diet

Benefits of fruit & vegetables for cognition

  • Fruit & vegetables are a vital part of a brain-healthy diet.
  • Apart from valuable vitamins and minerals, they contain antioxidants which help protect against damage to brain cells, as well as helping with cholesterol and blood flow.
  • Color is your best sign that the fruit or vegetable has more 'goodness': go for reds and purples and dark greens.

I don't think anyone's going to try arguing that fruit and vegetables are not good for your health! We know they're good. But that's just general "oh, I know it's good for me" — do you know that the benefits are not only for your general health, your protection against obesity and diabetes, cancer and heart disease, but also for your brain. Actually, there's two aspects to this. An unhealthy diet (one rich in junk food, in saturated fat and sugar) is actively bad for your brain, and (the right) healthy diet is actively good for your brain.

Fruit and vegetables are only one part of a brain-healthy diet, of course, but they're a very important part. A major reason for this benefit is thought to lie in the antioxidants present in these foods. Antioxidants help fight the oxidative stress that increasingly damages our brain cells as we age. Antioxidants is a group term, and some that fall into this category are more important than others.

The anthocyanins appear to be the most useful — these are responsible for the reds, purples, and blues in some plants. Several studies have affirmed the cognitive benefits of blueberries and Concord grape juice in particular (Concord grapes are especially purple grapes). Basically, the darker the fruit, the more anthocyanins, and the more powerful it will be.

Other valuable compounds include pterostilbene (found in blueberries), and resveratrol (found in grapes and red wine), which lower cholesterol. Quercetin (found in apples, blueberries, and cranberries) protects against cell damage and apparently helps with blood flow.

All of this perhaps explains why it is so much better to eat well rather than hope to receive what you need from dietary supplements!

Of the vegetables, green leafy vegetables, especially spinach, have been found to be especially beneficial. Onions are also a good source of quercetin (and presumably red onions, like red apples, are better than their paler cousins).

As a rule of thumb, the best fruits and vegetables are those with the most color. And, obviously, it's the color you want to eat (so no peeling your nice red apple!).

References: 

tags lifestyle: 

Benefits of fish & oils for cognition

  • Regular consumption of fish, especially oily fish, is associated with a reduced risk of Alzheimer's and better cognitive performance in old age.
  • High levels of omega-3 oils are associated with less brain shrinkage, and less brain damage in old age.
  • The benefits of supplements (as opposed to deriving these oils from food) is less clear, with inconsistent findings. It seems likely that their benefits depend on the individual's health and genetic profile, as well as on the nature and type of supplement.

There have been quite a few studies looking into the possible benefits of omega-3 fatty acids and fish (a good source of the oils), particularly for older adults. Several large studies have found that regular intake of oily fish is associated with lower rates of dementia, and some evidence that eating fish regularly slows the rate of 'normal' age-related cognitive decline.

However, findings into the effects of omega-3 oils have not been consistent, and one reason for that may lie in its interactions with other factors. For example, B vitamins have been found to improved cognition in older adults, but only when omega-3 levels are high. A number of studies have found regular consumption of fish is associated with reduced Alzheimer's risk, but one study found that, although it  was associated with less Alzheimer's pathology, this was only in those with the 'Alzheimer's gene' (APOE4).

The same study found that fish oil supplementation was not associated with any differences in neuropathology — but higher levels of alpha-linolenic acid (an omega-3 fatty acid found in flaxseed, chia seeds, walnuts, etc) were associated with a reduced chance of brain infarctions. Another large study found that omega-3 supplements (fish-based, not plant), together with vitamins C, E, beta carotene, and zinc, had no effect on cognitive decline among older adults with age-related macular degeneration. But it was suggested that this may be because the participants were too old to benefit from them.

Among other groups, the question of whether supplements of omega-3 fatty acids can help memory and cognition has been even more contentious, with some studies showing a positive effect and others failing to find an effect.

My own take on this issue is that, like so many other things, it all depends on what you’re working with. The most important of these factors is surely diet — it would be unsurprising if supplements are only of benefit when the individual's diet is seriously deficient. It may also well be the case that genes are a factor. (I'm ignoring, but we shouldn't forget, that many of the studies are probably poorly done, for this is a problematic area and it is tricky to do well.) There does seem to be more evidence that a diet high in omega-3 oils is good, than that supplements are going to help. And the weight of the evidence certainly favors the importance of high omega-3 levels for older adults.

Although it's not yet clear which fatty acids are most important, one is definitely docosahexaenoic acid, or DHA. Salmon, mackerel, herring, sardines, and anchovies are all good sources (not, I am sorry to say, your standard fried fish from the chippie). Other sources include almonds, walnuts, soy, flaxseed oil, and eggs laid by chickens that eat DHA-supplemented feed.

 

 

References: 

tags lifestyle: 

Benefits of herbs & spices for cognition

  • Two spices have been implicated in fighting Alzheimer's (and thus age-related cognitive decline): turmeric and cinnamon.
  • Two herbs have been implicated in fighting Alzheimer's as well as being linked to better cognitive performance: sage and lemon balm.
  • Another two herbs have also been linked to better cognitive performance: rosemary and peppermint.
  • For those who suffer from sleep or stress problems (both of which contribute to cognitive problems), there is some evidence that, in keeping with traditional beliefs, chamomile and lavender both have calming effects.

There hasn't been a lot of research into the effects of herbs and spices on cognition and the brain, unfortunately. But on the positive side, the risk of side-effects is very low, so we don't need a lot of evidence for it to be worth trying.

Spices

Probably the most researched of these substances is the curry spice turmeric, more specifically one of its components, called curcumin. This has been found to be a powerful antioxidant and anti-inflammatory, which affects the brain protein BDNF (involved in the creation of new neurons). Research also suggests it may be protective against amyloid plaques, and so help fight Alzheimer's.

These findings have had an effect on my own cooking — I habitually cook up a lot of vegetables in the wok for our evening meal, and I add turmeric to the mix (heating it, along with some other curry spices, in the oil before adding the veges), so I have turmeric most days. Cumin, by the way, is (notwithstanding the similarity in names) something completely different.

Another spice that may be helpful, and one that is even easier to add to your daily diet, is cinnamon. I’ve been happily generous with cinnamon on my breakfast ever since the first hints came out that cinnamon might help protect against Alzheimer’s (it’s not like it’s an ordeal to add cinnamon!). Now we have more evidence, with a finding that two compounds found in cinnamon —cinnamaldehyde and epicatechin — appear to help prevent tau tangles (one of the characteristics of Alzheimer’s).

Herbs

As for herbs, there's a researcher in Britain who takes an interest in herbs, and it's really solely down to him and his students that we have any idea about the effects of herbs on cognition. Because they're all from one lab, and because the studies are invariably quite small, and the issue difficult to study, we can't put too much weight on these findings. But, as I say, where's the harm?

Four herbs have been put forward as helpful for the brain. Sage and lemon balm seem to increase the activity of acetylcholine, and so may be helpful to protect against Alzheimer's. They have also been linked to better cognitive performance. The scent of rosemary (i.e. from essential oil) has also been linked to better cognition, as has drinking peppermint tea.

From a more indirect perspective, chamomile tea and the scent of lavender have both been linked to feelings of calmness, which might help those who suffer from sleep problems. Lemon balm has also been linked to greater feelings of calmness.

References: 

tags lifestyle: 

Benefits of vitamins & minerals for cognition

  • Iron is important at all ages, and it seems clear now that iron deficiency can affect cognition long before anemia is diagnosed. However, too much iron may also increase Alzheimer's risk, so you need to steer a middle road.
  • Magnesium and zinc also seem to be important minerals for cognition, and zinc deficiency has been linked to Alzheimer's.
  • B vitamins, especially B12 and folate, are important to fight age-related cognitive impairment and Alzheimer's.
  • Vitamins C, D, and E, are probably also important in this fight.
  • Interactions need to be taken into consideration. Zinc may impact iron absorption; vitamin C may not be well absorbed if iron is not bound; the vitamins are more effective if omega-3 levels are high.

Let me start by saying that if you're healthy and are eating a good balanced diet, there should be no need for you to take supplements. I also want to emphasize that the best way of meeting your body's needs for certain vitamins and minerals is to get them from food. In some cases, for one reason or another, this may not be possible. For example, as a (mostly) vegan, I take iron and B12 supplements, to make up for these deficiencies in my diet. Elderly adults with small appetites may also find it hard to get all the nutrients they need from their diet.

What nutrients are important for brain health and cognition?

Minerals

Number one mineral for cognition, that goes right across the age groups, is iron. A number of studies have found that iron deficiency in children and adolescents is associated with lower scores of cognitive tests, and indeed, it may be that iron deficiency during infancy has long lasting effects on cognition. The effects on adults have been less studied, but there is some evidence that iron deficiency may be linked to poorer attention. What's worth noting is that the levels at which iron is "deficient" may be overstated. It now seems that negative effects occur long before a person is officially diagnosed with anemia.

Other minerals that may impact learning and memory are magnesium and zinc, although evidence is limited thus far. Magnesium deficits are common in industrialized countries, and increase with age. Vegetarians, adolescents, and older adults, are particularly at risk of zinc deficiency. An analysis of Alzheimer's has revealed that one type of the disease, which is found most commonly at a younger age (50- to early 70s) and typically shows itself first in language and number difficulties, is associated with a significant zinc deficiency.

Good sources of magnesium are dark green leafy vegetables, some nuts (especially almonds and cashews), beans, seeds and whole unrefined grains (especially buckwheat). Red meats, fish and grains are good sources of zinc.

Do bear in mind that it is not a case of "if some is good, more is better"! Having too much is not a good idea either; this is another reason why getting your vitamins and minerals from food rather than supplements is a good idea. Too much iron, in particular, has been linked to an increased risk of Alzheimer's. It has been argued that many neurodegenerative diseases are partly caused by poorly bound iron, and it is vital to consume nutrients which bind iron, such as brightly-colored fruits (especially purple) and vegetables — but not, perhaps, green tea, which does bind iron, but taking them at the same time seems to cancel out each other's benefits!

Just to complicate the matter further, there is evidence that zinc inhibits iron absorption. These complications suggest there is something in the idea that you need to consider food combinations.

Vitamins

Vitamins B, C, D, and E all seem to be important for cognition, mainly in relation to prenatal development and prevention of Alzheimer's and age-related cognitive impairment. A long-running study of older adults found that those with diets high in omega 3 fatty acids and in vitamins C, D, E and the B vitamins had higher scores on cognitive tests than people with diets low in those nutrients, and moreover that these were dose-dependent, with each standard deviation increase in the vitamin BCDE score ssociated with an increase in cognitive score. Additionally, they showed less brain shrinkage than those with lower intakes of these nutrients.

The B vitamins are often called the B-complex vitamins, and they are a messy sort of group. The main ones of interest for cognition are B12, folate, and choline. Again, most of the research has focused on prenatal development, and age-related cognitive impairment and dementia.

The importance of folate and B12 has a lot to do with homocysteine, which is produced in the body by the breakdown of a dietary protein called methionine. High levels of homocysteine have been linked to increased risk of Alzheimer's, stroke, and vascular dementia, and greater brain shrinkage. B-vitamins are required to convert homocysteine back to methionine, and high levels of homocysteine go hand in hand with low levels of B12 and folate. Diet isn't the only reason for increased levels of homocysteine; smoking has also been implicated. But the association between homocysteine and age-related cognitive decline is not straightforward — it appears that seniors with normal levels of vitamin B12 perform better if their folate levels are high, but when vitamin B12 is low, high levels of folate were associated with poor cognitive performance, as well as a greater probability of anemia. Vitamin B12 is often deficient in older people.

There is also some evidence that B12 is more effective in slowing cognitive decline if levels of omega-3 oils are high.

Folate is a water-soluble B vitamin found particularly in citrus fruit, green leafy vegetables, whole-wheat bread, water-soluble dried beans and peas; however, they are often destroyed by cooking or processing. In the United States, Canada and Australia, flour is fortified with folic acid. Vitamin B12 is naturally found in animal foods including fish, milk and milk products, eggs, meat, and poultry.

Among older adults, choline, particularly in conjunction with omega-3 fatty acids and uridine (not available from food), has been found to improve memory in those cognitively impaired. Top sources of choline are eggs, peanuts, and meat. Fish and soy are also good sources.

References: 

tags lifestyle: 

Total Cognitive Burden

Because it holds some personal resonance for me, my recent round-up of genetic news called to mind food allergies. Now food allergies can be tricky beasts to diagnose, and the reason is, they’re interactive. Maybe you can eat a food one day and everything’s fine; another day, you break out in hives. This is not simply a matter of the amount you have eaten, the situation is more complex than that.

tags problems: 

tags lifestyle: 

Eating right for your brain

Although I’m a cognitive psychologist and consequently think that memory and cognition is mostly about your mastery of effective strategies, when it comes to age-related cognitive decline, I’m a big believer in the importance of diet and exercise. But while we know these things can play an important role in why some people develop cognitive impairment and even dementia as they age, and others don’t, we don’t yet know with any great certainty exactly what exercise programs would be the best use of our time, and what diet would have the most benefit.

tags problems: 

tags lifestyle: 

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.

tags lifestyle: 

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: 

  1. Scarmeas, N. et al. 2009. Mediterranean Diet and Mild Cognitive Impairment. Archives of Neurology, 66(2), 216-225.
  2. Scarmeas, N. et al. 2009. Physical Activity, Diet, and Risk of Alzheimer Disease. Journal of the American Medical Association, 302(6), 627-637.
  3. Barberger-Gateau, P. et al. 2007. Dietary patterns and risk of dementia: The Three-City cohort study. Neurology, 69, 1921-1930.
  4. Dai, Q. et al. 2006. Fruit and Vegetable Juices and Alzheimer's Disease: The Kame Project. The American Journal of Medicine, 119 (9), 751-759
  5. Gray, S.L. et al. 2008. Antioxidant Vitamin Supplement Use and Risk of Dementia or Alzheimer's Disease in Older Adults. Journal of the American Geriatrics Society, 56 (2), 291–295.
  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.
  7. Engelhart, M.J., Geerlings, M.I., Ruitenberg, A., van Swieten, J.C., Hofman, A., Witteman, J.C.M. & Breteler, M.M.B. 2002. Dietary Intake of Antioxidants and Risk of Alzheimer Disease. JAMA, 287, 3223-3229.
  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.
  10. Ghosh, D., McGhie, T.K., Zhang, J., Adaim, A. & Skinner, M. 2006. Effects of anthocyanins and other phenolics of boysenberry and blackcurrant as inhibitors of oxidative stress and damage to cellular DNA in SH-SY5Y and HL-60 cells. Journal of the Science of Food and Agriculture, in press.
  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.
  13. McIlroy, S.P., Dynan, K.B., Lawson, J.T., Patterson, C.C. & Passmore, A.P. 2002. Moderately Elevated Plasma Homocysteine, Methylenetetrahydrofolate Reductase Genotype, and Risk for Stroke, Vascular Dementia, and Alzheimer Disease in Northern Ireland. Stroke, 33, 2351–2356.
  14. Seshadri, S., Beiser, A., Selhub, J., Jacques, P.F., Rosenberg, I.H., D'Agostino, R.B., Wilson, P.W.F. & Wolf, P.A. 2002. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. The New England Journal of Medicine, 346, 476-483.
  15. Kruman, I.I., Kumaravel, T.S., Lohani, A., Pedersen, W.A., Cutler, R.G., Kruman, Y., Haughey, N., Lee, J., Evans, M. & Mattson, M.P. 2002. Folic Acid Deficiency and Homocysteine Impair DNA Repair in Hippocampal Neurons and Sensitize Them to Amyloid Toxicity in Experimental Models of Alzheimer's Disease. Journal of Neuroscience, 22, 1752-1762.
  16. Schaefer, E.J. et al. 2006. Plasma Phosphatidylcholine Docosahexaenoic Acid Content and Risk of Dementia and Alzheimer Disease. Archives of Neurology, 63, 1545-1550.
  17. Freund-Levi;, Y. et al. 2006. w-3 Fatty Acid Treatment in 174 Patients With Mild to Moderate Alzheimer Disease: OmegAD Study: A Randomized Double-blind Trial. Archives of Neurology, 63, 1402-1408.
  18. Quinn, J.F. et al. 2009. A clinical trial of docosahexaenoic acid (DHA) for the treatment of Alzheimer's disease. Presented at the Alzheimer's Association International Conference on Alzheimer's Disease July 11-16 in Vienna.
    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.
  19. Lim, G.P., Calon, F., Morihara, T., Yang, F., Teter, B., Ubeda, O., Salem, N.Jr, Frautschy, S.A. & Cole, G.M. 2005. A Diet Enriched with the Omega-3 Fatty Acid Docosahexaenoic Acid Reduces Amyloid Burden in an Aged Alzheimer Mouse Model. Journal of Neuroscience, 25(12), 3032-3040.
  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.
  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/content/322/7300/1447.full
  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://publications.ki.se/xmlui/handle/10616/38590
  46. Erickson, K.I. et al.  2009. Aerobic fitness is associated with hippocampal volume in elderly humans. Hippocampus, Published online 2 January.
  47. Burns, J.M. et al. 2008. Cardiorespiratory fitness and brain atrophy in early Alzheimer disease. Neurology, 71, 210-216.
  48. 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.
  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.

tags lifestyle: 

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] 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 function 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. Harada, T., Okagawa, S., & Kubota, K. (2004). Jogging improved performance of a behavioral branching task: implications for prefrontal activation. Neuroscience Research, 49(3), 325–337.
  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/article/dn6735-some-people-are-immune-to-exe...

tags lifestyle: 

Subscribe to diet