Lifestyle factors

Estrogen's effect on memory & learning

Estrogen's effect on the brain is a complex story, one which we are only beginning to understand. We know it's important for women, but we're not sure about the details. One of the problems is that it appears to interact with stress. There are two aspects to estrogen's effects on women: normal monthly fluctuations in estrogen levels, and menopause.

It's also important to distinguish post-menopause (once you have completely stopped menstruating) from perimenopause (the years of menstrual irregularity leading up to this).

In general, the last few years of research seem to be coming to the conclusion that any cognitive problems women experience as they approach menopause is limited, both in time and in task, and depends in part on other factors. For example, those who experience many hot flashes may have poorer verbal memory, but the main cause for this may be the poorer sleep quality; those who are distressed or experience mood changes may find their memory and concentration affected for that reason.  These findings suggest the best approach to dealing with cognitive problems in perimenopause is to tackle the physical and/or emotional causes.

Post-menopause is different. Post-menopause is all about low estrogen levels, and the importance of estrogen for brain function. Nevertheless, estrogen therapy for postmenopausal women has had inconsistent results; there has even been some research suggesting it may increase the risk of later dementia. There is also some suggestion that it may not help those women who have cognitively stimulating environments, or are highly educated. And other indications that timing might be critical -- the age at which you begin hormone therapy. At the moment, we simply have too little clear evidence to warrant recommending hormone therapy for cognitive reasons (particularly in light of the possible cancer risk), or to know when it might be effective.

Excitingly, however (because there is no downside!), there is some evidence that physical exercise can counter the cognitive decline postmenopausal women may experience. There's also a study suggesting that the effect of low estrogen after menopause is not to impair cognition but simply to change it -- however, because women aren't prepared for, or understand, these changes, they perceive it as impairment. That would suggest that what is needed is an education program in how the brain changes (but first we have to understand exactly how it does change!).

See news reports

Sleep and cognition in children

A U.S. survey provides evidence that both children and adolescents tend to be getting less sleep than needed.

Depression, lower self-esteem, and lower grades, have all been found to be correlated with sleep deprivation in middle-school children.

Sleep disturbance in infants and young children has also been found to be associated with lower cognitive performance.

We all know that lack of sleep makes us more prone to attentional failures, more likely to make mistakes, makes new information harder to learn, old information harder to retrieve ... We all know that, right? And yet, so many of us still go to bed too late to get the sleep we need to function well. Of course, some of us go to sleep early enough, we just can’t get to sleep fast enough, or are prone to waking in the night. (Personally, I can count the times I’ve slept through the night without waking in the last fifteen years on my fingers).

I talk about the effect of sleep on memory elsewhere; I want to talk here about a sleep problem that we don’t tend to think about so much — the sleep deficit children are running.

A survey commissioned by the National Sleep Foundation found that 3-to-6-year-olds in the U.S. get about 10.4 hours sleep nightly, while experts recommend 11 to 13 hours. 1st graders to 5th graders who should be getting 10 to 11 hours are averaging just 9.5 hours.

And a study of middle-school children (11 to 14 year olds) found a direct correlation between sleep deprivation and depression, lower self-esteem, and lower grades. "The fewer hours of sleep that children got, the more depressed they were, the higher number of depressive symptoms [they had], and the lower their self-esteem and the lower their grades."

The second largest growth spurt occurs during these years (usually 10-14 for girls; 11-16 for boys), so this is a time when a lot of sleep is needed. But it’s also a time when children become more capable and more independent; when they’re likely to start taking on a lot more activities, work harder and longer, and are monitored less by their parents and caregivers. So ... it’s not surprising, when we stop and think about it, that a lot of these children are starting to pick up the bad habits of their parents — not getting enough sleep.

Which also points, in part, to the solution: if you’re a parent, remember that your children are, as always, modeling themselves on you. And sleep habits usually reflect a household pattern. If you’re a teacher, remember you need to educate the family, not just the child.

The National Institutes of Health (NIH) have identified adolescents and young adults (ages 12 to 25 years) as a population at high risk for problem sleepiness based on "evidence that the prevalence of problem sleepiness is high and increasing with particularly serious consequences."

Sleep disturbance in infants and young children has also been found to be associated with lower cognitive performance. Previous studies have looked at the severe end of the spectrum of sleep disorders — obstructive sleep apnea. More alarmingly, a new study of 205 5-year-old children found even mild sleep-disordered breathing symptoms (frequent snoring, loud or noisy breathing during sleep) were associated with poorer executive function and memory skills and lower general intelligence.

Before you panic, please note that some 30% of the participants had SBD symptoms, so it’s hardly uncommon (although there may have been a bias towards children with these symptoms; it does seem surprisingly high). You might also like to note that I personally had a blocked nose my entire childhood (always breathed through my mouth, and yes, of course I snored) and it didn’t stop me being top of the class, so ...

Nor is the research yet developed enough to know precisely what the connection is between SBD and cognitive impairment. However, it does seem that, if something can be done about the problem, it is probably worth doing (in my case, taking me off dairy would probably have fixed the problem! but of course noone had any idea of such factors back then).

Here’s a few links that may be of interest to parents and teachers:

ScienCentral article on the middle-school study:
http://sciencentral.com/articles/view.htm3?article_id=218392389

The NSF Sleep poll
http://www.sleepfoundation.org/article/press-release/national-sleep-foundation-2013-international-bedroom-poll 

a look at the school start times debate (I find this fairly amazing actually, because here in New Zealand, our children usually start school around 9am; the thought of kids starting school at 7.30 sends me into a spin!)
http://www.sleepfoundation.org/article/sleep-topics/school-start-time-and-sleep

The National Sleep Foundation also has a site for children who want to learn about sleep and healthy sleep habits: www.SleepforKids.org For children from 7 up; with educational games and activities, as well as a downloadable copy of NSF’s new Sleep Diary designed especially for children.

This article originally appeared in the November 2004 newsletter.

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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  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.
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  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.

Food & Supplements

There is little evidence that dietary supplements or changes to the diet improve mental function in young, healthy people.

Changes in diet and dietary supplements may be beneficial to older adults, or those suffering from physical disorders, allergies, depression, stress, etc.

Despite the claims made for many supplements, we can't point unequivocally to any as beneficial. Whether they are of benefit does depend on whether you are lacking in some vitamin and mineral (e.g., Vitamin B12), so it is advisable to have your levels checked.

Food is safer, and the evidence does now seem clear that fruit and vegetables rich in anti-oxidants are of particular benefit.

A perennial topic in the arena of memory improvement is the question of “food for the brain”, and in particular, whether there are dietary supplements that can improve your mental abilities. While my own emphasis is improvement through development and practice of skills, I don’t dismiss the possibility of improvement through more physical means. I myself am a great fan of the “you are what you eat” principle. This is mainly because I suffer from multiple food sensitivities, so the consequences of food are very much a reality for me. That doesn’t mean I believe perfectly healthy people should obsess about their diet. There is another principle that is of great importance: we are all individuals.

For example, a year ago, I wrote of the effects of caffeine on memory, concluding that: “while caffeine may help older adults in the later part of the day, those with hypertension, diabetes, impaired glucose tolerance, or high homocysteine levels, would be wiser to avoid coffee, even if decaffeinated. In general, while caffeine may help you overcome factors that lower your cognitive performance, it does not seem that caffeine has any significant direct effect on memory, although it may well help you pay attention.”

So, caffeine is more helpful for some types of people than others, and is in fact contra-indicated for some. Moreover, the effects are different for those who are accustomed to a high caffeine intake, compared to those who only occasionally consume caffeine. And – here’s the real kicker – I also know from personal experience that the effects of caffeine are highly individual: I myself respond to caffeine not with the usual increased alertness, but in fact with decreased alertness. It makes me sleepy!

I do think there are physical factors of far greater importance than diet. Sleep is the obvious one. Individual differences don’t show up in the basic need to have enough sleep, and the right sort of sleep, to optimize brain functioning, but they do of course show up as regards how much sleep is right for us. That also, is something that changes with age, and, I imagine, health, throughout our lifespan.

Another physical factor which should be given due weight is exercise. While its effect is not as great as sleep (I don’t think anything rivals the importance of sleep!), I would give it more importance than diet because its effect is far more consistent. I don’t think anyone would fail to benefit mentally from increased physical fitness (which is not to say there isn’t a level of fitness beyond which no more mental improvement will occur).

Diet, on the other hand, depends a great deal on the individual. There is little evidence that dietary supplements or changes to the diet improve mental function in those who don’t suffer from any of the conditions which can adversely affect brain function — e.g., aging, physical disorders, depression, stress, etc.

In other words, if you are a relatively young person with no health problems, I suggest you concentrate on getting enough sleep and exercise, and learning and practicing effective memory strategies.

If you have any conditions which can adversely affect brain function I would also emphasize doing this! But, additionally, I do think there are foods and supplements you can take which may well significantly improve your brain function.

Which ones? Here we enter the area of individual difference. To find out what is effective for you, you should start with the research. What foods and supplements have been demonstrated to be effective in improving cognition?

Here we enter an area fraught with difficulty. News reports come out about foods and supplements all the time, and today’s world is filled with people hawking “health” products. How do we know what to believe?

The first thing, of course, is to ascertain whether the claims are backed up by research. But that’s not as easy as it sounds, because every seller of such products knows the importance of sounding as if research has proven the effectiveness of their product. (Actually, I automatically disavow any text which talks of research “proving” something. No researcher worth his salt would ever make such a claim.)

How do we determine the genuineness and reliability of the research? First, and most importantly, by assessing the source. For example, I only cite research from reputable academic journals, or academic conferences. I also give greater weight to research from researchers whose work I know of. Hopefully, by so doing, I also make myself a reliable source.

This is not, however, infallible, for even well-respected journals can make mistakes. For example, very topically, the truthfulness of a widely reported study of a nutritional supplement's effects on thinking and memory in the elderly has recently been cast into doubt (actually, this is a rather polite phrase for the comments now being made: “scientists who reviewed the paper had found the methods and statistical findings so unlikely that they wondered whether the study had actually been done”; "The statistics were not just implausible, they were impossible.")

Nevertheless, the very shock with which these questions are being raised demonstrates that, by and large, the system does work. We cannot expect certainty.

Having approved the source, the second thing to consider is the extent to which the research has been replicated. One study does not make an answer! It is indicative only. It is interesting.

Even a second study is little more than another support. Before we can say, “You know, I really think there’s something to this”, we need a number of studies building together from different angles.

So, a study showing that sage can help cognitive function in healthy young adults (there is indeed such a study) is interesting. Given that sage is easy to grow, and commonly consumed (one doesn’t need to worry about toxicity), I would go so far as to say, give it a try! But I wouldn’t give a lot of weight to the research until more studies had been carried out. (I would, however, happily drink sage tea everyday on the off chance, except it turns out – I really can’t believe this! – I’m sensitive to sage, too.)

On the other hand, for a product that is expensive, or has potential side-effects, I would wait for more evidence to come in before trying it. Okay, we’ve looked at the research, we’ve found the foods and supplements of potential benefit. What next?

Next, you look at your own particular problems.

For example, my main problem is food sensitivities. The first, most dramatic, thing I did to overcome my increasing mental sluggishness was: stop eating foods which turned out to be bad for me! After concentrating on that for a year or two, with my physical and mental problems much improved (but not gone), I turned my attention to the damage done to my body over the long period during which I was unaware of my food sensitivities. I now take B12, which I am sure has had a significant effect on my brain, and have recently started taking iron (as a woman of childbearing age). I also take other mineral supplements, principally to overcome deficiencies in my environment (New Zealand’s soil is deficient in a number of minerals), and lecithin (partly because of the deficiencies in my diet as a result of having to avoid certain foods).

The final step, once you’ve established the possible foods and supplements which are worth trying, is to see whether they are effective for you. Remember me and the coffee. What works for one doesn’t necessarily work for another (and may indeed be harmful). But don’t try everything at once! One at a time, and the most likely first.

So, what foods and supplements might be of benefit to your brain?

Most of the research into the cognitive benefits of diet and supplements has been concerned with seniors, with alleviating the effects of age on the brain. This is consistent with the belief that there is little, if any, benefit to be gained by young, healthy adults. Having said that, however, the following have been shown to be of benefit in at least one study:

  • creatine
  • sage
  • lemon balm
  • a diet high in soy products

Remember my comment about the reliability of single studies! However, since three of these four are all perfectly “natural” food items, there would be little danger in trying these out.

Several substances are worth mentioning as having been of particular interest to researchers for their potential benefits to brains suffering from the effects of age:

  • gingko biloba
  • ginseng
  • choline (lecithin)
  • vitamin B12
  • phosphatidylserine (PS)
  • acetyl-L-carnitine (ALC)
  • antioxidants (particularly vitamin E)

This article originally appeared in the May 2004 newsletter.

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

Reviewing alcohol's effects on normal sleep

A review on the immediate effects of alcohol on sleep has found that alcohol shortens the time it takes to fall asleep, increases deep sleep, and reduces REM sleep.

Because sleep is so important for memory and learning (and gathering evidence suggests sleep problems may play a significant role in age-related cognitive impairment), I thought I’d make quick note of a recent review bringing together all research on the immediate effects of alcohol on the sleep of healthy individuals.

The review found that alcohol in any amount reduces the time it takes to fall asleep, while greater amounts produce increasing amounts of deep sleep in the first half of the night. However, sleep is more disrupted in the second half. While increased deep sleep is generally good, there are two down sides here: first, it’s paired with sleep disruption in the second half of the night; second, those predisposed to problems such as sleepwalking or sleep apnea may be more vulnerable to them. (A comment from the researchers that makes me wonder if the relationship between deep sleep and slow-wave activity is more complicated than I realized.)

Additionally, at high doses of alcohol, REM sleep is significantly reduced in the first half, and overall. This may impair attention, memory, and motor skills. Moreover, at all doses, the first REM period is significantly delayed, producing less restful sleep.

The researchers conclude that, while alcohol may give the illusion of improving sleep, it is not in fact doing so.

Reference: 

[3269] Ebrahim, I. O., Shapiro C. M., Williams A. J., & Fenwick P. B. (2013).  Alcohol and Sleep I: Effects on Normal Sleep. Alcoholism: Clinical and Experimental Research. n/a - n/a.

How urban living affects attention

A comparison of traditional African villagers and those who have moved to town indicates that urban living improves working memory capacity even as it makes us more vulnerable to distraction.

Another study looking into the urban-nature effect issue takes a different tack than those I’ve previously reported on, that look at the attention-refreshing benefits of natural environments.

In this study, a rural African people living in a traditional village were compared with those who had moved to town. Participants in the first experiment included 35 adult traditional Himba, 38 adolescent traditional Himba (mean age 12), 56 adult urbanized Himba, and 37 adolescent urbanized Himba. All traditional Himba had had little contact with the Western world and only spoke their native language; all adult urbanized Himba had grown up in traditional villages and only moved to town later in life (average length of time in town was 6 years); all adolescent urbanized Himba had grown up in town the town and usually attended school regularly.

The first experiments assessed the ability to ignore peripheral distracting arrows while focusing on the right or left direction of a central arrow.

There was a significant effect of urbanization, with attention being more focused (less distracted) among the traditional Himba. Traditional Himba were also slower than urbanized Himba — but note that there was substantial overlap in response times between the two groups. There was no significant effect of age (that is, adolescents were faster than adults in their responses, but the effect of the distracters was the same across age groups), or a significant interaction between age and urbanization.

The really noteworthy part of this, was that the urbanization effect on task performance was the same for the adults who had moved to town only a few years earlier as for the adolescents who had grown up and been educated in the town. In other words, this does not appear to be an educational effect.

The second experiment looked at whether traditional Himba would perform more like urbanized Himba if there were other demands on working memory. This was done by requiring them to remember three numbers (the number words in participants’ language are around twice as long as the same numbers in English, hence their digit span is shorter).

While traditional Himba were again more focused than the urbanized in the no-load condition, when there was this extra load on working memory, there was no significant difference between the two groups. Indeed, attention was de-focused in the traditional Himba under high load to the same degree as it was for urbanized Himba under no-load conditions. Note that increasing the cognitive load made no difference for the urbanized group.

There was also a significant (though not dramatic) difference between the traditional and urbanized Himba in terms of performance on the working memory task, with traditional Himba remembering an average of 2.46/3 digits and urbanized Himba 2.64.

Experiment 3 tested the two groups on a working memory task, a standard digit span test (although, of course, in their native language). Random sequences of 2-5 digits were read out, with the participant being required to say them aloud immediately after. Once again, the urbanized Himba performed better than the traditional Himba (4.32 vs 3.05).

In other words, the problem does not seem to be that urbanization depletes working memory, rather, that urbanization encourages disengagement (i.e., we have the capacity, we just don’t use it).

In the fourth experiment, this idea was tested more directly. Rather than the arrows used in the earlier experiments, black and white faces were used, with participants required to determine the color of the central face. Additionally, inverted faces were sometimes used (faces are stimuli we pay a lot of attention to, but inverting them reduces their ‘faceness’, thus making them less interesting).

An additional group of Londoners was also included in this experiment.

While urbanized Himba and Londoners were, again, more de-focused than traditional Himba when the faces were inverted, for the ‘normal’ faces, all three groups were equally focused.

Note that the traditional Himba were not affected by the changes in the faces, being equally focused regardless of the stimulus. It was the urbanized groups that became more alert when the stimuli became more interesting.

Because it may have been a race-discrimination mechanism coming into play, the final experiment returned to the direction judgment, with faces either facing left or right. This time the usual results occurred – the urbanized groups were more de-focused than the traditional group.

In other words, just having faces was not enough; it was indeed the racial discrimination that engaged the urbanized participants (note that both these urban groups come from societies where racial judgments are very salient – multicultural London, and post-apartheid Namibia).

All of this indicates that the attention difficulties that appear so common nowadays are less because our complex environments are ‘sapping’ our attentional capacities, and more because we are in a different attentional ‘mode’. It makes sense that in environments that contain so many more competing stimuli, we should employ a different pattern of engagement, keeping a wider, more spread, awareness on the environment, and only truly focusing when something triggers our interest.

Reference: 

[3273] Linnell, K. J., Caparos S., de Fockert J. W., & Davidoff J. (2013).  Urbanization Decreases Attentional Engagement. Journal of experimental psychology. Human perception and performance.

Alcohol and marijuana use in adolescence linked to impaired white-matter integrity

A brain-imaging study shows adolescents who abuse alcohol and marijuana show poorer white-matter integrity, with alcohol associated with continuing damage to wiring in prefrontal regions.

Chronic use of alcohol and marijuana during youth has been associated with poorer neural and cognitive function, which appears to continue into adulthood. A new study looking specifically at white-matter changes provides more support for the idea that adolescent brains may be at particular risk from the damage that substance abuse can bring.

The brain-imaging study compared 41 adolescents (aged 16-20) with extensive marijuana- and alcohol-use histories by mid-adolescence with 51 adolescents with no such history. The study found that substance users showed poorer white matter integrity in seven tracts (right and left superior longitudinal fasciculus, right posterior thalamic radiations, right prefrontal thalamic fibers, right superior temporal gyrus white matter, right inferior longitudinal fasciculus, left posterior corona radiata).

Two brain scans were taken, at baseline and at 18 months. Substance use interviews were given every six months.

More alcohol use during the interval was associated with worse integrity in both the right and left superior longitudinal fasciculi, above and beyond baseline values in these bundles. Marijuana use didn’t predict change over time. Those who had a history of more risk-taking behaviors showed poorer integrity of the right prefrontal thalamic fibers.

The findings add to previous research showing white matter problems in youth with substance-use histories. The study points to alcohol use during adolescence being particularly problematic. It also suggests that youth who engage in risk-taking behaviors may tend to have poorly developed fronto-thalamic tracts.

All of this is particularly worrying because it is thought that maturation of the brain during adolescence is the foundation for self-control, suggesting that substance abuse during this period may have long-lasting effects on the individual’s ability to plan, organize, and self-regulate.

Reference: 

[3210] Bava, S., Jacobus J., Thayer R. E., & Tapert S. F. (2012).  Longitudinal Changes in White Matter Integrity Among Adolescent Substance Users. Alcoholism: Clinical and Experimental Research. n/a - n/a.

Cognition impaired by low-level exposure to organophosphate pesticides

A meta-analysis has concluded that low-level exposure to organophosphates has a small-to-moderate negative effect on cognitive function.

Organophosphate pesticides are the most widely used insecticides in the world; they are also (according to WHO), one of the most hazardous pesticides to vertebrate animals. While the toxic effects of high levels of organophosphates are well established, the effects of long-term low-level exposure are still controversial.

A meta-analysis involving 14 studies and more than 1,600 participants, reveals that the majority of well-designed studies undertaken over the last 20 years have found a significant association between low-level exposure to organophosphates and impaired cognitive function. Impairment was small to moderate, and mainly concerned psychomotor speed, executive function, visuospatial ability, working memory, and visual memory.

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