The research comes out of the University of Michigan and involved the study of 1,674 elderly Mexican-Americans from Sacramento, California. At the beginning of the 5-year study none of the participants showed signs of dementia or cognitive impairment.

A total of 130 participants had developed dementia or impaired cognitive ability by the end of the study. 452 (27%) of the participants had taken statins during the study period. After adjusting the results for risk factors such as a history of a stroke or diabetes, smoking, and years of education, the researchers found that the participants who took statins had an impressive 52% reduction in the probability of developing dementia or cognitive impairment compared to the participants who did not take statins.

The study comes on the back of recent studies that have found that statins taken after the onset of dementia have little effect on the progression of the disease. According to lead researcher Mary Haan of the Department of Epidemiology at the University of Michigan, while statins may not slow the progression of dementia, they may be effective as a preventative measure against the disease.

Statins work by increasing the production of LDL-receptors in the body which leads to a direct reduction in LDL cholesterol levels. It is thought that high cholesterol levels in the blood, and diets containing large amounts of cholesterol trigger an inflammatory response in the body that can cause oxidative stress in the brain leading to an increased risk of dementia. Scientific studies attempting to link cholesterol to dementia have produced conflicting results however with some studies finding no link at all between the two. It is possible that statins reduce dementia risk through some unknown mechanism that is unrelated to statins cholesterol lowering abilities.

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The study was conducted by researchers out of the University of Kansas School of Medicine. The researchers compared the brain sizes and fitness levels of 64 individuals who were free of dementia and 57 patients who had recently been diagnosed with early-stage Alzheimer’s disease.

The fitness of the participants was measured using VO2-peak which is a measure of an individuals ability to transport and use oxygen during exercise. It is generally thought to be one of the best measures of cardiovascular fitness.

Physical fitness was not found to be correlated with brain size in patients without Alzheimer’s disease. In those who had recently been diagnosed with Alzheimer’s disease however, high levels of physical fitness were associated with both larger brain and white matter volumes.

Normal brains tend to reduce in size as a person ages, however in Alzheimer’s disease the rate of brain shrinkage is much faster than in normal brains. The researchers found that those with Alzheimer’s disease who were not physically fit experienced brain shrinkage at four times the rate of Alzheimer’s patients who were physically fit.

The authors concluded that physical exercise might allow recently diagnosed Alzheimer’s sufferers to maintain brain function and continue to live independently for much longer than might be the case for sedentary individuals.

The research team plans to continue following the participants of this study for a further two years in order to see how cognitive ability and brain volume in Alzheimer’s patients correlates with physical activity over time.

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American researchers analyzed 2,798 individuals with a mean age of 72 years. During the study 480 (17.2%) of the participants developed dementia over an average follow up period of 5.4 years. The researchers found that for women, a 1 inch increase in arm span led to a 7% decrease in dementia and a 10% decrease in Alzheimer’s disease risk. A 1 inch increase in knee height led to a 16% and 22% decrease in the risk of developing dementia and Alzheimer’s disease respectively.

In men the results were less conclusive with no correlation observed between knee height and Alzheimer’s disease. A longer arm span was associated with a modest reduction in the risk of dementia and Alzheimer’s disease with a 1 inch increase in arm span decreasing dementia risk by 6% and Alzheimer’s disease risk by 8%.

The study found no association between the risk of vascular dementia and knee height while longer arm spans were associated with a statistically insignificant decrease in risk. Vascular dementia is the second most common form of dementia behind Alzheimer’s disease and is caused by impaired blood flow to the brain.

The size of a persons limbs depends on both genetic and lifestyle factors. It is thought that the link between limb size and Alzheimer’s disease is due to the part of the brain that influences limb growth being the same region of the brain that is most severely affected by Alzheimer’s disease.

Poor nutrition and health in a child’s early life may stunt the growth of limbs and it is thought that poor health in early life may increase the probability of developing various health problems, including neurological disorders such as Alzheimer’s disease, in later in life.

The results back up the findings of a Korean study that found a link between longer limbs and improved cognitive performance in elderly people. Other studies have suggested a link between height and Alzheimer’s disease however the correlation appears to be a small one.

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The study found that certain NSAID’s, in particular ibuprofen, cut the risk of Alzheimer’s disease by almost 50% however other NSAID’s including aspirin and COX-2 inhibitors such as celecoxib did not have an effect on Alzheimer’s disease.

The study, conduced by researchers in Boston, involved more than 240,000 participants and is one of the largest studies ever undertaken on the relationship between NSAID’s and Alzheimer’s disease. The participants were all aged over 55 and 49,349 of the individuals had been diagnosed with Alzheimer’s disease while the remaining 196,850 had not.

The researchers compared NSAID use for those with Alzheimer’s disease to those free of the disease. They found that using NSAID’s for more than five years was associated with a 24% reduction in the risk of Alzheimer’s disease. Ibuprofen was found to be particularly effective at reducing Alzheimer’s disease with a 44% reduction in risk observed in those using ibuprofen for more than five years.

Low-dose aspirin did not reduce Alzheimer’s risk which was quite surprising given aspirin is considered a stronger NSAID than ibuprofen however the authors indicated that the dosages of aspirin may have been too low to produce any beneficial effects on Alzheimer’s disease. Other NSAID’s that appeared to reduce Alzheimer’s disease included diclofenac, piroxicam, and inolic acid derivatives. Tylenol, which is a pain killer without anti-inflammatory properties was also found to cut the risk of Alzheimer’s disease.

It is thought that NSAID’s may help prevent Alzheimer’s disease by reducing the formation of amyloid protein deposits in the brain which are a precursor to Alzheimer’s disease. A second mechanism by which NSAID’s may reduce the risk of Alzheimer’s disease is by lowering the levels of anti-inflammatory activity in the brain. Inflammation in the brain is thought to increase in free radical production as well as inducing brain cell toxicity and death.

The theory of inflammation leading to cognitive decline and a higher risk of Alzheimer’s disease is supported by studies that have found Alzheimer’s disease to be more common in people with high levels of C-reactive protein which is a marker of inflammation in the body.

The researchers warn that people need to be careful before starting a regime of NSAID’s because the side-effects of long-term use can often outweigh the benefits. NSAID’s can cause liver and kidney damage, gastric ulcers, and heart problems.

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The study, published in the journal Annals of Internal Medicine in January 2006, analyzed 1,740 people over the age of 65 who were initially free of dementia. The participants were followed for an average of 6.3 years during which 107 people (6.1%) developed Alzheimer’s disease and a further 51 people (2.9%) developed other forms of dementia.

The researchers found that those who were physically active were much less likely to develop dementia than those who were less active. Those who exercised 3 or more times a week were 32% less likely to develop dementia and were 31% less likely to develop Alzheimer’s disease. Exercise was defined as performing a physical activity such as aerobics, swimming, hiking, walking, or biking for at least 15 minutes at a time.

The research backs up other studies that have found physically active people tend to develop Alzheimer’s disease later in life than sedentary individuals. It is believed that exercise improves cognitive function, blood flow in the brain, and may prevent brain tissue loss in the hippocampus which is the part of the brain that affects emotions and memory. The hippocampus is one of the first parts of the brain affected by Alzheimer’s disease.

Studies have also shown that mice who are more active throughout their lifetimes exhibit improved learning and are less likely to develop beta-amyloid plaques, the precursor to Alzheimer’s disease, in later life.

According to lead researcher Dr Eric B. Larson who is the executive director of the Group Health Center for Health Studies in Seattle, Washington, it is never too late to begin exercise and enjoying the health benefits associated with it. Most studies have found that maintaining some form of physical activity in later life allows older people to keep their independence and enjoy a good quality of life for longer than would otherwise be the case.

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In February 2003, a study was published in the journal Archives of Neurology that linked the consumption of both saturated and trans fats with an increased risk of Alzheimer’s disease. The study involved 815 individuals aged 65 and older who were followed for an average of four years.

After adjusting for factors such as age, sex, race, and education, the researchers reported that trans fat intake of more than 4.8g per day was associated with a 150% increase in Alzheimer’s disease risk compared to those who consumed 1.8g per day or less. Saturated fat intake of more than 25g per day was associated with a 120% increase in Alzheimer’s disease compared to those who consumed 13g or less of saturated fat a day.

Both poly-unsaturated fats and mono-unsaturated fats appeared to have a small preventative effect on Alzheimer’s disease although the effect was not statistically significant.

A study published in the journal Annals of Neurology found similar results. That study found that high intake of saturated fat increased Alzheimer’s risk by 90% and also linked a high intake of dietary cholesterol with a 70% increase in Alzheimer’s risk.

Animal studies have found that rats fed diets high in fat and cholesterol exhibited impaired learning and memory performance and had more beta-amyloid deposits in their brains. Studies in humans have found a link between high cholesterol levels and greater Alzheimer’s disease risk. Saturated fats are known to increase blood cholesterol levels, particularly LDL cholesterol.

Trans-fats are uncommon in fresh foods \but are commonly found in foods such as biscuits, pies, potato chips, salad dressings, and margarines which contain high amounts of hydrogenated vegetable oils.

Food products high in saturated fat include cream, whole milk, butter, cheese, fatty meats, chocolate, and coconut oil.

Most doctors recommend that less than 30% of an individuals daily calorie intake should come from fats and in particular no more than 10% from saturated fat This equates to less than 60g of total fat and 20g of saturated fat a day for a person who consumes 1800 calories a day.

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The study involved 980 individuals aged 65 or older from the northern Manhattan area in New York. The participants were followed for an average of four years and during that period, 242 of the individuals developed Alzheimer’s disease.

Those individuals who were in the highest quartile for calorie intake (average intake of 1870 kcal) were found to be 48% more likely to develop Alzheimer’s disease than those in the lowest quartile (average intake of 758 kcal) while those in the second highest quartile for calorie intake (average intake of 1363 kcal) were 20% more likely to develop Alzheimer’s disease than those in the bottom quartile.

Calories derived from fat were found to be the most strongly associated with Alzheimer’s disease. Individuals in the highest quartile for mono unsaturated fat intake were 60% more likely to develop Alzheimer’s disease and individuals in the highest quartile for saturated fat were 30% more likely to develop Alzheimer’s disease than those in the lowest quartiles.

Those who carry the ApoE-4 allele, which increases the risk of Alzheimer’s disease, appeared to be at the greatest risk when consuming a high calorie diet. Those with the ApoE-4 allele and who were in the highest quartile for calorie intake were 2.3 times more likely to develop Alzheimer’s disease than those with the ApoE allele in the lowest quartile for calorie intake.

It is thought that calorie restriction helps reduce oxidative damage in the body by reducing the number of free radicals present. Oxidative damage to cells in the brain (neurons) may be one of the processes related to the development of Alzheimer’s disease. Those who consume calorie restricted diets also tend to have higher levels of the SIRT1 protein in the brain. SIRT1 is thought to be associated with a longer lifespan and improved health in old age.

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The study involved 938 people aged 60 or older who had been diagnosed with Alzheimer’s disease. The researchers looked at three potential risk factors: heavy cigarette use, heavy alcohol consumption and the presence of a particular allele of the ApoE gene which is known to increase the risk of Alzheimer’s disease.

The research team found that 20% of the patients diagnosed with Alzheimer’s disease had been heavy smokers (20 or more cigarettes smoked per day), 7% were heavy drinkers (more than two standard drinks consumed per day), and 27% had the ApoE allele that is known to increase Alzheimer’s risk.

The researchers determined that consumption of more than two standard drinks of alcohol a day led to Alzheimer’s disease developing 4.8 years earlier than in people who consume less than two standard drinks a day. The researchers also found a link between heavy smoking and Alzheimer’s disease with heavy smokers developing the disease on average 2.3 years earlier than those who did not smoke heavily.

Those who had a combination of all three risk factors studied developed Alzheimer’s disease at the average age of 68.5 which was 8.5 years earlier than for individuals with none of the risk factors.

The authors of the study admit that there is some controversy over the link between heavy drinking and Alzheimer’s, especially in regard to how “heavy” drinking is defined and the type of alcohol that is consumed. Some studies have found that light to medium consumption of alcohol, in particular wine, can actually reduce an individuals risk of developing Alzheimer’s. It is generally accepted however that consumption of more than three standard drinks a day, especially in the form of hard liquor, damages the brain and increases the risk of dementia.

The link between heavy smoking and Alzheimer’s disease risk is thought to be more clear cut with several studies demonstrating a link between the two. A 1997 study published in the journal Lancet found that smokers had a 2.2 times greater risk of dementia, and a 2.3 times greater risk of Alzheimer’s disease compared to people who had never smoked. That study also found that smoking had the greatest impact on people without the high risk ApoE gene and had little impact on people with the high risk variant.

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The researchers analyzed almost 10,000 men and women from Northern California who were initially between the ages of 40 and 45. The participants underwent health evaluations between 1964 and 1973 which included measurements of blood cholesterol and blood pressure. 30 years later, the researchers obtained medical records of the participants and determined that 504 (5.2%) people had developed Alzheimer’s disease while a further 162 (1.7%) had developed vascular dementia.

The researchers found that those people who had very high total cholesterol levels (between 249 and 500 mg/dL) in middle age were around 50% more likely to develop Alzheimer’s disease than those with low cholesterol levels (less than 198 mg/dL).Those with moderately high cholesterol levels (between 221 and 248 mg/dL were around 25% more likely to develop Alzheimer’s disease.

High cholesterol levels are an established risk factor for other diseases such as coronary heart disease and strokes however the ratio of HDL (the good cholesterol) to LDL (the bad cholesterol) is thought to be more important than total cholesterol levels in these diseases. This study however suggests that high cholesterol levels are a risk factor for Alzheimer’s disease regardless of the type of cholesterol.

According to lead author Dr. Alina Solomon from the University of Kuopio in Eastern Finland “The association between cholesterol and cardiovascular disease is well known. What we know now is that minding heart health may protect your brain as well.”

Total cholesterol levels below 200mg/dL and LDL cholesterol levels below 120mg/dL are generally considered optimal.

A person can lower their cholesterol by losing weight, performing regular exercise, eating several small meals a day rather than one or two large ones, consuming mono-unsaturated and polyunsaturated fats rather than saturated and trans fats, quitting smoking, consuming fiber rich foods or taking a fiber supplement, and switching to fresh fruits and vegetables rather than processed foods.

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The Swedish study involved 1,458 women initially aged between 38 and 60. The participants were subjected to a physical examination and completed questionnaires on social and lifestyle factors including alcohol use, cigarette use, and education levels. The study began in 1968-1969 and follow up studies were conducted in 1975, 1980-1981, 1992-1993, and at the end of the study in 2002.

At the conclusion of the study, all but 5% of the participants had died with 162 (11.1%) of the women having been diagnosed with dementia. The researchers found that after adjusting for other risk factors such as education, smoking, and BMI, wine consumption was associated with a decrease in dementia rates while spirits were associated with an increase in dementia risk. Beer consumption did not appear to be correlated with the incidence of dementia.

Women who drank wine regularly and did not drink any other form of alcohol were 70% less likely to develop dementia and as much as 81% less likely to develop dementia when former wine drinkers were included. Those who drank wine in combination with beer and/or spirits were 40% less likely to develop dementia. In contrast, regular consumption of spirits was associated with a 50% increased risk of dementia.

The study also found that although beer did not seem to protect against an individual getting dementia, both wine and beer increased the dementia-free lifetimes of participants while smoking and consumption of spirits lowered the dementia-free lifetimes of participants.

The researchers believe that it may be ingredients in wine other than ethanol that are responsible for the reduction in dementia risk because only wine and not other forms of alcohol were shown to reduce dementia risk.

The study did not differentiate between red and white wine. Red wine is known to have many beneficial compounds including flavonoids such as quercetin and epicatechin as well as polyphenols such as resveratrol that may protect against Alzheimer’s disease. It is also possible that wine drinkers may lead a healthier life style than beer or hard liquor drinkers resulting in a lower probability of dementia.

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The researchers analyzed the survival rates of 847 people who had been diagnosed with Alzheimer’s disease.The majority of the patients in the study were women and the average age of participants was 74 years.

Around two-thirds of the patients took 1,000 international units (IU) of Vitamin E a day combined with a cholinesterase inhibitor. Less than 10% took vitamin E alone and 15% of the patients took no Vitamin E. The researchers found that those who took Vitamin E extended their survival times by around 26% compared to those who did not take Vitamin E. Interestingly the cholinesterase inhibitor offered no survival benefit when used alone.

The study also suggested that a combination of both Vitamin E and the cholinesterase inhibitor may be more beneficial than either treatment by itself as the greatest improvement in survival time came in the group using both agents.

A daily dose of 1,000 IU of Vitamin E is around 50 times the recommended daily intake of 20 IU. Concerns had been raised that very high doses of vitamin E may actually increase increase mortality, particularly in the elderly, however this does not appear to be the case for those with Alzheimer’s disease. The current upper safety limit for Vitamin E is 1,500 IU per day in the United States and 800 IU in the United Kingdom.

According to Valory Palik, one of the studies co-authors, “[…] we did not find evidence that high doses of vitamin E reduced survival. In fact, patients who took vitamin E seemed to live longer, particularly when they took it in combination with a cholinesterase inhibitor.”

Natural sources of Vitamin E include vegetable oils, nuts, tomato sauce, peanut butter, whole grain breads, olives, papaya, blueberries, avocados, eggs, tuna, and most leafy green vegetables.

Cholinesterase inhibitors try to increase levels of acetylcholine in the brain by reducing the function of cholinesterase enzymes which break down the chemical acetylcholine.

Acetylcholine is a neurotransmitter that plays an important role in brain function and depleted supplies of acetylcholine are often found in the brains of those diagnosed with Alzheimer’s disease.

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The study, conducted by Swedish researchers, involved data from the Uppsala Longitudinal Study of Adult Men which followed 2,269 men aged 50 years in 1970 for an average period of 32 years. At the beginning of the study, the men were tested for both insulin response and glucose tolerance. At the conclusion of the study, 102 (4.5%) of the men had developed Alzheimer’s disease, 57 (2.5%) had developed vascular dementia, and 235 (10.4%) had been diagnosed with other forms of dementia.

The researchers found that those men with a poor response to insulin were much more likely to develop Alzheimer’s disease than those with a normal insulin response. Those in the bottom quarter for insulin response were almost twice as likely to develop Alzheimer’s disease as those in the top 25% for insulin response.

While impaired glucose tolerance was not associated with Alzheimer’s disease, it was associated with another form of dementia known as vascular dementia. Those in the bottom 25% in terms of glucose tolerance were around 2.2 times more likely to develop vascular dementia than those in the top 25%.

Vascular dementia is the second most common form of dementia behind Alzheimer’s disease. It occurs when blood flow to the brain is impaired causing brain cells to die due to a lack of oxygen.

The relationship between Alzheimer’s disease and poor insulin response was strongest in those who did not have a specific form of a gene called ApoE-4 which is associated with Alzheimer’s disease. Around 30% of the population is though to have at least one copy of ApoE-4.

According to lead researcher Elina Ronnemaa of the Uppsala University in Sweden: “Our results have important public health implications given the increasing numbers of people developing diabetes and the need for more powerful interventions.” Ronnemma added that insulin problems are an important risk factor for Alzheimer’s disease, particularly amongst those who do not have the high risk form of the ApoE gene.

Similar findings have been reported in earlier studies. In one study, published in 1996, Dutch researchers found that diabetics who required insulin were 3.2 times more likely to develop dementia than non-diabetics. That study found that the relationship was strongest with vascular dementia but was also observed in Alzheimer’s disease.

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The researchers, based in Rotterdam, The Netherlands, analyzed 486 people between the ages of 60 or 90 who were free of dementia at the beginning of the study. The participants were followed for a period of six years during which 33 people (6.6%) developed Alzheimer’s disease.

Of the participants, 134 (27%) indicated that they had a history of depression, with 88 of these individuals reporting depression before the age of 60 and 46 individuals indicating depression had began after the age of 60.

After controlling for other variables, the researchers reported that individuals with a history of depression before the age of 60 were 3.76 times more likely to develop Alzheimer’s disease compared to those with no history of depression. Those who developing depression after the age of 60 were 2.34 times more likely to develop Alzheimer’s disease than those with no history of depression.

The researchers believe that depression may damage the limbic system, which is a part of the brain housing the hippocampus and amygdala which play a role in controlling emotions, long term memory, and behavior.

In a previous study, published in the journal Archives of General Psychiatry, researchers had found that the brains of Alzheimer’s disease patients who had a history of depression had more tangles and plaques in the hippocampus than Alzheimer’s disease sufferers who did not have a history of depression.

In that study however, brain scans of the subjects did not reveal a link between depression and damage to either the hippocampus or the amygdala.

Cortisol levels are raised in depressed individuals and another possible explanation for the link between depression and Alzheimer’s disease is that high cortisol levels, which are associated with inflammatory activity in the body, may cause oxidative stress leading to greater free radical production and neuron cell damage in the brain.

Another possible explanation for the link is that early changes in the brain caused by Alzheimer’s disease may manifest themselves as depression. It is therefore possible that depression may be an early warning symptom of changes in the brain caused by processes associated with early Alzheimer’s disease such as beta-amyloid plaque development.

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In the study, published in the Journal of Neuroinflammation, researchers used New Zealand white rabbits to examine the effects of a high cholesterol diet and/or high levels of caffeine consumption on the blood-brain barrier.

The blood brain barrier protects the brain from chemicals circulating in the blood that can disrupt brain function. Leakages of the blood-brain barrier are believed to occur in neurological disorders such as Alzheimer’s disease, Parkinson’s disease, and strokes.

In Alzheimer’s disease it is believed that leakages in the blood-brain barrier allow blood containing amyloid beta protein to cross into the brain. Deposits of amyloid beta plaques are found in the brains of Alzheimer’s sufferers and are associated with brain cell toxicity and death. High levels of dietary cholesterol are linked with increased linkages of the blood-brain barrier so it is hypothesized that high cholesterol diets may increase the risk of Alzheimer’s disease.

The 24 rabbits used in the study were divided into four groups. One group received a normal diet, the second group received a normal diet supplemented with 3mg a day of caffeine added to the rabbits drinking water, a third group received a high cholesterol diet, and the final group received both a high cholesterol diet and 3mg of caffeine daily. The diets were administered for the full 12 week duration of the study.

The researchers found that the high cholesterol diets increased the levels of fibrinogen and IgC in the rabbits’ brains. These two substances are usually blocked from entering the brain by the blood brain barrier so high levels of the chemicals indicates leakages in the blood brain barrier. The rabbits who received both the high cholesterol diets and the caffeine had normal levels of fibrinogen and IgC indicating that caffeine prevented the breakdown of the blood-brain barrier caused by the high cholesterol diet.

The authors of the study concluded that: “chronic ingestion of caffeine protects against high cholesterol diet-induced disruption of the blood-brain barrier”.

The 3mg of caffeine a day administered to the rabbits is equivalent to around 50mg of caffeine a day in humans. This is equivalent to just one cup of coffee, one can of coke, two cups of black tea, or 80g (2.8oz) of dark chocolate a day.

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6,583 middle-aged adults from the Kaiser Permanente organization in Northern California took part in the study during the 1960s and 70s which involved the measurement of individuals Sagittal Abdominal Diameter (SAD). SAD is a measurement of the thickness of the body in the middle of the point between the bottom of the ribs and the pelvic bone. It is similar to a waist circumference measurement in that it is is a measure of central or abdominal fat levels. A SAD measurement greater than 25 cm (10 inches) is considered to indicate central obesity.

By 2006, 1049 (15.9%) of the individuals in the study had been diagnosed with some form of dementia. Those with an abdominal diameter in the top 25% were at a 2.72 times greater risk of dementia compared to those in the lowest 25% of abdominal diameters. Even after adjusting for Body Mass Index (BMI) those in the highest quartile of abdominal diameters were still 92% more likely to develop dementia.

Even skinny people can be at a greater risk of dementia if they have high levels of belly fat. Those in the study who had a BMI in the healthy weight range but a abdominal diameter greater than 25cm were 89% more likely to develop dementia than those with a healthy BMI but an abdominal diameter less than 25cm.

Those in the obese BMI range (BMI greater than 30) who also had a high SAD had the highest risk of dementia with a 260% greater risk of developing dementia.

The increased risk of dementia came independent of other possible dementia risk factors such as age, education, marital status, and the presence of diseases such as heart disease, diabetes, hypertension and strokes.

Abdominal fat is predominately visceral fat. Visceral fat is known to secrete certain hormones which increase inflammation and oxidative stress in the body. Leptin, which is secreted by visceral fat cells is known to play a role in the formation of plaques in the brain. These plaques are considered to be precursors of Alzheimer’s disease.

According to lead researcher Rachel Whitmer of the Kaiser Permanente Division of Research: “Fat biologists know, that visceral fat, it is more lively, it is more toxic, it is more metabolically active. It secretes a lot of hormones and inflammatory compounds.”

Those with a large waist size are already known to be at a far greater risk of diabetes, strokes, and heart disease than those with a smaller waist size. Studies suggest that men with a waist size greater than 40 inches (102cm) are 12 times more likely to develop diabetes than those men with a waist size less than 34 inches (86cm). Another study found that women with a waist size greater than 88cm are three times more likely to develop cardiovascular disease.

The study should come as a wake up call to many people with more than fifty percent of adult Americans considered to be centrally obese.

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The study, which was funded by the National Institute on Aging and the U.S. Department of Veterans Affairs, followed 111 families in which both parents had been diagnosed with the disease.

Of the 297 children born to the parents, 67 of the children (23 percent) had been diagnosed with Alzheimer’s disease. In the 98 of the children who had reached the age of 70 years, 41 of them (42 percent) had been diagnosed with Alzheimer’s disease. In the general population just 14 percent of those over the age of 70 are thought to be living with Alzheimer’s disease.

Around 31 percent of the children older than 60 years and 36 percent of those over 65 years had developed Alzheimer’s disease compared to around 8 percent and 11 percent in the general population respectively.

The genetic component to Alzheimer’s disease has yet to be understood fully. Currently only one gene, called ApoE, has been linked to increased Alzheimer’s disease risk however it is likely that many more such genes exist. Those who have a particular form of the ApoE gene, called E4, are thought to be at increased risk of atherosclerosis, Alzheimer’s disease, and reduced growth of axons and dendrites in the brain.

According to Dr. Thomas Bird, who is the director of the Genetics Core of the University of Washington Disease Research Center and senior author of the study, “I think it confirms that there’s a strong genetic component in the disease and that’s not a surprise.”

The study appears in the March edition of the journal, Archives of Neurolgy.

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A recent study presented in the journal Neurology, analyzed data taken from the Cardiovascular Risk Factors, Aging, and Dementia study (CAIDE) to determine the extent of the relationship between education and the development of dementia.

This study involved following 1,449 middle aged individuals from Finland for 21 years. The participants were first surveyed in either 1972, 1977, 1982 or 1987. A final follow-up re-examination of the individuals, now aged between 65 and 79, was carried out in 1998.

Researchers found that those individuals who had between 6 and 8 years formal education had, on average, a 43% lower risk of developing dementia and a 51% reduced risk of developing Alzheimer’s disease compared to those with 5 or less years of formal education. For individuals with 9 or more years of formal education, the risk of developing dementia was a massive 84% lower than those with 5 or less years of education while the risk of developing Alzheimer’s disease was 85% lower.

The associations did not significantly change when potential confounding variables such as lifestyle and socio-economic factors were taken into account and the results were the same for both men and women.

An earlier American study involving 594 people, which was published in 1994 in the Journal of the American Medical Association had found a similar relationship between low education levels and the risk of developing Alzheimer’s disease.

That study also found that those working in low-skilled occupations were at a greater risk of developing Alzheimer’s disease. Those with the combination of a low skilled job and low education levels were at almost three times the risk of developing Alzheimer’s disease.

A third study, published in the Archives of Neurology in 2001, involved the study of 1,296 subjects from Sweden aged over 75. That study found that those with less than 8 years of formal education were at more than twice the risk of developing Alzheimer’s disease compared to those with 8 or more years of formal education. The results of that study are presented below.

While educated people tend to develop Alzheimer’s and dementias much later in life, some studies have found that highly educated individuals appear to deteriorate much quicker upon diagnosis of Alzheimer’s disease.

It is thought that those with higher levels of education may be better able to tolerate deterioration in the brain meaning early stage Alzheimer’s disease might go unnoticed for a long period of time. Because of this, Alzheimer’s disease may be quite well advanced at the time of diagnosis which might explain the faster rates of mental decline observed in well educated people following the diagnosis of Alzheimer’s disease.

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One such study involved over 8,800 female residents of a retirement community situated in Laguna Hills, southern California. The residents were surveyed on various health related questions in 1981. Over the 11 year study period, 138 of the participants were diagnosed with Alzheimer’s disease or other dementias likely to be Alzheimer’s disease.

The study found a significant reduction in the likelihood of developing Alzheimer’s disease amongst those using estrogen replacement therapy compared to those not using the therapy with the odds of estrogen users developing Alzheimer’s disease 32 percent lower than those not using the therapy.

The study also found the risk of developing Alzheimer’s disease decreased significantly when the estrogen dose was higher and when the duration was longer. The study also found that the risk of Alzheimer’s was higher the later each women experienced their first menstrual period.

The researchers concluded that: “This study suggests that the increased incidence of Alzheimer’s disease in older women may be due to estrogen deficiency and that estrogen replacement therapy may be useful for preventing or delaying the onset of this dementia.”

Another study, which formed part of the Baltimore Longitudinal Study of Aging (BLSA),  found that women using hormone replacement therapy (HRT) were 50 percent less likely to develop Alzheimer’s disease during the sixteen year study period.

Estrogen raises levels of several neurotransmitters such as acetylcholine, serotonin, noradrenaline and dopamine. Low levels of acetylcholine are often found in individuals diagnosed with Alzheimer’s disease and it is thought that the ability of estrogen to increase acetylcholine levels in the brain may be responsible for the relationship between estrogen levels and Alzheimer’s disease.

Estrogen has also been shown to reduce or prevent the formation of beta amyloid plaques which are found in the brains of Alzheimer’s sufferers. Estrogen can also improve blood flow in the brain and raises the levels of nerve growth factors in the brain.

Endogenous estrogen levels are largely determined by genetics however hormone replacement after menopause can help women maintain higher estrogen levels in later life.

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Researchers at the Massachusetts General Hospital Institute for Neuro-degenerative Disease analyzed the brains of mice bred to develop amyloid plaques using an advanced microscopic imaging technique known as “multiphoton laser confocal microscopy” in order to view the formation of the plaques and the subsequent damage as it occurred in the brains of the mice.

“We’ve had snapshots of individual steps in the past. This microscopic technology gives us the ability to watch the process from beginning to end, to see the variety of things that happen as inflammatory cells get activated,” said research leader Dr. Bradley Hayman.

The researchers found that while the formation of these plaques was a relatively rare event, once plaque formation is initiated, the process was a rapid one with large plaques being observed in mice just one day after a scan showing no plaque formation. Furthermore, the researchers found that neuron cell damage due to plaque formation begins to appear within days of plaque formation.

The study also helps shed light on the way Alzheimer’s disease develops in the brain. Previously it had been unknown whether protein plaques were a symptom or a cause of neuron cell damage in the brain. It now appears that the amyloid protein plaques are the primary cause of the brain cell damage rather than being a symptom of the disease.

In a healthy brain, fragments of amyloid protein known as beta-amyloid form naturally in the brain but are broken down and eliminated by brain cells. In Alzheimer’s disease however, it appears the bodies natural defense mechanisms begin to slow down and become overwhelmed by the protein fragments which start to accumulate between neurons in the brain.

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Researchers at Cornell University in Ithaca, New York tested phenolic phytochemicals derived from bananas, oranges, and apples on neuron cells. The researchers found that all three of the fruits protected the neuron cells from oxidative stress and prevented neurotoxicity. Apples were found to have the highest levels of beneficial antioxidants.

The authors reported that “Our study demonstrated that antioxidants in the major fresh fruits consumed in the United States and Korea protected neuronal cells from oxidative stress.”

Oxidation is caused by free radicals which are highly reactive molecules that have unpaired electrons in their outer ring. These free radicals “steal” electrons from cells in the body (which are made up of molecules) which in turn causes that molecule to become a free radical itself. Antioxidants help prevent this process because they do not themselves turn into free radicals when a free radical steals an electron, thus helping reduce the number of free radicals present in the body.

In Alzheimer’s disease ,free radicals are believed to damage brain cells and lower levels of a chemical known as acetylcholine which helps transmit impulses throughout the brain. Low acetylcholine levels are often found in the brains of individuals with Alzheimer’s disease.

More than one in seven people over the age of 70, and one in two people over the age of 85 suffer from Alzheimer’s disease or some other form of dementia. With the number of people living past 80 increasing dramatically in the western world, in the absence of a cure dementias such as Alzheimer’s disease are expected to become an increasingly important health problem.

The study appears in the December 1 issue of the Journal of Agricultural and Food Chemistry.

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