin.
Type-2 Diabetes (known as non-insulin-dependent diabetes mellitus) is much more common than type-1 diabetes. This occurs when the cells in the body do not react to insulin or when the pancreas does not produce enough insulin. Because the insulin controls the amount of glucose in the body’s bloodstream, it moves the glucose from the blood into the body’s cells where it is converted into energy. So if one has Type-2 diabetes, a lack of insulin is produced and therefore there is not enough insulin to maintain a normal blood glucose level. The insulin cannot be produced effectively and so it is known as ‘insulin resistance’.
There are other types of diabetes, which are less common. They are caused by genetic defects in beta-cell function or insulin action etc. If these different types of diabetes are not treated, they could lead to severe and often life-threatening consequences, for example, cardiovascular disease, kidney disease, nerve damage and blindness.
In figure 6, it shows that during the years, there has been a dramatic rise of the cases of type-2 diabetes in America. More and more cases of type-2 diabetes have risen over the years.
So what about Type 3 diabetes? What does the graph (figure 6) tell us about the dementia? Thanks to Suzanne de la Monte and her colleagues in Brown University, they have stated that the damage caused in Alzheimer’s are “mediated by depletion of insulin and insulin-like growth factors”. Surprisingly, the idea of the link between diabetes and Alzheimer’s disease is not new. It has been known for a while that many consequences of type 2 diabetes, especially in older adults, is a cognitive impairment. That means that brain cells are damaged by the impaired glucose metabolism. The impaired glucose metabolism damages all kinds of cells throughout the body as well, however, the brain cells rely on the levels of glucose metabolism more than others for a healthy function.
However, it is hard to establish the link between diabetes and dementia, as a correlation does not imply causation. There is a possibility that cognitive impairment does lead to Alzheimer’s disease, but there could be other factors for the cause of dementia.
Dr. de la Monte, Dr. Jack R. Wands (and co.) made some observations. The first one was that in the brains of patients with Alzheimer’s, there were extensive abnormalities in insulin signalling, which is the cascade of biochemical reactions triggered by insulin when it starts the process of glucose transport in our cells. And also there was a decrease in activity of the molecules that participate in these reactions. Because of this discovery, it is thought that the main culprit to this abnormality is insulin resistance. Insulin resistance is the inability of our cells to respond to insulin. Not only does this condition impair our glucose metabolism and is insufficient in cellular energy production, but it also increases the levels of certain deadly enzymes, increases oxidative stress (from free radicals) reduces neuronal survival (cell death) and harmful processes associating proteins.
Even though epidemiological and pathological studies about the role of insulin resistance in Alzheimer’s disease were conflicting and inconclusive, there has been support that either glucose or insulin can improve cognition and memory in patients with Alzheimer’s disease.
And so based on their analysis, the researchers from Rhode Island concluded that Alzheimer’s disease is mediated by Insulin resistance (occurring in type 2 diabetes) and insulin depletion. Not only are there a loss of neurons, but also an advanced level of insulin resistance, which injures the cerebral microvasculature (arterioles and capillaries), resulting in damage in blood flow and affecting the function of the blood-brain barrier. Insulin also contributes to the accumulation of beta-amyloid in certain regions of the brain. These plaque deposits can cause neurotoxic cell death.
Researchers also discovered that insulin is not only produced in the pancreas, but also in the brain. Insulin is produced in various regions of the brain. The highest production of insulin occurs in the hippocampus and the hypothalamus. The hippocampus plays a role in memory; learning and cognitive functions whereas the hypothalamus is associated with physical and emotional functions, such as sleep, appetite, sex drive and mood.
Research has shown that insulin deficiency and insulin resistance are mediators of Alzheimer’s disease-type neurodegeneration.
Roles of brain insulin deficiency and insulin resistance in Alzheimer's disease:
Suzanne de la Monte is the neuropathologist at Brown University in the United States of America who discovered that Alzheimer’s disease correlates with insulin resistance and insulin deficiency in the brain. Her experiment with rats showed that Alzheimer’s could be a controversial category of “Type 3 diabetes”. De la Monte compared Type 3 diabetes to Type 2. However, Type 3 concerns the brain and resembles dementia rather than a lack of insulin being produced in the pancreas.
As mentioned before, Alzheimer’s disease develops as a result of insulin resistance. Now, De La Monte has discovered that this prevents lipid metabolism. As more and more time passes by, these lipids accumulate in the brain, rather than absorbed, which increases stress and inflammation and symptoms of dementia trigger.
Suzanne de la Monte demonstrated this experimentally, using rats. She had modified the way in which the rats’ brains responded to insulin. Insulin is a hormone known to control blood sugar levels, and that also plays a role in brain signalling. De la Monte had disrupted the rodents’ insulin path to their neurons and performed a common memory test for rodents – navigating their way around a circular water maze. As a result, these rodents were confused and were not aware of where they were. “They were demented. They couldn’t learn or remember.” - Observed De la Monte.
She uncovered surprising damage to the rats’ brains. The areas of the brain associated with memory were a punctate of bright pink plaques. The rodents’ neurons were collapsing and crumbling as it was on the point on bursting with toxic proteins. These rodents were near death as they disintegrated, losing their connections with other neurons and losing its shape.
These changes indicated a similarity to Alzheimer’s disease and the results for blocking the neuron connection in the brain lead to dementia.
Calorific foods are known to weaken the body’s response for insulin. Therefore, one may be poisoning his/her brains every time they consume junk food. And so, people with Type 2 Diabetes already have a high risk of developing dementia, as they are already resistant to insulin. Consuming foods with high saturated fats and sugars are bad for one’s brain as they keep one’s insulin levels high. A recent study from the University of California was conducted where rats had to consume water containing high-fructose corn syrup (a sweetener in soft drinks) and some processed foods. As a result, the rodents had memory problems after six weeks and their brain tissue became less responsive to insulin.
De la Monte’s first experiment that linked to Type 3 diabetes was with demented rats. She wanted to discover the impact of alcohol in the brain. Alcohol is known to decrease the number of insulin receptors. She used a chemical to wipe out all the brain cells carrying the insulin receptor. As a result, there was a build-up of the deadly beta amyloid plaques, which were very similar to Alzheimer’s. Because of this experiment, there have been other discoveries confirming that a disrupted insulin resistance can lead to the symptoms of Alzheimer’s.
Other researchers such as McNay and Suzanne Craft fed rats with a high fat diet for 12 months. As a result, this destroyed their ability to regulate insulin. This led to diabetes. The rats also had trouble navigating their way around a maze. These animals behaved such as to an Alzheimer’s patient. McNay and Craft also discovered that in the rat’s brain, there were, again, high levels of beta amyloid (build up of amyloid plaques).
William Klein from Northwestern University did an experiment associated with rabbits. He found that, in rabbits, triggering diabetes created brain changes linked to Alzheimer’s including a sharp rise in the number of beta amyloid proteins. He had also done an experiment studying rat neurons in dishes. He found that clustered toxic proteins attack and destroy regions of synapses that are covered in insulin receptors. The protein also stopped new receptors from appearing and therefore they were neuron insulin resistant. This results in impairment in cognition. The resistance of insulin tells cells to make even more beta amyloid, which harms even more brain cells, triggering a toxic cycle.
Studies cannot tell everything about a human disease when using animals in experiments. However, the demonstrations shown do confirm that human brains with Alzheimer’s are insulin resistant.
Steven Arnold (from the University of Pennsylvania) used brains from corpses in his experiment. He bathed various tissue samples from the brain in insulin to see how the tissues would react. Tissue samples included a brain that had already developed Alzheimer’s and a healthy brain. The tissue sample from the people without Alzheimer’s sprung back to life. It triggered a rush of chemical reactions possibly related to synaptic activity. As for people with Alzheimer’s, the neurons barely reacted. Arnold quotes: “Insulin signalling is paralysed.”
The Toxic Cycle
A high sugar and fat diet leads to high levels of insulin in the brain. The high level of insulin blocks the enzyme that engulfs the beta amyloid protein. Not only that, the high levels of insulin also affects the neurons and the neurons become resistant to the effects of insulin. The neurons make even greater quantities of beta amyloid protein. Even worse, the beta amyloid produces toxic quantities, which block the insulin receptors on neurons. Eventually, there is a fall in the production of insulin. This is a big problem, as the insulin can stop the damage of beta amyloid by blocking its landing site on neurons. So, without it, the cell is more vulnerable to damage. This leads to brain damage and dementia. (As shown in Figure 7)
Although people with Alzheimer’s are not definitely diagnosed with type 2 diabetes, there have been problems with insulin signalling in their bodies. Plus, the mechanism between diabetes and dementia is quite similar. Due to our addiction to fast food, type 2 diabetes increases more and more. People need to be aware of what they eat to prevent diabetes and dementia. Already people, especially in the United States, show early signs of insulin resistance and are considered “prediabetic”.
Suzanne Craft set up a study proving that if someone doesn’t develop diabetes, a bad diet may still be enough to trigger the motion for brain degeneration. The study lasted for one month and there were two groups. One group ate food, which were high in fats and sugars; the other group was known as the control group and ate food that was low in fats and sugars. After this period of time, the people who ate high sugary and fatty foods had higher levels of insulin and “significantly higher beta amyloid levels in their spinal fluid”; whereas, the control group showed low levels in both insulin and beta amyloid levels. Therefore Craft concluded, “An unhealthy diet disrupts normal insulin function in the brain, increases inflammation and oxidative stress, and impairs amyloid regulation.”
Even though high levels of insulin in the brain could cause dementia, on the contrary, Craft investigated whether or not symptoms could be improved by a boost of insulin. This was known as the SNIFF study. Craft had tested a nasal spray that delivered insulin via the nose to the brain. This study lasted four months and only recruited 104 people. The results to this study were promising. The participants who did receive the treatment could recall more details of stories in memory tests, regained more interest in their hobbies, had longer attention spans and were better able to care for themselves. The treated participants also improved their glucose metabolism in their brains.
This nasal spray may work for various reasons as the given insulin has a variety of roles in the brain. This blast of insulin may help the impaired cells to return to normal activity. Problems for Alzheimer’s patients could be solved as Craft states that the spray could decrease inflammation and oxidative stress caused by compounds that react with oxygen. William Klein from Northwestern University also agrees that Craft’s approach could work as an addition of insulin up the nose could help prevent the beta amyloid toxins from attaching with brain cells. Klein says: “It is a struggle between insulin and the toxins for synaptic survival”.
Clinical trials are also investigating drugs for diabetes for example, metformin, which improves the insulin sensitivity of an organ by trying to restore the balance of insulin and glucose in the blood. Arnold plans to study the effect of metformin by measuring the levels of amyloid in the spinal fluid and testing before and after treatment of the blood flow in the brain. Arnold says: “We want to see if these medicines work to decrease levels of these abnormal proteins in Alzheimer’s disease and ultimately improve the patients’ cognitive abilities, or at least prevent them from getting worse. We’ll also see whether the drugs restore other insulin functions like promoting synapse formation and regrowing neural connections.”
Awareness and Prevention
Since insulin resistance is triggered by a poor diet, one can reduce the risk of developing Alzheimer’s by avoiding fats and sweets. On the other hand, diets rich with certain fatty acids might help the brain maintain a good insulin signalling.
One can prevent dementia by eating fresh fruit and vegetables that contain many vitamins and antioxidants. Research has shown that there is a higher risk of developing dementia with low levels of vitamin D in one’s diet. Therefore, sources of vitamin D (eggs, oily fish) are important for a healthy diet. This is because the polyunsaturated fatty acids, such as omega-3 fatty acids found in oily fish, reduce the risk of developing dementia.
Exercise can also help overcome the development of insulin resistance. 40 per cent chance of Alzheimer’s is reduced with regular physical activity. McNay says that even if people are diabetic or overweight, it is not too late to start exercising. A build up of amyloid can still be broken down. As quoted by McNay: “Get some of the insulin sensitivity back and stop accumulating so much amyloid.”
Many of the elderly who have Alzheimer’s disease have been diagnosed to take statin drugs to lower cholesterol levels. However, these drugs have been proved to cause diabetes and to exacerbate Alzheimer’s. Therefore, as many dementia patients take these drugs, this will make the patients’ symptoms worse.
Benson states that the human body requires cholesterol in order for the body to be healthy. However, if cholesterol levels are too high, then it can clog the arteries, causing problems in inflammation. Inflammation can prevent proper absorption and use of cholesterol. Therefore, high cholesterol levels trigger the body’s chronic inflammation. But consuming more healthy saturated fats, such as coconut oil, can help prevent or even cure Alzheimer’s. These saturated fats prevent the inflammation problem and can also improve the brain’s neuronal function by increasing the absorption of cholesterol in the brain.
Researchers have predicted more and more people as the years go by will develop dementia. Not only that, obesity cases will increase and so will the number of cases for people with diabetes. In figure 8, it shows that the older one is, the more likely one will develop dementia since there are more dementia cases (in millions) in the older aged categories. This graph also shows a positive correlation between the number of people (millions) and the years that go by as the line gradually increases.
A bad diet filled with high sugars and fats will lead to obesity if eating habits are uncontrolled and one does not do enough exercise to lose the weight. Obesity is a strong factor that links to the development of diabetes. A bad diet with high levels of sugars can lead to a higher risk of insulin resistance, and therefore lead to type-2 diabetes. In Figure 9, there is a positive correlation for both the mean body weight and diabetes. On the graph it shows that more and more people are putting on weight each year, therefore the number of diabetes cases increases, especially from 1996 to 2000.
The research shows a lot of evidence that a bad diet containing high sugars and fats does increase the chance of dementia. There have also been many links between diabetes and dementia, showing a positive correlation between the two disorders. However, a bad diet or having diabetes may not be the only factor that causes dementia. There could be other factors such as genetics or just simply due to old age.
The conclusion is that the term “type 3 diabetes” accurately reflects the fact that Alzheimer’s disease is a form of diabetes involving the brain, which overlap the molecular, and biochemical features with both Type 1 and Type 2 Diabetes.
So is Alzheimer’s the same as brain diabetes and is this brain diabetes known as a type 3? Dr. de la Monte and her colleagues in fact state that Alzheimer’s disease is more a neuroendocrine disorder that resembles type 2 diabetes, however, it is slightly more complex. These researchers see this as “brain diabetes” and call it type 3 diabetes. This provokes scientific controversy.
Other researchers have agreed on the findings of a close interaction between diabetes and Alzheimer’s. Not only do they point out that type 2 diabetes is a significant risk factor for Alzheimer’s, but also patients with Alzheimer’s are at higher risk for type-2 diabetes. However, there are some issues. The casual link is still inconclusive between the two diseases. All the mechanisms are still not well understood on the impact by diabetes to Alzheimer’s. De La Monte and her colleagues conclude, “It is premature to refer to Alzheimer’s disease as type 3 diabetes at the current time.”
A bad diet does increase the chance of developing dementia. A lot of research, having been conducted by de la Monte, McNay, Craft and many more, supports the link that a bad diet can cause dementia. However, a bad diet is not the only contributing factor and a bad diet is not an immediate cause dementia. Nevertheless, there have been a variety of results all concluding that high levels of fats and sugars trigger the over-production of insulin in the brain, which leads to the build up of plaques and the loss of neurons.