prevention

Meditation's cognitive benefits

A critical part of attention (and working memory capacity) is being able to ignore distraction. There has been growing evidence that meditation training (in particular mindfulness meditation) helps develop attentional control, and that this can start to happen very quickly.

For example:

  • after an eight-week course that included up to 30 minutes of daily meditation, novices improved their ability to quickly and accurately move and focus attention.
  • three months of rigorous training in Vipassana meditation improved attentional control.
  • after eight weeks of Mindfulness Training, Marine reservists during pre-deployment showed increased working memory capacity and decreased negative mood (this training also included concrete applications for the operational environment and information and skills about stress, trauma and resilience in the body).
  • after a mere four sessions of 20 minutes, students produced a significant improvement in critical cognitive skills — and a dramatic improvement when conditions became more stressful (provided by increasingly challenging time-constraints).

There seem to be several factors involved in these improvements: better control of brainwaves; increased gray matter density in some brain regions; improved white-matter connectivity.

Thus, after ten weeks of Transcendental Meditation (TM) practice, students showed significant changes in brainwave patterns during meditation compared to eyes-closed rest for the controls. These changes reflected greater coherence and power in brainwave activity in areas that overlap with the default mode network (the brain’s ‘resting state’). Similarly, after an eight-week mindfulness meditation program, participants had better control of alpha brainwaves. Relatedly, perhaps, experienced Zen meditators have shown that, after interruptions designed to mimic spontaneous thoughts, they could bring activity in most regions of the default mode network back to baseline faster than non-meditators.

Thus, after an 8-week mindfulness meditation program, participants showed increased grey-matter density in the left hippocampus , posterior cingulate cortex, temporo-parietal junction , and cerebellum , as well as decreased grey-matter density in the amygdala . Similarly, another study found experienced meditators showed significantly larger volumes of the right hippocampus and the right orbitofrontal cortex, and to a lesser extent the right thalamus and the left inferior temporal gyrus.

These areas of the brain are all closely linked to emotion, and may explain meditators' improved ability in regulating their emotions.

Thus, long-term meditators showed pronounced differences in white-matter connectivity between their brains and those of age-matched controls, meaning that meditators’ brains were better able to quickly relay electrical signals. The brain regions linked by these white-matter tracts include many of those mentioned as showing increased gray matter density. Another study found that a mere 11 hours of meditation training (IBMT) produced measurable changes in the integrity and efficiency of white matter in the corona radiata (which links to the anterior cingulate cortex, an area where attention and emotion are thought to be integrated).

It’s an interesting question, the extent to which poor attentional control is a reflection of poor emotional regulation. Obviously there is more to distractability than that, but emotion and attention are clearly inextricably entwined. So, for example, a pilot study involving 10 middle school students with ADHD found that those who participated in twice-daily 10 minute sessions of Transcendental Meditation for three months showed a dramatic reduction in stress and anxiety and improvements in ADHD symptoms and executive function.

The effects of emotion regulation are of course wider than the effects on attention. Another domain they impact is that of decision-making. A study involving experienced Buddhist meditators found that they used different brain regions than controls when making decisions in a ‘fairness’ game. The differences reflected less input from emotional reactions and more emphasis on the actual benefits.

Similarly, brain scans taken while experienced and novice meditators meditated found that periodic bursts of disturbing noise had less effect on brain areas involved in emotion and decision-making for experienced meditators compared to novices — and very experienced meditators (at least 40,000 hours of experience) showed hardly any activity in these areas at all.

Attention is also entwined with perception, so it’s also interesting to observe that several studies have found improved visual perception attendant on meditation training and/or experience. Thus, participants attending a three-month meditation retreat, showed significant improvements in making fine visual distinctions, and ability to sustain attention.

But such benefits may depend on the style of meditation. A study involving experienced practitioners of two styles of meditation (Deity Yoga (DY) and Open Presence (OP)) found that DY meditators were dramatically better at mental rotation and visual memory tasks compared to OP practitioners and controls (and only if they were given the tasks immediately after meditating). Similarly, a study involving Tibetan Buddhist monks found that, during "one-point" meditation, monks were significantly better at maintaining their focus on one image, when two different images were presented to each eye. This superior attentional control was not found during compassion-oriented meditation. However, even under normal conditions the monks showed longer stable perception compared to meditation-naïve control subjects. And three months of intense training in Vipassana meditation produced an improvement in the ability of participants to detect the second of two visual signals half a second apart (the size of the improvement was linked to reduced brain activity to the first target — which was still detected with the same level of accuracy). Similarly, three months of intensive meditation training reduced variability in attentional processing of target tones.

References

You can read about these studies in more detail in the aggregated news reports on meditation. Three studies were mentioned here without having appeared in the news reports:

Lutz, A., Slagter, H. A., Rawlings, N. B., Francis, A. D., Greischar, L. L., & Davidson, R. J. (2009). Mental Training Enhances Attentional Stability: Neural and Behavioral Evidence. J. Neurosci., 29(42), 13418-13427. doi:10.1523/JNEUROSCI.1614-09.2009

Tang, Y.-Y., Lu, Q., Geng, X., Stein, E. A., Yang, Y., & Posner, M. I. (2010). Short-term meditation induces white matter changes in the anterior cingulate. Proceedings of the National Academy of Sciences, 107(35), 15649 -15652. doi:10.1073/pnas.1011043107

Travis, F., Haaga, D., Hagelin, J., Tanner, M., Arenander, A., Nidich, S., Gaylord-King, C., et al. (2010). A self-referential default brain state: patterns of coherence, power, and eLORETA sources during eyes-closed rest and Transcendental Meditation practice. Cognitive Processing, 11(1), 21-30. doi:10.1007/s10339-009-0343-2
 

 

 

Preventing Dementia: Mental stimulation

Stimulating activities

A 5-year study1 involving 488 people age 75 to 85 found that, for the 101 people who developed dementia, the greater the number of stimulating activities (reading, writing, doing crossword puzzles, playing board or card games, having group discussions, and playing music) they engaged in, the longer rapid memory loss was delayed. Similarly, a study2 involving 1321 randomly selected people aged 70 to 89, of whom 197 had mild cognitive impairment, has found that reading books, playing games, participating in computer activities or doing craft activities such as pottery or quilting was associated with a 30 to 50% decrease in the risk of developing memory loss compared to people who did not do those activities.

Moreover, two activities during middle age (50-65) were also significantly associated with a reduced chance of later memory loss: participation in social activities and reading magazines. The value of social activities is consistent with another, small, study3 that found that social networks, like education, offers a 'protective reserve' capacity that spares individuals the clinical manifestations of Alzheimer's disease. As the size of the social network increased, the same amount of Alzheimer’s pathology in the brain had less effect on cognitive test scores. For those without much pathology (plaques and tangles), social network size had little effect on cognition.

This supports another study4 involving 469 people aged 75 and older, that found that those who participated at least twice weekly in reading, playing games (chess, checkers, backgammon or cards), playing musical instruments, and dancing were significantly less likely to develop dementia. Although the evidence on crossword puzzles was not quite statistically significant, those who did crossword puzzles four days a week had a much lower risk of dementia than those who did one puzzle a week.

Similarly, a study5 of 700 seniors found that more frequent participation in cognitively stimulating activities, such as reading books, newspapers or magazines, engaging in crosswords or card games, was significantly associated with a reduced risk of Alzheimer’s disease. On average, compared with someone with the lowest activity level, the risk of disease was 47% lower for those whose frequency of activity was highest.

In the first comprehensive review6 of the research into 'cognitive reserve', which looks at the role of education, occupational complexity and mentally stimulating activities in preventing cognitive decline, researchers concluded that complex mental activity across people’s lives almost halves the risk of dementia. All the studies also agreed that it was never too late to build cognitive reserve. The review covered 29,000 individuals across 22 studies.

A review7 of research on the impact of cognitive training on the healthy elderly (not those with mild cognitive impairment or Alzheimer's disease), has found no evidence that structured cognitive intervention programs affects the progression of dementia in the healthy elderly population.

Post-mortem analysis of participants in a large, long-running study8 has provided more support for the idea that mental stimulation protects against Alzheimer’s. The study found a cognitively active person in old age was 2.6 times less likely to develop dementia and Alzheimer’s disease than a cognitively inactive person in old age. This association remained after controlling for past cognitive activity, lifetime socioeconomic status, and current social and physical activity. Frequent cognitive activity during old age was also associated with reduced risk of mild cognitive impairment.

Research involving genetically engineered mice9 has found that mice whose brains had lost a large number of neurons regained long-term memories and the ability to learn after their surroundings were enriched with toys and other sensory stimuli, pointing to the importance of maintaining cognitive stimulation as long as possible. Similarly, another mouse study10 found that short but repeated learning sessions can slow the development of those hallmarks of Alzheimer's, beta amyloid plaques and tau tangles. And another11 found that an enriched environment, with more opportunities to exercise, explore and interact with others, dramatically reduces levels of beta-amyloid peptides.

Education & iq

A study12 involving some 6,500 older Chicago residents being interviewed 3-yearly for up to 14 years (average 6.5 years), has found that while at the beginning of the study, those with more education had better memory and thinking skills than those with less education, education was not related to how rapidly these skills declined during the course of the study. The result suggests that the benefit of more education in reducing dementia risk results simply from the difference in level of cognitive function.

Another study13 has come out supporting the view that people with more education and more mentally demanding occupations may have protection against the memory loss that precedes Alzheimer's disease, providing more evidence for the idea of cognitive reserve. The 14-month study followed 242 people with Alzheimer's disease, 72 people with mild cognitive impairment, and 144 people with no memory problems.

Another study14 has come out confirming that people with more years of education begin to lose their memory later than those with less education, but decline faster once it begins. Researchers note that since the participants were born between 1894 and 1908, their life experiences and education may not represent that of people entering the study age range today.

A study15 of 312 New Yorkers aged 65 and older, who were diagnosed with Alzheimer's disease and monitored for over 5 years, found that overall mental agility declined faster for each additional year of education, particularly in the speed of thought processes and memory, and was independent of age, mental ability at diagnosis, or other factors likely to affect brain function, such as depression and vascular disease. It’s suggested this may reflect the greater ability of brains with a higher cognitive reserve to tolerate damage, meaning the damage is greater by the time it becomes observable in behavior.

The Nun Study16 found that nuns who completed 16 or more years of formal education or whose head circumference was in the upper two-thirds were four times less likely to be demented than those with both smaller head circumferences and lower education.

Post-mortem study17 of the brains of 130 participants in the Religious Orders Study found that the relationship between cognitive performance and the number of amyloid plaques in the brain changed with level of formal education. The more years education you had, the less effect the same number of plaques had on actual cognitive performance. It’s worth noting that this considerable difference was observed in a population where even the least educated had some college attendance; presumably the difference would be even more marked in the general population.

A long-running Finnish study18 has found that compared with people with five or less years of education, those with six to eight years had a 40% lower risk of developing dementia and those with nine or more years had an 80% lower risk. Generally speaking, people with low education levels seemed to lead unhealthier lifestyles, but the association remained after lifestyle choices and characteristics such as income, occupation, physical activity and smoking had been taken into account.

An analysis of high school records and yearbooks from the mid-1940s19, and interviews with some 400 of these graduates, now in their 70s, and their family members, has found that those who were more active in high school and who had higher IQ scores, were less likely to have mild memory and thinking problems and dementia as older adults.

An analysis20 of 184 people with dementia found that the mean age of onset of dementia symptoms in the 91 monolingual patients was 71.4 years, while for the 93 bilingual patients it was 75.5 years — a very significant difference.

A study21 of 122 people with Alzheimer's and 235 people without the disease found that people with Alzheimer's are more likely to have had less mentally stimulating careers than their peers who do not have Alzheimer's.

 

A study22 of 173 people from the Scottish Mental Survey of 1932 who have developed dementia has found that, compared to matched controls, those with vascular dementia were 40% more likely to have low IQ scores when they were children than the people who did not develop dementia. This difference was not true for those with Alzheimer's disease. The findings suggest that low childhood IQ may act as a risk factor for vascular dementia through vascular risks rather than the "cognitive reserve" theory. 

References: 
  1. Hall, C.B. et al. 2009. Cognitive activities delay onset of memory decline in persons who develop dementia. Neurology, 73, 356-361.
  2. Geda, Y.E. et al. 2009. Cognitive Activities Are Associated with Decreased Risk of Mild Cognitive Impairment: The Mayo Clinic Population-Based Study of Aging. Presented April 28 at the American Academy of Neurology's 61st Annual Meeting in Seattle.
  3. Bennett, D.A., Schneider,J.A., Tang,Y., Arnold,S.E. & Wilson,R.S. 2006. The effect of social networks on the relation between Alzheimer's disease pathology and level of cognitive function in old people: a longitudinal cohort study. Lancet Neurology,5, 406-412.
  4. Verghese, J., Lipton, R.B., Katz, M.J., Hall, C.B., Derby, C.A., Kuslansky, G., Ambrose, A.F., Sliwinski, M. & Buschke, H. 2003. Leisure Activities and the Risk of Dementia in the Elderly. New England Journal of Medicine, 348 (25), 2508-2516.
  5. Wilson, R.S., de Leon, C.F.M., Barnes, L.L., Schneider, J.S., Bienias, J.L., Evans, D.A. & Bennett, D.A. 2002. Participation in Cognitively Stimulating Activities and Risk of Incident Alzheimer Disease.
    JAMA, 287,742-748.
  6. Valenzuela, M.J. & Sachdev, P. 2006. Brain reserve and dementia: a systematic review. Psychological Medicine, In press
  7. Papp, K.V., Walsh, S.J. & Snyder, P.J. 2009. Immediate and delayed effects of cognitive interventions in healthy elderly: A review of current literature and future directions. Alzheimer's & Dementia, 5 (1), 50-60.
  8. Wilson, R.S., Scherr, P.A., Schneider, J.A., Tang, Y. & Bennett, D.A. 2007. The relation of cognitive activity to risk of developing Alzheimer’s disease. Neurology, published online ahead of print June 27.
  9. Fischer, A., Sananbenesi, F., Wang, X., Dobbin, M. & Tsai, L-H. 2007. Recovery of learning and memory is associated with chromatin remodelling. Nature, 447, 178-182.
  10. Billings, L.M., Green, K.N., McGaugh, J.L. & LaFerla, F.M. 2007. Learning Decreases Aß*56 and Tau Pathology and Ameliorates Behavioral Decline in 3xTg-AD Mice. Journal of Neuroscience, 27, 751-761.
  11. Lazarov, O.et al. 2005. Environmental Enrichment Reduces Aβ Levels and Amyloid Deposition in Transgenic Mice. Cell, 120(5), 701-713.
  12. Wilson, R.S., Hebert, L.E., Scherr, P.A., Barnes, L.L., de Leon, C.F.M. & Evans, D.A. 2009. Educational attainment and cognitive decline in old age. Neurology, 72, 460-465.
  13. Garibotto, V. et al. 2008. Education and occupation as proxies for reserve in aMCI converters and AD: FDG-PET evidence. Neurology, 71, 1342-1349.
  14. Hall, C.B., Derby, C., LeValley, A., Katz, M.J., Verghese, J. & Lipton, R.B. 2007. Education delays accelerated decline on a memory test in persons who develop dementia. Neurology, 69, 1657-1664.
  15. Scarmeas, N., Albert, S.M., Manly, J.J. & Stern, Y. 2006. Education and rates of cognitive decline in incident Alzheimer’s disease. Journal of Neurology Neurosurgery and Psychiatry, 77, 308-316.
  16. Mortimer, J.A., Snowdon, D.A. & Markesbery, W.R. 2003. Head Circumference, Education and Risk of Dementia: Findings from the Nun Study.Journal of Clinical and Experimental Neuropsychology, 25 (5), 671-679.
  17. Bennett, D.A., Wilson, R.S., Schneider, J.A., Evans, D.A., de Leon, M.C.F., Arnold, S.E., Barnes, L.L. & Bienias, J.L. 2003. Education modifies the relation of AD pathology to level of cognitive function in older persons. Neurology, 60, 1909-1915.
  18. Ngandu, T. et al. 2007. Education and dementia: What lies behind the association? Neurology, 69, 1442-1450.
  19. Fritsch, T., Smyth, K.A., McClendon, M.J., Ogrocki, P.K., Santillan, C., Larsen, J.D. & Strauss, M.E. 2005. Associations Between Dementia/Mild Cognitive Impairment and Cognitive Performance and Activity Levels in Youth. Journal of the American Geriatrics Society, 53(7), 1191.
  20. Bialystok, E., Craik, F.I.M. & Freedman, M. 2007. Bilingualism as a protection against the onset of symptoms of dementia. Neuropsychologia, 45 (2), 459-464./li>
  21. Smyth, K.A. et al. 2004. Worker functions and traits associated with occupations and the development of AD. Neurology, 63 (3), 498-503.
  22. McGurn, B., Deary, I.J. & Starr, J.M. 2008. Childhood cognitive ability and risk of late-onset Alzheimer and vascular dementia. Neurology, first published on June 25, 2008 as doi: doi:10.1212/01.wnl.0000319692.20283.10 .

Preventing dementia: Diet & exercise

It's increasingly clear that eating a healthy diet can have a big impact on whether or not you develop dementia.

A study1 of nearly 2000 older adults has found that eating a Mediterranean diet was associated with less risk of developing mild cognitive impairment or of transitioning from MCI to Alzheimer's disease. The third with the highest scores for Mediterranean diet adherence had a 28% lower risk of developing MCI compared to the third with the lowest scores, and of those who already had MCI, those with the highest scores for Mediterranean diet adherence had a 48% less chance of developing Alzheimer’s.

Another, similar-sized study2, has found that those who adhered more strongly to a Mediterranean-type diet had a 40% risk reduction, and those who were very physically active had a 33% risk reduction of Alzheimer's -- doing both gave people a 60% reduction.

A Mediterranean-type diet is typically characterized by high intake of fish, vegetables, legumes, fruits, cereals and monounsaturated fatty acids; relatively low intake of dairy products, meats and saturated fats; and moderate alcohol consumption. Most of these components have been independently associated with reduced dementia risk. Let's look at them one by one.

Fruit & vegetables

A very large study3 of older adults found that those who ate fruits and vegetables daily reduced their risk of dementia by 30% compared to those who didn’t regularly eat fruits and vegetables. Another large, long-running epidemiological study4 found that those who drank three or more servings of fruit and vegetable juices per week had a 76% lower risk of developing Alzheimer’s disease than those who drank juice less than once a week. The benefit seemed greatest for those who carried the so-called “Alzheimer’s gene”.

This may not have anything to do with vitamin C. A five-year study5 involving nearly 3000 people has found that use of Vitamin C or E or both was not associated with a reduced risk of developing dementia or Alzheimer’s. However a study6 involving 4,740 elderly found the greatest reduction in both prevalence and incidence of Alzheimer's in those who used individual vitamin E and C supplements in combination. There was no significant benefit in these vitamins alone.

Of course, it is now well understood that taking vitamins as supplements is not the same as receiving them in food.

Two studies have come out in favor of a diet rich in foods containing vitamin E to help protect against Alzheimer's disease. One study7 involved 815 Chicago residents age 65 and older with no initial symptoms of mental decline, who were questioned about their eating habits and followed for an average of about four years. When factors like age and education were taken into account, those eating the most vitamin E-rich foods had a lower risk of developing Alzheimer’s, provided they did not have the ApoE e4 allele. This was not true when vitamin E was taken as a supplement. The effect of vitamin C was not statistically significant.

The other study8 involved 5,395 people in the Netherlands age 55 and older who were followed for an average of six years. Those with high intakes of vitamins E and C were less likely to become afflicted with Alzheimer's, regardless of whether they had the gene variation. This association was most pronounced for current smokers.

So beneficial effects of these vitamins may depend on genetics, smoking history, and possibly other lifestyle factors. But there are other valuable compounds common in fruits & vegetables. Another class of antioxidant chemicals, polyphenols, are now suspected. Polyphenols generally exist primarily in the skins of fruits and vegetables and are particularly abundant in teas, juices and wines.

A cell study9 also found that quercetin (a flavonoid with greater antioxidant and anticancer properties than vitamin C) protects against cellular damage. Quercetin is particularly abundant in apples (mainly in the skin, and especially the red ones). Other good sources are onions, blueberries and cranberries.

Another cell study10 found that compounds in blackcurrants (anthocyanins as well as polyphenols) strongly protect neuronal cells against the effects of amyloid-beta. Boysenberries contain the same compounds, and those that are darker are likely to be more potent.

The inconsistent findings regarding vitamins C and E may also have to do with the presence of folates. Data from the Baltimore Longitudinal Study of Aging11 revealed that although those with higher intake of folates, vitamin E and vitamin B6 had a lower risk of developing Alzheimer’s, statistical analysis showed it was only folate consumption that was significant. Those who had at least 400mcg of folates a day (the recommended daily allowance) had a 55% reduction in risk of developing Alzheimer’s. Unfortunately, most people who reached that level did so by taking supplements, suggesting the difficulty of doing so through diet alone.

Folates are abundant in foods such as liver, kidneys, yeast, fruits (like bananas and oranges), leafy vegetables, whole-wheat bread, lima beans, eggs and milk; however, they are often destroyed by cooking or processing.

The benefits of folates probably has to do with its effect on homocysteine. A mouse study12 indicates that increased levels of homocysteine are produced by low intake of folate and B vitamins, and impair cognition through microvascular changes. 

High levels of homocysteine are associated not only with deficiencies in vitamin B12 and folate, but also with smoking.

High levels of homocysteine were associated in one study13 with a more than five-fold increase in the risk for stroke, a nearly five-fold risk for vascular dementia, and almost triple the risk for Alzheimer's disease. Findings from the long-running Framingham study14 found people with elevated levels of homocysteine in the blood had nearly double the risk of later developing Alzheimer’s disease.

Moreover, evidence from a study15 using genetically engineered mice suggests that increased levels of homocysteine in the brain cause damage to nerve cells in the hippocampus -- which can be repaired when there is an adequate amount of folate, but not when there is a deficiency.
 

Omega-3 oils & fish

One of the clearest findings in this area has been the benefits of regularly consuming omega-3 oils, fish oil, and fish. Several epidemiological studies have indicated that regularly eating fish (at least once a week) reduces risk of dementia. More recently, two very large studies have come out in support. One very large study3 of older adults found that those who regularly consumed omega-3 rich oils, such as canola oil, flaxseed oil and walnut oil, reduced their risk of dementia by 60% compared to people who did not regularly consume such oils. Additionally, those who ate fish at least once a week had a 40% lower risk of dementia -- but only if they did not carry ApoE4 gene.

Moreover, for those who didn’t have the gene, regular use of omega-6 rich oils, but not omega-3 rich oils or fish, were twice as likely to develop dementia compared to those who didn’t eat omega-6 rich oils (e.g., sunflower or grape seed oil).

The second study16 comes from the famous long-running Framingham Heart Study, which found that those with the highest levels of DHA (an omega-3 polyunsaturated fatty acid found in relatively high concentrations in cold-water fish) had a 47% lower risk of developing dementia. Those with these levels tended to eat an average three fish servings a week, as well as an average of .18 grams of DHA a day. Those at lower levels ate markedly less fish.

There is also some suggestion that omega-3 oils might help slow the progression of dementia. A Swedish study17 found that, although fatty acids DHA and EPA didn't slow cognitive decline in those with mild-to-moderate Alzheimer’s, they did slow decline in those with very mild cognitive impairment (a frequent precursor of dementia). It's been suggested that anti-inflammatory effects are an important reason for the benefit, why might explain why benefits only occur in the very early stages, when levels of inflammation seem to be higher.

Similar results were more recently reported18 from a large 18-month trial. This one, however, suggested that genetic status might be a factor -- that those without the “Alzheimer’s gene” ApoE4 might benefit even if impairment had progressed to mild-to-moderate Alzheimer’s.

There are a number of reasons why DHA might help brains.

A study involving genetically engineered mice19 has found that a diet high in DHA dramatically slowed the progression of Alzheimer's by cutting the harmful brain plaques that mark the disease. An earlier study20 showed that DHA protected against damage to the synaptic areas where brain cells communicate and enabled mice to perform better on memory tests. More recent research21 has revealed that DHA increases the production of LR11, a protein that is found at reduced levels in Alzheimer's patients and which is known to destroy the protein that forms the plaques associated with the disease.

Food sources of omega-3 fatty acids include fish such as salmon, halibut, mackerel and sardines, as well as almonds, walnuts, soy, flaxseed, and DHA-enriched eggs. These fish have high levels of DHA because they consume DHA-rich algae. Because these fishes' oiliness makes them absorb more mercury, dioxin, PCP and other metals, a less risky yet more costly strategy is to consume fish oil or purified DHA supplements made from algae.

Possible benefits of wine, tea, and coffee

There have been a number of reports that moderate alcohol consumption (generally defined as 1 drink or less per day for women and 1-2 drinks or less per day for men) may help reduce your risk of developing dementia, and a 2008 review of 44 studies22 supported this conclusion. 

However, given that alcohol has known negative effects on the brain, no one is recommending that non-drinkers take up the habit! All one can say is that there's no reason to alter your habits if you are a moderate drinker. On the other hand, if you drink more than this, you are probably best to knock it back to this level.

However, the evidence suggests that it is wine rather than alcohol in general that is beneficial for the brain. A large Danish study23 found that those who drank wine occasionally in the 1970s had a lower risk of developing dementia in the 1990s (when participants were 65 or older). However, occasional beer drinking was associated with an increased risk of developing dementia. But we cannot draw too hard & fast a conclusion from this, as eating habits were not investigated, and research suggests that wine drinkers may have better dietary habits than beer and liquor drinkers. Moreover, a very large study of older adults3, that found a significant effect of some dietary factors, found no effect of wine.

There are, however, some good reasons for believing regular drinking of red wine may help the aging brain. Red grapes contain several polyphenols that have been shown to significantly reduce cognitive deterioration in genetically engineered mice, by preventing the formation of amyloid beta. One of these is resveratrol; the others are catechin and epicatechin. Resveratrol was much vaunted when its effects were first discovered, but unfortunately it requires extremely high doses. The more recent discovery24 of the catechins is much more exciting, as they appear to be effective at much lower doses. The catechins are also abundant in tea and cocoa.

Tea, most particularly green tea, has also been found25 to inhibit the activity of enzymes associated with the development of Alzheimer's Disease. Green tea also obstructed the activity of beta-secretase.

These inhibitory properties were not found in coffee. However, a large, long-running Finnish study26 has found that those who were coffee drinkers at midlife had lower risk for dementia and Alzheimer’s later in life compared to those drinking no or only little coffee midlife. The lowest risk was found among moderate coffee drinkers (drinking 3-5 cups of coffee/day).

Restricting your calories

There has been some talk that calorie-restricted diets might help prevent Alzheimer's. So far, the only indications have come from experiments with genetically engineered mice. While there have been a number of studies providing evidence that high cholesterol, obesity, and other cardiovascular risk factors increase the likelihood of Alzheimer’s, it is decidedly premature to say whether calorie-restricted diets would benefit humans. Particularly since one of the early signs of Alzheimer's is weight loss. So it is certainly not recommended that people severely restrict their diets. More useful is removing certain food types (e.g., the "bad" oils; sugar -- there is some evidence that Alzheimer's may be a type of diabetes), and increasing consumption of others (fish, "good" oils, fruit & vegetables).

There may also be a genetic link. A four-year study27 of nearly 1000 older adults found that among those who carried the ApoE e4 gene, those who consumed the most calories had a 2.3 times greater chance of developing Alzheimer’s compared to those who ate the fewest calories. But calories weren't a factor for those without the gene.

Cholesterol

A study28 involving nearly 10,000 people who underwent health evaluations between 1964 and 1973 when they were between the ages of 40 and 45, has found that those with total cholesterol levels between 249 and 500 milligrams were one-and-a-half times more likely to develop Alzheimer's disease than those people with cholesterol levels of less than 198 milligrams. People with total cholesterol levels of 221 to 248 milligrams were more than one-and-a-quarter times more likely to develop Alzheimer's disease. High cholesterol increased risk regardless of midlife diabetes, high blood pressure, obesity, smoking and late-life stroke.

A review29 of autopsy cases of patients over 40 years old found that high blood cholesterol levels were correlated with the presence of amyloid deposits in the brain in the youngest subjects (aged 40-55).

An analysis30 of data on 1037 older women who had participated in a clinical trial of hormone replacement therapy found that high cholesterol levels increase the risk of cognitive impairment.

A large-scale Finnish study31 following 1449 men and women over 21 years found that raised systolic blood pressure and high serum cholesterol concentration, particularly in combination, in midlife, increase the risk of Alzheimer's disease in later life. Raised diastolic blood pressure had no significant effect.

However, the long-running, large-scale Framingham Heart study32 found that, after adjustment for age, sex, APOE genotype, smoking, body mass index, coronary heart disease, and diabetes, there was no significant association between AD risk and cholesterol level.

Previous studies suggesting that fat may be involved in the development of dementia and Alzheimer’s disease have been contradicted by a new study33 involving over 5,000 elderly people over a period of six years. The study found no correlation between fat and cholesterol intake and risk of dementia, and no evidence for a reduction in risk for those taking cholesterol lowering medication.

A cell study34 provides more understanding of why there might be a link between cholesterol and Alzheimer's disease. The study found that proteins which help control cholesterol levels in arterial walls were also present in neurons, and when the genes for these proteins were over-expressed, production of amyloid beta protein fell. The finding suggests a new approach to slowing Alzheimer’s. The study also showed that the apoE protein is extremely good at regulating cholesterol removal from neurons — the gene for this protein is a well-known genetic risk factor for Alzheimer's.

Diabetes

A large Swedish study35 has found that men with low insulin secretion capacity at age 50 were nearly one-and-a-half times more likely to develop Alzheimer’s disease than men without insulin problems. The risk was strongest in those who didn't have the APOE4 gene. Another large study36 found that diabetes was related to a significantly higher risk of developing amnestic mild cognitive impairment in older seniors (average age 76), after controlling for other risk factors. And a large study37 of post-menopausal women (mean age 67 years) found that those with poor blood sugar control were four times more likely to develop MCI or dementia. Findings38 from the long-running Religious Orders Study also support a link between diabetes and an increased risk of developing Alzheimer's disease.

Evidence from a mouse study39 suggests that diabetes might increase risk because elevated blood glucose levels interact with beta amyloid in a way damaging to blood vessels in the brain.
In fact it has been suggested that Alzheimer’s could be considered a third form of diabetes. Another study40 provides evidence that amyloid oligomers remove insulin receptors from nerve cells, rendering those neurons insulin resistant. Another mouse study41 suggests that low levels of insulysin, an enzyme that degrades insulin, are a factor. The enzyme, it seems, also degrades amyloid-beta peptides, and even a partial decrease in insulysin activity was found to raise amyloid-beta peptide levels in the brain.

Obesity

A review42 of 10 international studies published since 1995, covering just over 37,000 people, has found that obesity increased the relative risk of dementia by an average of 42% compared with normal weight. Being underweight increased the risk by 36%. For Alzheimer's Disease and vascular dementia, specifically, obesity was an even more significant risk: 80% and 73%, respectively. With regards to Alzheimer’s, obesity was more likely to be a risk factor for women, but men were more affected when it came to vascular dementia.

A very large study43 that measured abdominal fat at age 40 to 45 and dementia occurrence some 36 years later, found that those with the highest amount of abdominal fat were nearly three times more likely to develop dementia than those with the lowest amount of abdominal fat. Having a large abdomen increased the risk of dementia regardless of overall weight and existing health conditions, although being obese as well did increase the risk. Those more likely to have abdominal obesity, were women, non-whites, smokers, people with high blood pressure, high cholesterol or diabetes, and those with less than a high school level of education. And another large study44 found that those who at 40 were obese, or had high blood pressure, or high cholesterol levels, were twice as more likely to develop dementia by the age of 60. Having all three of these risk factors increased their chances six-fold.

And just to be really scary, when45 genetically engineered mice were fed a diet rich in fat, sugar and cholesterol for a mere nine months (although that is, of course, much longer for a mouse than it is for us!), they developed a preliminary stage of Alzheimer's pathology in their brains, suggesting that a ‘fast food’ diet could be a contributory factor in those with the Alzheimer’s gene.

Physical exercise & fitness

A number of studies have found that physical fitness reduces the risk of dementia. One way physical exercise can help fight dementia is through its ability to grow neurons in the hippocampus. This is well-established in rodent studies, and has been confirmed in small human studies. One such study46 found the association between physical fitness and hippocampus size was specifically associated with performance on certain spatial memory tests.  Another47 found that those with early Alzheimer's disease who were less physically fit had four times more brain shrinkage when compared to normal older adults than those who were more physically fit, suggesting the value of physical fitness extends to slowing down the progression of the disease.

Another reason for exercise to prevent dementia is through its effect on cardiovascular fitness, and a reasonably large four-year study48 did indeed find that the most active (top third) were significantly less likely to develop vascular dementia than the least active (bottom third). Interestingly, no such association was found with Alzheimer’s disease. However, at least two large studies have found a significantly reduced risk of dementia in those who had higher levels of fitness49 or exercised three or more times a week50. It may be that exercise has a greater effect on vascular dementia, but many cases of Alzheimer's dementia are actually mixed dementia, with a vascular component.

References: 
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  6. Zandi, P.P., Anthony, J.C., Khachaturian, A.S., Stone, S.V., Gustafson, D., Tschanz, J.T., Norton, M.C., Welsh-Bohmer, K.A. & Breitner, J.C.S. 2004. Reduced Risk of Alzheimer Disease in Users of Antioxidant Vitamin Supplements: The Cache County Study. Archives of Neurology, 61, 82-88.
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  8. Morris, M.C., Evans, D.A., Bienias, J.L., Tangney, C.C., Bennett, D.A., Aggarwal, N., Wilson, R.S. & Scherr, P.A. 2002. Dietary Intake of Antioxidant Nutrients and the Risk of Incident Alzheimer Disease in a Biracial Community Study. JAMA, 287, 3230-3237.
  9. Heo, H.J. & Lee, C.Y. 2004. Protective Effects of Quercetin and Vitamin C against Oxidative Stress-Induced Neurodegeneration. Journal of Agricultural and Food Chemistry, 52 (25), 7514–7517.
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  11. Corrada, M.M., Kawas,C.H., Hallfrisch,J., Muller,D. & Brookmeyer,R. Reduced risk of Alzheimer’s disease with high folate intake: The Baltimore Longitudinal Study of Aging. Alzheimer’s & Dementia, 1 (1), 11-18.
  12. Troen, A.M. et al. 2008. B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice. Proceedings of the National Academy of Sciences, 105, 12474-12479.
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    Yurko-Mauro, K. et al. 2009. Results of the MIDAS Trial: Effects of Docosahexaenoic Acid on Physiological and Safety Parameters in Age-Related Cognitive Decline. Presented at the Alzheimer's Association International Conference on Alzheimer's Disease July 11-16 in Vienna.
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  20. Calon, F. et al. 2004. Docosahexaenoic Acid Protects from Dendritic Pathology in an Alzheimer's Disease Mouse Model. Neuron, 43 (5), 633-645.
  21. Ma, Q-L. et al. 2007. Omega-3 Fatty Acid Docosahexaenoic Acid Increases SorLA/LR11, a Sorting Protein with Reduced Expression in Sporadic Alzheimer's Disease (AD): Relevance to AD Prevention. Journal of Neuroscience, 27 (52), 14299 - 14307.
  22. Collins, M.A. et al. 2008. Alcohol in Moderation, Cardioprotection, and Neuroprotection: Epidemiological Considerations and Mechanistic Studies. Alcoholism: Clinical and Experimental Research, Published Online 20 November.
  23. Truelsen, T., Thudium, D. & Grønbæk, M. 2002. Amount and type of alcohol and risk of dementia: The Copenhagen City Heart Study. Neurology, 59, 1313-1319.
  24. Wang, J. et al. 2008. Grape-Derived Polyphenolics Prevent Aβ Oligomerization and Attenuate Cognitive Deterioration in a Mouse Model of Alzheimer's Disease. Journal of Neuroscience, 28, 6388-6392.
  25. Okello, E.J., Savelev, S.U. & Perry, E.K. 2004. In vitro Anti-beta-secretase and dual anti-cholinesterase activities of Camellia sinensis L. (tea) relevant to treatment of dementia. Phytotherapy Research, 18 (8), 624-627.
  26. Eskelinen, M.H. et al. 2009. Midlife Coffee and Tea Drinking and the Risk of Late-Life Dementia: A Population-based CAIDE Study. Journal of Alzheimer's Disease, 16(1).
  27. Luchsinger, J.A. et al. 2002. Caloric Intake and the Risk of Alzheimer Disease. Archives of Neurology, 59 (8), 1258-1263.
  28. Solomon, A. et al. 2008. Midlife Serum Total Cholesterol and Risk of Alzheimers Disease and Vascular Dementia Three Decades Later. Presented at the American Academy of Neurology Annual Meeting in Chicago, April 16. Abstract
  29. Pappolla, M.A. et al. 2003. Mild hypercholesterolemia is an early risk factor for the development of Alzheimer amyloid pathology. Neurology, 61, 199-205.
  30. Yaffe, K., Barrett-Connor, E., Lin, F. & Grady, D. 2002. Serum Lipoprotein Levels, Statin Use, and Cognitive Function in Older Women. Archives of Neurology, 59,378-384.
  31. Kivipelto, M., Helkala, E., Laakso, M. P., Hanninen, T., Hallikainen, M., Alhainen, K., Soininen, H., et al. (2001). Midlife vascular risk factors and Alzheimer's disease in later life: longitudinal, population based study. BMJ, 322(7300), 1447-1451.  http://www.bmj.com/cgi/content/full/322/7300/1447
  32. Tan, Z.S., Seshadri, S., Beiser, A., Wilson, P.W.F., Kiel, D.P., Tocco, M., D'Agostino, R.B. & Wolf, P.A. 2003. Plasma Total Cholesterol Level as a Risk Factor for Alzheimer Disease: The Framingham Study. Archives of Internal Medicine, 163, 1053-1057.
  33. Engelhart, M.J., Geerlings, M.I., Ruitenberg, A., van Swieten, J.C., Hofman, A., Witteman, J.C.M. & Breteler, M.M.B. 2002. Diet and risk of dementia: Does fat matter?: The Rotterdam Study. Neurology, 59, 1915-1921.
  34. Kim, W.S. et al. 2007. Role of ABCG1 and ABCA1 in Regulation of Neuronal Cholesterol Efflux to Apolipoprotein E Discs and Suppression of Amyloid-β Peptide Generation. Journal of Biological Chemistry, 282, 2851-2861.
  35. Rönnemaa, E. et al. 2008. Impaired insulin secretion increases the risk of Alzheimer disease. Neurology, first published on April 9 as doi: doi:10.1212/01.wnl.0000310646.32212.3a
  36. Luchsinger, J.A. et al. 2007. Relation of Diabetes to Mild Cognitive Impairment. Archives of Neurology, 64, 570-575.
  37. Yaffe, K. et al. 2006. Glycosylated Hemoglobin Level and Development of Mild Cognitive Impairment or Dementia in Older Women. Journal of Nutrition, Health, and Aging, 10 (4).
  38. Arvanitakis, Z., Wilson, R.S., Bienias, J.L., Evans, D.A. & Bennett, D.A. 2004. Diabetes Mellitus and Risk of Alzheimer Disease and Decline in Cognitive Function. Archives of Neurology, 61, 661-666.
  39. Burdo, J.R. et al. 2008. The pathological interaction between diabetes and presymptomatic Alzheimer's disease. Neurobiology of Aging, Available online 26 March 2008 .
  40. Zhao,W-Q. et al. 2007. Amyloid beta oligomers induce impairment of neuronal insulin receptors. FASEB Journal, published online ahead of print August 24.
  41. Miller, B.C., Eckman, E.A., Sambamurti, K., Dobbs, N., Chow, K.M., Eckman, C.B., Hersh, L.B. & Thiele, D.L. 2003. Amyloid-β peptide levels in brain are inversely correlated with insulysin activity levels in vivo. PNAS, 100, 6221-6226. published online before print.
  42. Beydoun, M.A., Beydoun, H.A. & Wang, Y. 2008. Obesity and central obesity as risk factors for incident dementia and its subtypes: a systematic review and meta-analysis. Obesity Reviews, 9 (3), 204–218.
  43. Whitmer, R.A., et al. 2008. Central obesity and increased risk of dementia more than three decades later. Neurology, published online ahead of print March 26.
  44. Kivipelto,M. et al. 2006. Risk score for the prediction of dementia risk in 20 years among middle aged people: a longitudinal, population-based study. Lancet Neurology, advance online publication 3 August
  45. Akterin, S. 2008. From cholesterol to oxidative stress in Alzheimer's disease: A wide perspective on a multifactorial disease. Doctoral thesis, Karolinska Institutet. http://diss.kib.ki.se/2008/978-91-7409-172-4/
  46. Erickson, K.I. et al.  2009. Aerobic fitness is associated with hippocampal volume in elderly humans. Hippocampus, Published online 2 January.
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  49. Wang, L., Larson, E.B., Bowen, J.D. & van Belle, G. 2006. Performance-Based Physical Function and Future Dementia in Older People. Archives of Internal Medicine, 166, 1115-1120.
  50. Larson, E.B., Wang, L., Bowen, J.D., McCormick, W.C., Teri, L., Crane, P., & Kukull, W. 2006. Exercise Is Associated with Reduced Risk for Incident Dementia among Persons 65 Years of Age and Older. Annals of Internal Medicine, 144 (2), 73-81.

Dementia: Risk Factors

Genes

Several genes have been implicated in Alzheimer's, but the big one is the e4 allele of the ApoE gene (on chromosome 19). This variant is found in about a quarter of the population.

Having it doesn't mean you are foreordained to develop Alzheimer's, but it certainly increases the risk substantially. The risk goes up considerably more if both of your genes are the e4 variant (remember you inherit two: one from each parent).

It also increases if you have both the ApoE-e4 and the D10S1423 234-bp allele (found on chromosome 10). The combined risk of these two gene variants has been described as being greater than the increased risk of lung cancer caused by smoking1. Chromosome 10 has also been implicated in setting the age at which it begins, for both Alzheimer's and Parkinson's diseases, in those genetically disposed.

Another gene that has been linked to Alzheimer's is the KIBRA gene (on chromosome 5) — carriers of the T-allele have a 25% lower risk of developing Alzheimer's compared to those who carry the C-allele2.

It does seem that having the right, or wrong, genes is more important than we believed. Data from the Swedish Twin Registry3, involving nearly 12,000 people aged 65 and older, estimated that genetic influence accounted for 79% of Alzheimer's risk, with 95% probability of being within the range 67 to 88%.

But it's not just a matter of genes. Not everyone with the 'wrong' genes will develop dementia, and not everyone who develops dementia has the wrong genes. There are a number of lifestyle actions that affect it.

Even the genetic picture is not as simple as it sounds. One study4, for example, found indications that having a mother who had Alzheimer's is more significant than father's status. Data from the long-running Framingham Heart Study has found5 that cognitive impairment is more likely in those whose who have the ApoE ε4 gene — but only if they had a parent with dementia (particularly if it was Alzheimer's). There was no effect of parental dementia in those who didn’t have the ApoE ε4 gene.

For those who carry the “Alzheimer’s” APOE-4 gene, and those who later develop dementia, there is an association between smaller head size and lower educational achievement6. In other words, having both a small head size and low educational achievement in early life makes it more likely that a person will develop Alzheimer’s — probably because of their lack of cognitive reserve.

Cardiac & Blood Pressure Problems

A very large study7 found that those with atrial fibrillation, regardless of age, were 44% more likely to develop dementia, with those younger than 70 particularly at risk (130% more likely to develop dementia). Previous studies have connected atrial fibrillation with vascular dementia; this finding extends it to all dementia types.

Another, smaller, study8 (135 patients) found that memory declined significantly faster in those with high blood pressure or atrial fabrillation.

Atrial fibrillation, the most common heart rhythm problem, has a strong genetic link, and is also a risk factor for stroke.

Smoking

A very large seven-year study9 found that older adults who smoked were 50% more likely to develop dementia than people who had never smoked or no longer smoked. Smoking did not increase the risk for those with the Alzheimer’s gene apolipoprotein E4, but for those without the gene, smoking increased the risk by nearly 70%. Another large study10 found that heavy smokers developed the disease 2.3 years sooner, while heavy drinkers developed Alzheimer’s nearly 5 years earlier than those who were not. Those with the APOE e4 gene developed the disease three years sooner than those without the gene variant. These three risk factors were additive — those with all three developed the disease 8.5 years earlier than those with none of the risk factors.

A large national study11 also found that exposure to second-hand smoke also increases your risk.

Depression, stress & anxiety

Several studies12 have found evidence that depression, high level of stress or anxiety, and even loneliness, increase the risk of later developing dementia.

Other Possible Risk Factors

Findings from a study13 using genetically engineered mice suggests that people genetically predisposed to Alzheimer's disease or with excessive amounts of beta amyloid in their brains are at increased risk of developing the disease earlier if they receive high concentrations of oxygen, for example during or after surgery.

A large long-running study14 has found that women with both the lowest and the highest levels of thyrotropin (a hormone secreted by the pituitary gland that helps regulate thyroid gland function) had more than double the risk of developing Alzheimer's disease. No such association was found in men.

References: 
  1. Zubenko, G.S., Hughes, H.B. III & Stiffler, J.S. 2001. D10S1423 identifies a susceptibility locus for Alzheimer's disease in a prospective, longitudinal, double-blind study of asymptomatic individuals. Molecular Psychiatry, 6 (4), 413-419.
  2. Corneveaux, J.J. et al. In press. Evidence for an association between KIBRA and late-onset Alzheimer's disease. Neurobiology of Aging.
  3. Gatz, M. et al. 2006. Role of Genes and Environments for Explaining Alzheimer Disease. Archives of General Psychiatry, 63, 168-174.
  4. Mosconi, L. et al. 2007. Maternal family history of Alzheimer's disease predisposes to reduced brain glucose metabolism. PNAS, 104, 19067-19072.
  5. Debette, S. et al. 2009. Parental Dementia and Alzheimer Disease Are Associated with Poorer Memory in Middle-Aged Adults: The Framingham Offspring Study. Presented April 29 at the American Academy of Neurology's 61st Annual Meeting in Seattle, Washington.
  6. Mortimer, J,A., Snowdon, D.A.  & Markesbery, W.R. 2008. Small Head Circumference is Associated With Less Education in Persons at Risk for Alzheimer Disease in Later Life. Alzheimer Disease & Associated Disorders, 22(3), 249-254.
  7. Bunch, T.J. et al. 2009. Atrial Fibrillation is Independently Associated with Senile, Vascular, and Alzheimer's Dementia. Presented Friday, May 15, at "Heart Rhythm 2009," the annual scientific sessions of the Heart Rhythm Society in Boston.
  8. Mielke, M.M. et al. 2007. Vascular factors predict rate of progression in Alzheimer disease. Neurology, 69, 1850-1858.
  9. Reitz, C., den Heijer, T., van Duijn, C., Hofman, A. & Breteler, M.M.B. 2007. Relation between smoking and risk of dementia and Alzheimer disease: The Rotterdam Study. Neurology, 69, 998-1005.
  10. Harwood, D. et al. 2008. Impact of Alcohol Use, Smoking and Apolipoprotein-E Epsilon 4 Allele (APOE 4) on Age of Onset of Late Onset Alzheimers Disease (LOAD). Presented at the American Academy of Neurology 60th Annual Meeting in Chicago, April 16. Abstract P04.071
  11. Llewellyn, D.J. et al. 2009. Exposure to secondhand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement. British Medical Journal, 338, 462. Full text available here.
  12. Peavy, G.M. et al. 2007. The Effects of Prolonged Stress and APOE Genotype on Memory and Cortisol in Older Adults. Biological Psychiatry, 62 (5), 472-478.
    Rapp, M.A. et al. 2006. Increased Hippocampal Plaques and Tangles in Patients With Alzheimer Disease With a Lifetime History of Major Depression. Archives of General Psychiatry, 63,161-167.
    Wang, H. -X. et al. 2009. Personality and lifestyle in relation to dementia incidence. Neurology, 72, 253-259.
    Wilson, R.S., Arnold, S.E., Beck, T.L., Bienias, J.L. & Bennett, D.A. 2008. Change in Depressive Symptoms During the Prodromal Phase of Alzheimer Disease. Archives of General Psychiatry, 65(4), 439-445.
    Wilson, R.S., Schneider, J.A., Boyle, P.A., Arnold, S.E., Tang, Y. & Bennett, D.A. 2007. Chronic distress and incidence of mild cognitive impairment. Neurology, 68, 2085-2092.
    Wilson, R.S., Krueger, K.R., Arnold, S.E., Schneider, J.A., Kelly, J.F., Barnes, L.L., Tang, Y. & Bennett, D.A. 2007. Loneliness and Risk of Alzheimer Disease. Archives of General Psychiatry, 64, 234-240.
    Wilson, R.S., Evans, D.A., Bienias, J.L., Mendes de Leon, C.F., Schneider, J.A. & Bennett, D.A. 2003. Proneness to psychological distress is associated with risk of Alzheimer’s disease. Neurology, 61, 1479-1485.
    Wilson, R.S., Barnes, L.L., de Leon, C.F.M., Aggarwal, N.T., Schneider, J.S., Bach, J., Pilat, J., Beckett, L.A., Arnold, S.E., Evans, D.A. & Bennett, D.A. 2002. Depressive symptoms, cognitive decline, and risk of AD in older persons. Neurology, 59, 364-370.
  13. Arendash, G.W. et al. 2009. Oxygen treatment triggers cognitive impairment in Alzheimer's transgenic mice. NeuroReport, 20 (12), 1087-1092.
  14. Tan, Z.S. et al. 2008. Thyroid Function and the Risk of Alzheimer Disease: The Framingham Study. Archives of Internal Medicine, 168(14), 1514-1520.

Vascular & Mixed Dementia

Prevalence

Vascular dementia, as its name suggests, is caused by poor blood flow, produced by a single, localized stroke, or series of strokes.

It is the second most common dementia, accounting for perhaps 17% of dementias. It also co-occurs with Alzheimer's in 25-45% of cases. Although there are other types of dementia that also co-occur with Alzheimer's, mixed dementia generally refers to the co-occurrence of Alzheimer's and vascular dementia.

Risk factors

In general, unsurprisingly, vascular dementia has the same risk factors as cerebrovascular disease.

A study1 of 173 people from the Scottish Mental Survey of 1932 who have developed dementia has found that, compared to matched controls, those with vascular dementia were 40% more likely to have low IQ scores when they were children than the people who did not develop dementia. Because this was not true for those with Alzheimer's disease, it suggests that low childhood IQ may act as a risk factor for vascular dementia through vascular risks rather than the "cognitive reserve" theory.

Prevention

The exciting thing about vascular dementia is that it is far more preventable than other forms of dementia. As with risk, as a general rule, the same things that help you protect you from heart attacks and stroke will help protect you from vascular dementia. This means diet, and it means exercise.

A four-year study2 involving 749 older adults has found that the top one-third of participants who exerted the most energy in moderate activities such as walking were significantly less likely to develop vascular dementia than those people in the bottom one-third of the group.

Treatment

Apart from normal medical treatment for cerebrovascular problems, there are a couple of interesting Chinese studies that have looked specifically at vascular dementia.

The herb gastrodine has been used in China for centuries to treat disorders such as dizziness, headache and even ischemic stroke. A 12-week, randomized, double-blind trial3 involving 120 stroke patients who were diagnosed with mild to moderate vascular dementia has found that  gastrodine and Duxil® (a drug used to treat stroke patients in China) produced similar overall levels of cognitive improvement -- although more patients showed 'much improvement' with gastrodine (23% vs 14%).

A Chinese pilot study4 involving 25 patients with mild to moderate vascular dementia found that ginseng compound significantly improved their average memory function after 12 weeks, but more research (larger samples, placebo-controls) is needed before this finding can be confirmed. Five years on I have still not seen such a study.

References: 
  1. McGurn, B., Deary, I.J. & Starr, J.M. 2008. Childhood cognitive ability and risk of late-onset Alzheimer and vascular dementia. Neurology, first published on June 25, 2008 as doi: doi:10.1212/01.wnl.0000319692.20283.10
  2. Ravaglia, G. et al. 2007. Physical activity and dementia risk in the elderly. Findings from a prospective Italian study. Neurology, published online ahead of print December 19.
  3. Tian, J.Z. et al. 2003. A double-blind, randomized controlled clinical trial of compound of Gastrodine in treatment of mild and moderate vascular dementia in Beijing, China. Presented at the American Heart Association's Second Asia Pacific Scientific Forum in Honolulu on June 10.
  4. Tian, J.Z. et al. 2003. Presented at the American Stroke Association's 28th International Stroke Conference on February 14 in Phoenix. Press release

Mental stimulation

Growing evidence points to greater education, and mentally stimulating occupations and activities providing a cognitive reserve that enables people with developing Alzheimer's to function normally for longer.

There is also evidence that physical exercise and mental stimulation protect against the development of Alzheimer's, by preventing accumulation of beta-amyloid.

Physical exercise and mental stimulation also seem to help protect against age-related decline in cognitive function, possibly for similar reasons — by stimulating growth of new blood vessels and keeps existing vessels open and functional.

Mental stimulation is not only gained by more obvious intellectual pursuits, but also by activities as simple as talking to people or going to the theater.

Education also seems to help seniors retain their mental flexibility, enabling their brains to change strategies as age effects make different strategies more effective.

The evidence that diet, physical exercise, and mental stimulation all help prevent age-related cognitive decline and reduce the risk of mild cognitive impairment and Alzheimer’s, is now very convincing.

Studies of mice and (rather intriguingly) beagles, have provided evidence that ‘enriched’ environments — ones that provide opportunities for regular exercise and mental stimulation — reduce or prevent age-related cognitive decline, and reduce the risk of Alzheimer’s.

Studies of genetically engineered mice have also now shown how an enriched environment protects against Alzheimer’s — by preventing accumulation of beta-amyloid, and helping these peptides to be cleared away.

It’s been suggested that the benefits of physical and mental activity, which now seem undeniable, may simply be a matter of blood flow — that physical and mental activity stimulates growth of new blood vessels and keeps existing vessels open and functional.

These findings from animal studies have been supported by a number of human studies.

Physical exercise

A large, six-year study of adults aged 65 and older found that physical fitness and exercise were both associated with a significantly lower risk of dementia. Encouragingly, for those who are more frail, even modest amounts of exercise (such as walking 15 minutes a day) appear beneficial, and the more frail the person was, the more they benefited from regular exercise.

Education

Findings from two long-running studies of aging and cognition — the Nun Study and the Religious Orders Study — have revealed that formal education helps protect people from the effects of Alzheimer’s disease.

Note that I said “from the effects”. Education doesn’t prevent or delay the disease from developing, but it does provide a “cognitive reserve”, which allows the individual to function normally in the presence of brain abnormalities (the presence of an Alzheimer’s pathology is thus only evident when the brain is autopsied post-mortem).

As you would expect, the more years of education, the greater the cognitive reserve — the less effect the same number of plaques have on cognitive performance. It’s worth noting that the populations in these studies are all relatively well-educated — even the least educated had some college attendance — suggesting that the effect of education would be even more marked in the general population.

However, there is some evidence that, once the disease progresses to the point that it has noticeable effects, those effects progress faster. This is thought to be simply because the damage is so much greater by the time it becomes observable in behavior.

A general population study still in train has provided preliminary findings indicating that prevalence of mild cognitive impairment also is less common among those with more education.

Higher education also seems to help protect older adults from cognitive decline in general. One reason is clearly the cognitive reserve aspect, but an imaging study has also revealed another reason. In young adults performing memory tasks, more education was associated with less use of the frontal lobes and more use of the temporal lobes. For older adults doing the same tasks, more education was associated with less use of the temporal lobes and more use of the frontal lobes. Previous research has indicated frontal activity is greater in old adults, compared to young; this study therefore implies that this effect is related to the educational level in the older participants. The higher the education, the more likely the older adult is to recruit frontal regions, resulting in a better memory performance.

An earlier brain-scan study also provided support for the theory that the brain may change tactics as it ages, and that older people whose brain is more flexible can compensate for some aspects of memory decline.

Results from a large study of older adults from a biracial community in Chicago suggest that the benefits of education are not necessarily education per se. Although both education and occupation were associated with Alzheimer's risk in this study, their effects were substantially reduced when cognitive activity was taken into account.

In keeping with these findings, several smaller studies have also provided evidence that other aspects of mental activity are also associated with a reduced risk of cognitive decline and dementia.

Mental activity

People with Alzheimer's have been found to be more likely to have had less mentally stimulating careers, and those who are more active in high school and have higher IQ scores are apparently less likely to have mild memory and thinking problems and dementia as older adults.

A study of 469 people aged 75 and older found that those who participated at least twice weekly in reading, playing games (chess, checkers, backgammon or cards), playing musical instruments, and dancing were significantly less likely to develop dementia. Although the evidence on crossword puzzles was not quite statistically significant, those who did crossword puzzles four days a week had a much lower risk of dementia than those who did one puzzle a week.

Another study of 700 seniors found that more frequent participation in cognitively stimulating activities, such as reading books, newspapers or magazines, engaging in crosswords or card games, was significantly associated with a reduced risk of Alzheimer’s disease.

And more recently, a comprehensive review of the research into 'cognitive reserve', involving 29,000 individuals across 22 studies, concluded that complex mental activity across people’s lives almost halves the risk of dementia. Encouragingly, all the studies also agreed that it was never too late to build cognitive reserve.

Looking at the question of cognitive decline in general, a large-scale British study of people aged 35—55 found that those who scored highest on tests of cognitive ability made regular cultural visits to theatres, art galleries and stately homes. Other activities were also associated with higher cognitive ability (in order of importance):

  • reading, and listening to music
  • involvement in clubs and voluntary organisations
  • participation in courses and evening classes

Interestingly, the association was stronger among men.

Another study, of people aged 30—88, has found that those who were fluent in two languages rather than just one, were sharper mentally. This was true at all age groups, but bilinguals were also much less likely to suffer from the mental decline associated with old age. The participants were all middle class, and educated to degree level.

Social networks

There has been some evidence suggesting that simply talking helps keep your mind sharp at all ages, and that older people with more extensive social networks are less likely to suffer cognitive impairment.

More recently, a study has provided evidence that social networks also offer a 'cognitive reserve' that protects people from the ravages of Alzheimer's disease. To determine social network, participants were asked about the number of children they have and see monthly; about the number of relatives, excluding spouse and children, and friends to whom they feel close and with whom they felt at ease and could talk to about private matters and could call upon for help, and how many of these people they see monthly. Their social network was the number of these individuals seen at least once per month.

Post-mortem analysis revealed that, as the size of the social network increased, the same amount of Alzheimer’s pathology in the brain (i.e., extent of plaques and tangles) had less effect on cognitive test scores. In other words, for persons without much pathology, social network size had little effect on cognition. However, as the amount of pathology increased, the apparent protective effect on cognition also increased.

What you can do

The thought that your education, occupation, degree of physical fitness, and social involvedness, over the years, affects your risk of losing cognitive function, may relieve your anxieties or depress you. But if it depresses you, take heart from a recently-reported pilot study involving people aged 35–69. These people had some mild memory complaints but performed normally on tests. Nevertheless, in a mere two weeks, a program combining a brain healthy diet plan (5 small meals a day; diet rich in omega-3 fats, antioxidants and low-glycemic carbohydrates like whole grains), relaxation exercises, cardiovascular conditioning (daily walks), and mental exercise (such as crosswords and brain teasers) resulted in these participants' brain metabolism decreasing 5% in working memory regions, suggesting an increased efficiency. Compared to the control group, participants also performed better in verbal fluency, and felt as if they were performing better.

 

Does physical exercise improve cognitive function?

A number of studies have provided evidence that physical exercise helps reduce age-related decline in cognitive function, and may prevent or delay dementia.

There is some reason to think older (post-menopausal) women may benefit more than older men.

While the cognitive benefits of physical exercise for children and younger adults are less clear, there is some evidence that there may be some benefit, although not to the same degree as for older adults.

Studies indicate that exercise programs involving both aerobic exercise and strength training are of greatest benefit, with exercise sessions lasting at least 30 minutes.

Apart from age and gender, individual differences also play a part in determining how much value exercise is to an individual.

The effects of exercise on cognitive function in older adults

A number of studies in the past few years have provided evidence that physical exercise can ameliorate the effects of aging on the brain, in terms both of preventing or postponing dementia, and reducing the more normal age-related decline in cognitive function. The reasons for the effect are almost certainly multiple, for example:

  • Exercise has clear effects on cardiovascular fitness, and many recent studies have provided converging evidence that there is an association between cardiovascular fitness and mental fitness — "what's good for the heart is good for the brain".
  • Exercise helps control blood sugar levels, and a recent study has found that those with impaired glucose tolerance tend to have a smaller hippocampus.
  • Exercise may increase the flow of oxygen-rich blood to the brain.
  • Exercise may increase self-confidence, and may reduce anxiety and depression.

Interestingly, while exercise benefits both genders, there is some evidence that it may be of greater benefit to women (at older ages). This may be related to estrogen status. There is some evidence that, in females, the benefits of exercise depend on the presence of estrogen. Levels of voluntary physical activity also seem to depend on estrogen status. This may be behind some of the benefit hormone therapy can have on older women's cognitive functioning.

But the undoubted benefits of physical activity for seniors do not imply that exercise has any effect on memory and learning in younger people. That is quite a different question. In seniors, the hope is that exercise will counteract some of the biological wear and tear caused by aging. Does physical fitness matter at younger age levels?

The effects of exercise on cognitive function in children and young adults

Unfortunately, there have been far fewer studies involving young people. However, one study [1], reported at the 2001 Society for Neuroscience conference, found that, following a 12 week regimen of jogging for 30 minutes two to three times a week, young adults significantly improved their performance on a number of cognitive tests. The scores fell again if participants stopped their running routine.

In this particular case, it does not seem that level of fitness is the primary cause — otherwise, you'd expect test performance not to be so quickly affected by the cessation of physical activity. The researchers suggested that increased oxygen flow to the brain might have been behind the improvement in mental sharpness. Oxygen intake did rise with the joggers' test scores. Supplemental oxygen administration has been found to significantly improve memory formation in healthy young adults, as well as improving reaction time [2].

On the other hand, preliminary results from a series of studies undertaken with elementary school children do indicate a strong relationship between academic achievement and fitness scores. One study found that physically fit children identified visual stimuli faster. Brain activation patterns provided evidence that the fit children allocated more cognitive resources towards the task, as well as processing information faster. [3]

What studies with non-humans tell us

Rodent studies have a big advantage over human studies - many subjects ready to hand, complete control of their environment - and accordingly, it is easier to receive more direct answers. These studies tell us not simply that exercise can be beneficial for learning, but why it might be so.

Studies with mice have made it clear that exercise can:

  • increase levels of BDNF (brain-derived neurotrophic factor; BDNF helps support and strengthen the synapses in the brain (the connections between neurons), as well as helping protect and grow new neurons),
  • stimulate neurogenesis (the creation of new neurons),
  • increase resistance to brain insult, and
  • perhaps promote brain plasticity. [4]

However, while there is no doubt that exercise increases levels of BDNF in the hippocampus, we can’t take it for granted that this is entirely a good thing. Mice bred for 30 generations to be more active (indeed, exercise “addicts”), showed high levels of BDNF and grew more neurons in the hippocampus, and yet performed terribly when attempting to navigate around a maze. Researchers suggested that too much exercise may cause the brain to “max out” in the production of BDNF and neurons, and this may prevent learning. Alternatively, the highly active mice may simply have been too focused on running to concentrate on anything else! [5]

The point is that at the moment, we don’t know for sure what the significance of the exercise-induced increase in BDNF and neurogenesis is. It may be that high levels of exercise place stress on the hippocampus, damaging or killing neurons. The increased levels of BDNF and neuron production may simply be attempts to counteract the damage done. All that's certain is that exercise provokes a lot of activity in the hippocampus, in particular in that particular region of the hippocampus called the dentate gyrus.

Having said that, let's note that this is the first study to demonstrate a case of neurogenesis that is not associated with learning improvement. In general, the production of new neurons is associated with improvement in learning and memory. It would be unwise, therefore, to take these findings as indicating the reverse. What they do suggest is that we cannot assume that such an association always occurs, and that in the case of exercise, it may well be that you can have too much of a good thing! It does seem clear, from this and other studies, that there is a direct association between amount of exercise and BDNF level.

On the subject of whether you can have too much exercise, it's worth noting that a human study found that, while moderate aerobic exercise for up to an hour improved performance on particular cognitive tasks, too much exercise had a deleterious effect. [6]

Brain regions affected by exercise

Notwithstanding the (understandable) emphasis placed on the hippocampus, a critical region for learning and memory, human studies have implicated many parts of the brain. Specifically, one study of seniors found that executive functions were particularly improved by exercise - executive functions are primarily located in the prefrontal cortex. Another study of seniors found reduced grey and white matter in the frontal, temporal, and parietal cortexes of those who were less physically fit. In similar vein, another study of seniors found differences in the middle-frontal and superior parietal regions of the brain as a function of aerobic fitness.

Interestingly, in the possibly first study to look at higher cognitive funtion during exercise (sustained, moderate), it was found that functions dependent on the prefrontal cortex were impaired, but not those requiring little prefrontal activity. [7]

Exercise and diet

Exercise should not, of course, be considered entirely without reference to diet. The effect of exercise on cardiovascular fitness and blood glucose levels is a counterweight to the effect diet has had in inducing impaired glucose tolerance and cardiovascular problems. A number of rodent studies* have found that a high-fat diet impairs learning and memory. Rodent experiments have also found that exercise can reverse the decrease in BDNF levels in the hippocampus resulting from a high-fat diet, and prevent the deficit in spatial learning induced by such a diet. [8]

The question might therefore arise, if the diet has been healthy, is exercise beneficial? Interestingly, a very recent study involving older beagles found that both a diet enriched with antioxidants and a stimulating environment were helpful in preventing or reducing age-related cognitive decline. That is, each were good, but both was best. This doesn't directly answer the question, of course, but it does seem likely that both diet and exercise are important factors in physical and mental health.

Physical exercise and mental exercise

The beagle study used what is termed an "enriched" environment — typically this involves opportunities for social interaction and mental stimulation, as well as physical activity. A mouse study endeavored to separate the components of such an enriched environment, in order to see whether all were necessary to achieve the observed increased neuron production in the dentate gyrus. Interestingly, they found that voluntary wheel running was in itself sufficient to achieve the level of neurogenesis achieved in typical enrichment conditions. [9]

This is intriguing, but as much as anything else it points to the limitations of rodent studies as models for human behavior. A number of human studies, again, mainly with older adults, point to the value of mental stimulation in protecting against cognitive decline. Interestingly, one such study found ballroom dancing was apparently of (surprising) value in protecting against age-related cognitive decline — it was suggested that there was an intellectual component to it lacking in other physical activities. But perhaps, if I may speculate, we should consider more seriously that activities that combine intellectual and physical (and perhaps social) attributes might be best of all.

It does seem clear that, while both mental stimulation and physical exercise might both help cognitive function, they do so in quite different ways, for different reasons.

Recommendations

An analysis of 18 studies [10] on the effects of exercise on cognitive function in older adults concluded that:

  • exercise programs involving both aerobic exercise and strength training produced better results on cognitive abilities than either one alone
  • more than 30 minutes of exercise per session produce the greatest benefit

Caveat: Not everyone benefits equally from exercise

It does seem clear that older adults benefit more from exercise than younger people, as far as cognitive function is concerned. It also seems that older women, especially those on hormone-replacement therapy, receive greater cognitive benefits from exercise than men.

Generalisations aside, it is as well to remember the findings of a very recent study showing that, while most people benefit (physically) from exercise, the degree of benefit is hugely variable between individuals, and some people don’t benefit at all! [11]

* In one study, young adult male mice were divided into four groups by diet: normal (control) diet, high-saturated-fat diet, high-sugar diet, and diet high in saturated fats and sugar. They were kept on the diet for four months, during which mice on the high-fat and high-fat-&-sugar diets gained significantly more weight than those on the control and high sugar diets. At the end of that time, the mice were tested on a maze task. Mice on the high-fat and high-fat-&-sugar diets performed worse than the other mice. The mice were then exposed to a neurotoxin called kainic acid, which is known to damage nerve cells in the hippocampus. Mice on the high-fat and high-fat-&-sugar diets were significantly more impaired by the neurotoxin.
In another mouse study, obese mice were fed a diet containing about 10% fat for seven months, while control mice were fed standard lab chow containing only 5% fat. On testing, it was found that the obese mice took significantly more trials than the normal-weight mice to both acquire and retain a memory of a foot shock. They also required significantly more trials than control mice to learn to press a lever for milk reinforcement.
A rat study explored whether a diet high in cholesterol and hydrogenated fats affected working memory in middle-aged rats (corresponding to 60 and older for humans). The high-fat, high-cholesterol diet produced significantly higher plasma triglycerides, total cholesterol, high density lipoprotein cholesterol, and low density lipoprotein cholesterol compared with controls. Weight increase and food consumption were similar between the groups. Animals on the high-fat regimen made more errors than animals fed the control diet, especially during the trial that placed the highest demand on their working memory.
Another rat study found that a diet high in fats and carbohydrates worsened cognitive deficits in rats exposed to repeated brief periods of low oxygen during sleep (as experienced by people with sleep apnea). Press release

See news reports

References: 
  1. Kubota et al. 2001. cited in http://nootropics.com/exercise/index.html
  2. Scholey, A.B., Moss, M.C., Neave, N. & Wesnes, K. 1999. Cognitive Performance, Hyperoxia, and Heart Rate Following Oxygen Administration in Healthy Young Adults. Physiology & Behavior, 67 (5), 783-789.
  3. Hillman, C. & Buck, S. 2004. Physical Fitness and Cognitive Function in Healthy Preadolescent Children. Presented at the annual meeting of the Society for Psychophysiological Research in Santa Fe, N.M., Oct. 20-24. Press release
  4. Cotman, C.W. & Berchtold, N.C. 2002. Exercise: a behavioral intervention to enhance brain health and plasticity. Trends in Neurosciences, 25 (6), 295-301.
  5. Rhodes, J.S., van Praag, H., Jeffrey, S., Girard, I., Mitchell, G.S., Garland, T.Jr. & Gage, F.H. 2003. Exercise increases hippocampal neurogenesis to high levels but does not improve spatial learning in mice bred for increased voluntary wheel running. Behavioral Neuroscience, 117(5), 1006-1016.
  6. Tomporowski,P.D. 2003. Effects of acute bouts of exercise on cognition. Acta Psychol (Amst), 112, 297-324.
  7. Dietrich, A. & Sparling, P.B. 2004. Endurance exercise selectively impairs prefrontal-dependent cognition. Brain and Cognition, 55 (3), 516-524.
  8. Molteni, R., Wu, A., Vaynman, S., Ying, Z., Barnard, R.J. & Gómez-Pinilla, F. 2004. Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor. Neuroscience, 123 (2), 429-440.
  9. van Praag, H., Kempermann, G. & Gage, F.H. 1999. Running increases cell proliferation and neurogenesis in the adult mouse dentate gyrus. Nature Neuroscience, 2 (3), 266-70.
  10. Colcombe, S. & Kramer, A.F. 2003. Fitness effects on the cognitive function of older adults: A meta-analytic study. Psychological Science, 14, 125-130.
  11. Bouchard, C. 2004. Reported at the Australian Health and Medical Research Congress in Sydney, Australia. http://www.newscientist.com/news/news.jsp?id=ns99996735

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