The study involved 3,468 middle aged men from the Honolulu-Asia Aging Study who were followed up over 25 years. The researchers theorized that a healthy lifestyle in mid-life could reduce an individuals probability of developing dementia in their later years.

Dr. Rebecca P. Gelber, and colleagues looked at four lifestyle characteristics that had been associated that dementia risk in previous studies. The factors were BMI, smoking, physical activity, and diet. The low risk group for BMI was defined as a BMI < 25, the low risk group for smoking was defined as former or non-smokers. For physical activity low risk was defined as being in the top 25% for hours spent doing light or moderate physical activity per day. The low risk diet consisted of relatively low meat and dairy consumption, high consumption of fish, cereals, fruits and vegetables, a high monounsaturated-to-saturated fat ratio, and light to moderate consumption of alcohol.

Over the course of the study, 223 of the participants developed dementia, including 117 cases of Alzheimer's Disease, and 78 cases of vascular dementia. BMI was the strongest risk factor for dementia with a BMI > 25 increasing the odds of developing dementia by 87%. Current smokers had 48% increased odds of developing dementia while individuals with low physical activity had 59% increased odds of developing the disease. Interestingly diet was not strongly correlated with dementia risk in this study.

As a general rule, the lifestyle factors predicted vascular dementia risk better than Alzheimer’s disease risk. For example, a BMI > 25 resulted in a 2.29-fold increase in the odds of vascular dementia but only 1.51 times increased odds of developing Alzheimer’s disease.

Interestingly, individuals who were low risk for all four factors had just 0.36 times the risk of developing dementia compared to other men in the study suggested that a large percentage of dementias could be avoided through a healthy lifestyle in middle age. Men in all four low risk groups comprised just 7.2% of all men in the study.

Vascular dementia and Alzheimer’s disease are the two most common forms of dementia. Vascular dementia occurs when the supply of blood to the brain is restricted. Vascular dementia and cardiovascular disease have similar risk factors and the two diseases often go hand in hand because the cardiovascular system is responsible for delivering blood to the brain.

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In 1989, a study published in The Lancet, found that the risk of Alzheimer’s disease was 50% higher in areas of England and Wales where aluminium concentrations exceeded 0.11mg/L compared to areas with levels below 0.01mg/L.

A second study, published in the American Journal of Epidemiology in 2000, found a 99% increased risk of dementia, and a 114% increased risk of Alzheimer’s disease when concentrations of aluminium in drinking water exceeded 0.1mg/L. The researchers concluded that “our study suggests that a concentration of aluminum in drinking water above 0.1 mg/liter may be a risk factor of dementia and, especially, Alzheimer’s disease.”

Several mechanisms explaining the role of aluminium in Alzheimer’s disease have been proposed. It is believed aluminium may disrupt the blood brain barrier allowing amyloid beta, which would normally be stopped, to pass through the barrier and into the brain. Amyloid beta proteins are the primary component of the plaques observed in the brain of Alzheimer’s patients. A 1978 study published in the journal Biological Psychiatry found that brains of Alzheimer’s disease patients contained 1.4 times more aluminium than the brains of individuals free of Alzheimer’s. Furthermore, studies in mice have found neuron death, increased levels of inflammatory markers in the brain, and the development of lesions following the chronic administration of high levels of aluminium.

Aluminium is a non-essential element but is present in virtually all foods. Higher levels of aluminium can be found in spinach, tea leaves, potatoes, fish, certain types of processed cheese, baking powders that contain aluminium sulfate, and table salt which often contains the anti-caking agent sodium aluminosilicate. Most Americans consume between 1 and 10mg of aluminium a day from dietary sources however this amount pales into insignificance when compared to the intake of individuals who take aluminium based drugs. For example, those who regularly consume antacids with aluminium hydroxide as the active ingredient will likely have intakes in excess of 1 gram a day. Interestingly however, no link has been found between regular antacid use and an increased risk of Alzheimer’s disease although studies to date have been small.

Deodorants are another source of aluminium and while aluminium is not readily absorbed through the skin, some aluminium is unintentionally inhaled through the mouth and nose when deodorant sprays are applied. This study, found a slightly increased risk of Alzheimer’s disease in individuals using aluminium based antiperspirants.

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The study, published in the Journal of Alzheimer’s Disease, involved 3494 men with an average age of 52 from the Honolulu-Asia Aging Study. At the beginning of the study, participants were questioned on their intake of coffee, tea, and colas, in order to determine caffeine intake levels. The participants were followed to death at which time a brain autopsy was carried out.

Although the researchers did not find a decreased risk of clinical dementia in heavy coffee drinkers, they did find that men in the top 25% of caffeine intake were 55% less likely to have brain lesions at death compared to the men in the bottom 25% for caffeine intake.

Brain lesions are the hallmark of various forms of dementia such as vascular denentia, Lewy body dementia, and Alzheimer’s disease. They occur when large groups of brain cells die prematurely, leaving large “holes” in the brain that are often filled with abnormal protein deposits. While the brain can compensate to a certain extent with brain lesions by forming new neuron network, the formation of large-scale lesions eventually results in the memory loss and decreases in cognitive function typically seen in those suffering from dementia.

The apparent lack of a statistically significant link between caffeine intake and clinical dementia despite a reduction in brain lesions could be due to the relatively small study size as only 226 men developed dementia over the course of the study. It is also possible that many of the lesions observed were small, and may not have resulted in a significant decline in cognitive function.

Other studies however have found a reduced risk of dementia in heavy coffee drinkers. A 2009 study, also published in the Journal of Alzheimer’s Disease found a 65% reduced risk of dementia in those who drank between 3 and 5 cups of coffee compared to individuals who drank 2 or less cups a day. The authors concluded that “Coffee drinking at midlife is associated with a decreased risk of dementia/AD later in life”.

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The first study, published in the journal Neurotoxicity Research in 2009, found that compared to a control diet, long term feeding of a diet containing 2% grape seed extract to mice genetically altered to be susceptible to Alzheimer’s disease resulted in a 33% and 44% reduction in amyloid beta levels in the brain and blood respectively.

A second study, led by Dr. Giulio Maria Pasinetti of the Mount Sinai School of Medicine and published online in the Journal of Alzheimer’s Disease earlier this year, found that administering grape seed extract to mice bred to develop an Alzheimer’s like illness resulted in reduced levels of a specific amyloid beta oligomer known as Aβ*56 which had previously been correlated with cognitive decline in mice.

Amyloid beta plays a central role in the development of Alzheimer’s disease because the accumulation of amyloid beta plaques in the brain is one of the hallmarks of the disease. Recently however, attention has focused on free-floating amlyoid beta oligomers which are smaller, soluble bundles of amyloid beta protein, as some studies have suggested that these may be the primary cause of cognitive impairment in Alzheimer’s disease rather than the plaques themselves.

Grape seed extract is one of the most concentrated sources of polyphenolic antioxidants. The primary phenolic compounds in grape seed extract are gallic acid, catechin, and epicatechin. GSE supplements are widely available on the internet and it is commonly marketed as a powerful antioxidant with anti-inflammatory and anti-carcinogenic potential. Although research into grape seed extract is still in its infancy, there is at least some evidence of anti-carcinogenic effects with respect to skin cancer, breast cancer, and leukaemia (see here, here, and here).

Unfortunately, no human clinical trials involving grape seed extract as an Alzheimer’s treatment are currently being carried out. Given the lack of enthusiasm by the pharmaceutical industry in general towards natural, unpatentable treatments, it is unlikely that any large scale Alzheimer’s trials will be carried out in the near future.

For those looking to use grape seed extract, look for a supplement standardized to contain 90-95% proanthocyanidins, as these are the key compounds responsible for the beneficial effects of grape seed extract.

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The Finnish researchers looked at data from 525 individuals who completed an extensive questionnaire on their dietary habits. The participants were assigned a healthy-diet score based out of 17 based on their consumption of certain foods. A score of 0 represented a very unhealthy diet and a score of 17 representing an extremely healthy diet.

Healthy diets consisted of high levels of fruit and vegetable, bread, fish, polyunsaturated fats, monounsaturated fats, and coffee (which has been linked to a decreased risk of Alzheimer’s disease in some studies). Moderate alcohol consumption, not adding salt to meals, and cooking with vegetable based oils were also considered healthy dietary choices. Unhealthy diet components included sausages, eggs, sugary soft drinks, confectionery, and a high intake of saturated fats. Saturated fats tend to raise cholesterol levels and high cholesterol in mid-life has been linked to Alzheimer’s disease in several studies. Conversely, polyunsaturated and mono-unsaturated fats have a cholesterol lowering effect.

The researchers found that individuals with a healthy diet score above 8 were a massive 90-92% less likely to develop Alzheimer’s disease and 86-90% less likely to develop dementia than those with a healthy diet score below 8. The findings remained unchanged even after adjustment for potential co-founders such as smoking status, physical activity, BMI, and education level.

Although this was a relatively small study, the results are promising and suggest that a large percentage of dementias may be preventable through healthy dietary choices.

Alzheimer’s disease is becoming an increasing problem in Western societies due to a rapidly ageing population. Currently 5 million Americans are living with Alzheimer’s disease and this figure is predicted to increase to 13 million by 2050. There is no cure for Alzheimer’s disease at present and current treatments do little to slow the progression of the disease, only extending survival by a few months at best.

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The study, conducted by researchers at the Department of Neurology at the University of Turku in Finland, involved a group of 554 twins who completeld questionnaires on their drinking habits in 1975 and again in 1981. During the course of the 25 year study, 103 of the participants developed some form of dementia.

The researchers found that participants who reported a binge drinking episode at least once a month were 3.2 times more likely to develop dementia. Furthermore, participants who had passed out at least twice in the previous year due to alcohol consumption were a massive 10.5 times more likely to develop dementia.

Binge drinking was defined as consuming at least 5 bottles of beer or one bottle of wine during a drinking session.

Light to moderate alcohol consumption is thought to have a negligible impact on cognitive function and some studies have actually found a reduction in the incidence of dementia and Alzheimer’s disease in moderate drinkers. On the other hand heavy alcohol consumption, particularly “episodic” consumption where a large quantity of alcohol is consumed in a short period of time, has many long term adverse effects on the brain.

Heavy alcohol consumption in adolescence has been linked to a reduction in the size of the hippocampus which controls aspects of memory and learning. Alcohol also reduces the bodies ability to absorb the B vitamin thiamine. A lack of thiamine leads to the degeneration of brain cells and can result in a form of dementia known as Wernicke-Korsakoff syndrome. Almost three quarters of alcoholics are thought to be deficient in thiamine.

The average binge drinker in America binge drinks 4 times a month and consumes 8 drinks per session. Recent CDC figures put the prevalence of binge drinking in the USA at 17.1%. Binge drinking is around twice as common in men than women (23.2% vs 11.4%). Binge drinking is also much more common in people under the age of 35. Interestingly, wealthy individuals and those with a high level of education have a higher prevalence of binge drinking than the rest of the population.

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Researchers from the Department of Neurosciences at the University of California randomly assigned 340 participants suffering from mild Alzheimer’s disease into a high dose group and a control group. The high dose group received supplements containing 25 mg per day of vitamin B6, 5 mg per day of folate, and 1 mg per day of vitamin B12, around 20 times the recommended daily intake for these vitamins while the control group received identical placebos.

During the 18 month study period, the group who received the B-vitamin supplements showed similar cognitive decline as measured by the Alzheimer Disease Assessment Scale to those who received the placebo suggesting no benefit from the vitamin supplementation.

It had been theorized that an amino acid known as homocysteine may play a role in the progression of Alzheimer’s disease because higher than normal levels of homocysteine are found in the brains of Alzheimer’s disease sufferers. The B-vitamins play an important role in the metabolism of homocysteine and studies have found a directly correlation between a high intake of the B-vitamins and low levels of homocysteine in the blood. Studies have also found average levels of vitamin B12 to be much lower in Alzheimer’s disease sufferers compared to the general population.

The participants in the B-vitamin group did show a 31% reduction in homocysteine levels however this did not lead to a slower rate of cognitive decline in these patients.

Although B-vitamin supplementation did not slow the progression of Alzheimer’s disease, it is thought that maintaining low homocysteine levels throughout life may prevent Alzheimer’s disease from occurring in the first place. One study, published in the New England Journal of Medicine in 2002 found that individuals in the top 25% for plasma homocysteine levels were almost twice as likely to subsequently develop Alzheimer’s disease compared to the remainder of the population.

High homocysteine levels have been linked to an increased risk of atherosclerosis and cardiovascular disease. A history of cardiovascular disease is known to increase the likelihood of developing Alzheimer’s disease and vascular dementia later in life. High homocysteine levels may also increase the amount of oxidative damage and cell death occurring in the brain.

Rich sources of the B vitamins include potatoes, mushrooms, bananas, turkey, tuna, eggs, spinach, broccoli, asparagus, and yeast spreads such as marmite and vegemite.

Most people get a sufficient intake of the B vitamins through diet alone, however vitamin B6, B12, and folate are all well tolerated by the body at levels much higher that the RDA. The B vitamins are all water soluble so any excess amounts are excreted through urine.

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The study, conducted by researchers from the University of Kuopio in Finland, involved 1,449 middle aged participants from eastern Finland. Both blood pressure and serum cholesterol levels were recorded at the beginning of the study.

The participants were followed for an average of 21 years during which 57 (3.9%) of the participants developed Alzheimer’s disease. The researchers found that a high systolic and diastolic blood pressure at the beginning of the study were both associated with an increased risk of Alzheimer’s disease in later life.

A systolic blood pressure greater than 160 mmHg was associated with 2.8 times greater odds of Alzheimer’s disease compared to a a systolic blood pressure lower than 140 mmHg. A diastolic blood pressure greater than 95 mmHg was associated with a 1.7 fold increase in the odds of Alzheimer’s disease compared to a level lower than 90mmHg.

The researchers also found that high total cholesterol levels in mid life were associated with a significant increase in the risk of Alzheimer’s disease. A total cholesterol level greater than 6.5mmol/L was associated with a 2.2 fold increase in the odds of Alzheimer’s disease compared to a level below 6.5mmol/L.

It is believed that high blood pressure increases the risk of white-matter lesions in the brain which have been implicated in the progression of Alzheimer’s disease. It is also thought that high blood pressure may lead to a breakdown in the blood-brain barrier which prevents potentially harmful chemicals in the bloodstream from entering the brain. A leaky blood brain barrier is thought to allow amyloid beta to cross into the brain and accumulate in the form of plaques.

An optimal blood pressure is considered to be less than 120 mmHg for systolic blood pressure and under 80 mmHg for diastolic blood pressure. The systolic component of blood pressure is defined as the peak pressure exerted by the blood on the arteries while the diastolic component is the lowest pressure exerted by the blood on the arteries.

There are many things an individual can do to lower their blood pressure. The most common ways include increasing physical activity levels, reducing salt and caffeine consumption, quitting smoking, reducing stress levels, and losing weight.

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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 while 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 48% 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.

Carbohydrate and protein intake on the other hand appeared to be unrelated to Alzheimer’s disease risk.

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.

Caloric restriction may also help preserve brain function by increasing the activity of certain DNA repair enzymes and upregulating the action of antiapoptotic proteins such as NAIP that help protect against neuronal cell death.

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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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