Growing Brain Cells While You Sleep

Every day, new brain cells (neurons) are born in the brains of adult mammals, a process called neurogenesis (neuro = neurons, genesis = birth).  These newborn cells appear particularly in the hippocampus – a brain area that is important for new memory formation.   Over the next few weeks, many of these newborn cells die off again.  But studies show that, if a rat has been exercising or has been exposed to new learning, more of the newborn cells survive.  The rate of survival of these new cells also depends on sleep.

As we sleep, we (like rats) cycle through several “stages,” including rapid-eye movement (REM) sleep, which is believed to be when we dream, and several kinds of non-REM sleep.

A recent study has suggested that REM is particularly important for neurogenesis in the hippocampus.  One group of rats were given four days of REM deprivation, by putting the rats in a small chamber where the floor was a treadmill that automatically activated whenever the rats entered REM sleep – forcing them to step forward to avoid being carried into the wall of the chamber.  (Non-REM sleep didn’t activate the treadmill.) For comparison, a group of control rats were placed in the same type of chamber, but treadmill activation was unrelated to sleep cycle.

The REM-deprived rats showed much less neurogenesis than controls. Both groups showed similar amounts of total sleep, and similar levels of stress hormones, indicating that the stress of being periodically awoken was similar for the REM-deprived and control rats. This study therefore suggests that REM sleep is particularly important for the birth and survival of new neurons in the adult brain.

There are two important implications of this study.  The first is that it adds to a growing literature suggesting that relatively short-term periods of sleep deprivation (equivalent to a few nights’ insomnia or intentional wakefulness) can significantly affect the brain.  This is a cautionary finding for those of us who routinely don’t get a full night’s sleep.

The second implication is that not all sleep is equal.  This study also adds to a growing literature suggesting that REM sleep has some special functions, particularly contributing to learning and memory.  Many medications, including some over-the-counter sleeping aids, disrupt REM sleep.  If REM sleep is indeed important for neurogenesis, then disrupting REM may disrupt neurogenesis – which might in turn have consequences for a person’s learning and memory abilities.

 

Further Reading:

R. Guzman-Marin et al. (2008). Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat. Sleep, 31(2):167-175.

Society for Neuroscience Meeting: Brain Research Past, Future, and Present

This past week, I traveled to Chicago to attend the annual meeting of the Society for Neuroscience, the association for researchers studying all aspects of the brain, from biochemical processes, genetics, and anatomy, to animal behavior, to human disorders such as schizophrenia, Alzheimer’s and epilepsy – and everything in between.  There were over 30,000 attendees, all in Chicago at the same time – more than the population of some small cities.  The SfN meeting is a chance for colleagues from around the world to gather, report on their latest findings, and exchange ideas.

Two of the keynote lectures stick in my mind.  The first was a talk by Richard Morris, the eminent British researcher who studies how brains form new memories.  Since 2009 marks SfN’s 40^th anniversary, Morris gave a brief overview of SfN’s history, reminding us all how far the science of neuroscience has come in that time.  Some of the researchers attending the 2009 meeting had not yet been born in 1969, and many of the seminal papers which we now take for granted had not yet been published. A salient example is Bliss & Lømo’s (1973) article documenting long-term changes in neurons as a result of experience: a phenomenon termed long-term potentiation (LTP) which is now generally believed to be one of the fundamental ways in which the brain encodes new learning.  Modern research methods such as functional neuroimaging (fMRI and PET) and genetic mapping, not to mention information-sharing via the Internet, were not yet available in 1969. In the past 40 years, we’ve developed new tools to diagnose diseases and new methods to treat them, as well as a broader understanding of how the brain works and why it sometimes doesn’t. Looking back now on how much we’ve learned in the last 40 years, one can’t help but wonder what we might learn in the next 40 years – and whether some of today’s most terrifying and incurable disorders, such as schizophrenia, Alzheimer’s, and epilepsy, could join polio and smallpox as relics of the past.

Against this vision of past and future, SfN attendees face a present reality in which competition for research funding is perhaps as fierce as it has ever been.  At the National Institutes of Health (NIH), the federal institution that is the major funder of biomedical research in the US, only about 20% of submitted research proposals actually receive funding.  The situation would have been much worse during the economic downturn, but for a large injection of stimulus funds provided by the Recovery Act (ARRA), which allowed many labs to continue their research (and to maintain and hire laboratory staff).  There is concern about what will happen when that infusion of money runs out. Francis Collins, NIH’s director, addressed SfN attendees and stressed that researchers themselves have a responsibility not only to conduct research, but also to communicate to the broader public why that research matters, and why in times of budgetary crisis, scientific research is an investment in the future of our species and our planet that our society must continue to support.  With luck, this year’s SfN meeting attendees came away charged with that vision as much as with inspiration for new and exciting research directions.

Red wine and the brain: Cheers!

A growing body of studies on the interactions between diet, behavior and health suggest that individuals who consume moderate amounts of alcohol (particularly wine) are statistically less likely to die from cardiovascular disease.  One possibility is that chemical compounds in wine (particularly red wine) may protect against heart disease.  An alternate theory is socioeconomic: in the US, wine is often considered a “high-class” form of alcohol – compared with, say, beer or whisky – and wine drinkers as a group tend to be more highly educated, to exercise more often, and to be more healthy overall.  In this case, wine drinking might not directly protect against heart health, but wine drinkers as a group might show reduced risk of heart disease because of these other factors.

In the last few years, there have been intriguing suggestions that low-to-moderate alcohol consumption may also protect against age-related cognitive decline, and even against Alzheimer’s disease.  One study considered mice that had been specially bred to develop beta amyloid plaques in their brains; beta amyloid plaques are a hallmark of Alzheimer’s disease in humans.  Some of the mice were given moderate amounts of cabernet sauvignon in their water supply for a period of about 7 months; others were given plain water. The group given wine showed less accumulation of plaques in their brain, and also showed much less decline in memory function than their counterparts.  The implication is that some (or some combination) of the chemical compounds in wine – specifically red wine – helps the brain combat plaque accumulation. 

And what about in humans?  A study published late last year in the Journal of the American Geriatric Society followed nearly 6,000 community-dwelling elderly adults for three years.  Each individual’s baseline alcohol consumption was recorded at the start of the study: about 42% of the women and 71% of the men were alcohol drinkers.  As would be expected, most of the volunteers showed some mild cognitive decline over the course of the study.  But female drinkers showed less decline than female nondrinkers on the Mini-Mental Status Exam or MMSE, a standard test of general cognitive function.  No such differences were observed between male drinkers and non-drinkers.  The authors’ conclusion: low-to-moderate alcohol consumption may help slow cognitive decline in elderly women.  This echoes an earlier study from 2005 which found a similar effect: that elderly women who drink about one serving of alcohol a day may have a slightly reduced risk of cognitive decline.  It’s not clear why women appear to benefit more than men, although one possibility is that, since women are at greater statistical risk of Alzheimer’s then men, more of the women are in a position to benefit from the plaque-busting properties of red wine.

There’s an obvious and serious caveat: the current findings do not represent an invitation to heavy drinking.  Long-term intake of large amounts of alcohol damages the brain, and is associated with a host of other health complications.  Current US guidelines suggest that women drink no more than two to three units a day (one unit is approximately one small glass of wine), while men (who typically have larger body weights) should drink no more than three or four units per day.  (These are general guidelines, and don’t apply to everyone; some individuals should drink much less or not at all.)

Nevertheless, for those who enjoy an occasional glass of wine, there now seems to be a reasonable cause to rejoice: modest amounts of red wine may not only pleasure the palate, but may also help protect the aging brain.

 

Further Reading:

J. Wang and others (2006). “Moderate consumption of cabernet sauvignon attenuates Abeta neuropathology in a mouse model of Alzheimer’s disease.” In, “FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology,” vol. 20, no. 13, pp. 2313-2320.

D. J. Stott and others (2008). “Does low to moderate alcohol intake protect against cognitive decline in older people?”In, Journal of the American Geriatric Society, vol. 56, no. 12, pp. 2217-2224.

M. J. Stampfer and others (2005). “Effects of moderate alcohol consumption on cognitive function in women.” In, New England Journal of Medicine, vol. 352, no. 3, pp. 245-253.

Eat less, remember more?

Researchers studying the effects of diet in animals have long known that caloric restriction (abbreviated CR) can improve longevity.  That is, lab rats fed a special, low-calorie diet tend to live longer than their comrades given a “normal” diet.  The same is true in other species, including dogs, fish, and yeast.  We don’t know yet if CR would also improve longevity in humans.

Caloric restriction also improves learning and memory in animal.  For example, a standard test of learning in rats is to place the rat in a shallow pool. Somewhere in the pool is a little platform, hidden just below the surface of the water. Rats are actually quite competent swimmers, and will swim around until they stumble across the platform; then they’ll climb out of the water.  With repeated trials, healthy rats learn the location of the platform quickly, and as soon as they’re placed in the pool, they rapidly swim to the platform and climb up.  It’s a skill that declines with age, so that older rats have a harder time learning to locate the hidden platform than younger rats do. Rats given lifelong CR – provided with only 60% as much food as a healthy rat would normally choose to eat – show less decline with age than animals given free access to food. 

A recent study suggests that caloric restriction might improve learning and memory in humans, too.  Two groups of healthy elderly individuals were assigned to follow either a “standard” diet or a calorie-restricted diet for 3 month.  At the end of that period, unsurprisingly, the CR group had lost weight.  More surprisingly, the CR group showed a significant improvement – almost 30% — in their memory scores.  The group on a regular diet showed no change from their baseline scores.

So, should we all start cutting back drastically on our caloric intake?  Here, the question gets complicated.  Obviously, there are many health benefits to maintaining a healthy diet, managing our cholesterol levels and keeping blood pressure in check.  But severe caloric restriction, with caloric reductions as dramatic as in the studies above, can have risks. The obvious risk is malnutrition. When reducing caloric intake, there may also be reduced intake of nutrients and vitamins that the body needs to function; as a result, calorie-restricted diets should only be attempted under medical supervision and with proper care to ensure that the body is still getting adequate supplies of nutrients and vitamins. 

Anecdotally, I’ve talked to two people who study caloric restriction in animals, and after seeing the dramatic positive effects, they had decided to attempt extending their own longevity in the same way. (They both had the medical background needed to attempt CR responsibly, without risking their health.) They reported feeling continually hungry, irritable, overtired, and cold.  In the end, they decided, a longer life wasn’t worth it if one was going to be miserable the whole time.

Instead, these and other researchers are focusing on the mechanisms involved – trying to understand exactly why CR produces the cognitive benefits it does.  Maybe, if we understood that, there would be a way to produce the same effects – in a more painless way than near-starvation.

Further reading:

J. Stewart and others (1989). The effects of life-long food restriction on spatial memory in young and aged Fischer 344 rats measured in the 8-arm radial and the Morris water mazes. In, Neurobiology of Aging, vol. 10, pp. 669-675.

A. V. Witte and others (2009). “Caloric restriction improves memory in elderly humans.” In, Proceedings of the National Academy of Sciences (USA), vol. 106, no. 4, pp. 1255-1260.

Diabetes and the Brain

It’s been well-established that type II diabetes (also called adult-onset diabetes) is linked with cognitive decline.  In type II diabetes, there is a reduction in the production or effectiveness of insulin, a hormone that the body uses to break down glucose so that our cells can take it in and use it for energy.  Less insulin (or insensitivity to insulin) means the cells can’t absorb glucose properly.  Over time, this can cause a host of medical complications – and can also damage the brain.  Several studies have now shown that individuals with type II diabetes – particularly elderly patients – perform worse than would be expected for their age group on a number of cognitive tests, and may have an increased risk of dementia.

The reason for the relationship between diabetes and cognitive impairment has been less clear, but a popular hypothesis has been that type II diabetes is associated with a heightened risk of cardiovascular disease, which in turn reduces the amount of blood flow to the brain, limiting the supply of oxygen and nutrients to brain cells.  Over time, this reduced supply could cause brain cells to malfunction and even die.

But a recent study has suggested a second way in which diabetes could damage the brain, and specifically the hippocampus, a part of the brain that is critical for our ability to lay down new memories.  William Wu and colleagues used magnetic resonance imaging (MRI) to examine of the brains of elderly individuals with type II diabetes.  Compared to individuals of the same age but without diabetes, the patients showed abnormalities in the dentate gyrus, a small region within the hippocampus.  Across individuals, the higher the blood glucose levels, the more abnormality in the dentate gyrus. 

Combined with other emerging data, this is relatively convincing proof that chronic high levels of blood glucose can directly damage the brain, and particularly the dentate gyrus. And – because this part of the brain is so critical for memory –  this could be one key reason why individuals with type II diabetes so often show memory impairments.

Why should the dentate gyrus be so sensitive?  That’s not clear. But it’s intriguing to note that the dentate gyrus is one of the few places in the adult brain that continues to generate newborn brain cells throughout life.  One might speculate that these newborn cells are particularly delicate – and particularly easy to destroy when glucose levels get out of balance.

If there’s any good news here, it’s that type II diabetes can often be controlled by a combination of diet, medication, and exercise.  For anyone who needed it, the recent results provide one more reason to try and do just that.

Further reading:

William Wu and others (2009). “The brain in the age of old: The hippocampal formation is targeted differentially by diseases of late life.”  In, Annals of Neurology, vol. 64, issue 6, pp. 698-706.

G. J. Biessels and others (2006). “Risk of dementia in diabetes mellitus: A systematic review.” In, The Lancet Neurology, vol. 5, no. 1, pp. 64-74.

T. Cukierman and others (2005). “Cognitive decline and dementia in diabetes – Systematic overview of prospective observational studies.”  In, Diabetologia, vol. 48, no. 12, pp. 2460-2469.

Ginkgo and Memory: Not So Fast

Dietary supplements – products like vitamins and herbal supplements – form a multibillion-dollar industry in the US.  Under current US law, dietary supplements are regulated as foods, rather than as drugs, which means that they’re exempt from some of the strict Federal regulations that apply to drugs.  In particular, makers of dietary supplements are not required to obtain FDA approval, proving that their products are either safe or effective, before they’re allowed to start putting those products on the shelves of supermarkets and drug stores. This makes it very hard for a consumer to know what’s effective – and what’s safe.

One of the top-selling dietary supplements in the US is ginkgo, a compound extracted from the leaves of the ginkgo biloba tree.  Gingko extracts have long been marketed for their supposed memory-boosting powers.  However, the hard science to back up this claim has been lacking.

One study, published in the prestigious Journal of the American Medical Association (JAMA) in 2002, examined cognitive function in healthy elderly individuals given ginkgo supplements, compared to peers who were given a placebo (an inactive sugar pill).  The study found no significant benefits of ginkgo on memory.  Another placebo-controlled study, published around the same time in a different journal, came to a different conclusion – that gingko could indeed enhance some kinds of memory and attention – but this study was funded by a company that markets a ginkgo supplement, which raised some red flags in the scientific community about whether the results were truly objective.  Most scientists now believe that there is little evidence that ginkgo improves memory in healthy adults.

Another possibility is that, even if ginkgo has little effect in boosting the memory power of healthy adults, it might be useful in helping to prevent dementia, including Alzheimer’s disease.  That claim now appears to have been overturned too.  In a study published in JAMA last year, over 3000 non-demented elderly individuals were given daily supplements of either ginkgo or a placebo.  This was a large, carefully-designed and well-controlled study, meant to provide definitive evidence about ginkgo’s effects. The study lasted for six years, and during this time about 20% of the participants developed dementia.  This included 246 of the participants who’d been taking the placebo, and 277 of those who’d been taking the ginkgo.  Statistically, this means that the people taking ginkgo were just as likely to develop dementia (including Alzheimer’s) as people taking the placebo.

This is the biggest, longest study of gingko so far, and it’s hard to argue with the results, although some have tried – for example, suggesting that ginkgo may have an effect that only emerges after people have been taking the supplements for more than six years, or that the particular dosage (or brand of ginkgo supplement) used in the study may not have been optimal.  Still, the burden of proof now seems to be on those who promote the supplement to provide compelling evidence that it has some measurable benefit.

It’s also worth noting that ginkgo, like all drugs, has some side effects.  In particular, ginkgo appears to improve blood flow and to reduce clotting; as such, it may have some uses related to cardiovascular health or other medical conditions – but this also means that it may increase the risk of stroke in people who are taking anticoagulant medication (including some heart medications and aspirin or ibuprofen).  There’s also been some concern that certain kinds of antidepressants may interact dangerously with ginkgo.  For many people, the possible risks of ginkgo may outweigh any, as-yet-unproven, benefits to the brain.

 

Further reading:

 

P. R. Solomon and others (2002). “Ginkgo for memory enhancement: A randomized controlled trial.” JAMA, vol. 288, no. 7, pp. 835-840.

J. A. Mix & W. D. Crews (2002). “A double-blind, placebo-controlled, randomized trial of Ginkgo biloba extract EGb 761® in a sample of cognitively intact older adults: Neuropsychological findings.” Human Psychopharmacology: Clinical and Experimental, vol. 17, no. 6, pp. 267-277.

S. T. DeKosky and others (2008). “Ginkgo biloba for prevention of dementia: A randomized controlled trial.” JAMA, vol. 300, no. 19, pp. 2253-2262.

Teaching Old Dogs New Tricks

The old folk wisdom – that it’s hard to teach an old dog (or an old human) new tricks – has some grounding in science.  Namely, humans and other animals have “sensitive periods” in brain development, windows of opportunity for new learning that close after a certain age.

One example is language learning: children can learn new languages more easily than adults do.  Human languages have about 25-40 sounds – but not all languages use the same sounds. For example, the sounds /l/ and /r/ are meaningfully different in English (so that “lay” and “ray” are different words with different meanings) but these sounds are not meaningfully different in Japanese, so that native Japanese speakers often have difficulty hearing the difference between these two sounds.  But Japanese infants younger than 6-8 months old can distinguish them – an ability that is lost by the time the infants reach about 11 months old (unless those infants are exposed to English as well as to their native language).  Similarly, an “English-speaking” baby can distinguish between sounds such as the soft /p/ and sharp /p/ of the Thai language, or the Hindi /ta/ vs. /Ta/ — even though most adult English speakers can’t tell these sounds apart.  Apparently, there is a “sensitive period” early in life during which the brain learns the sounds of language.  This period lasts until about age 10-11 months — and then the window closes.

The phenomenon of sensitive periods is widespread.  Other species have sensitive periods for learning their own “languages.”  For example, male sparrows raised in the wild learn their characteristic birdsongs from listening to other males of the same species. If young birds are raised in isolation, but allowed to hear birdsong, they can still learn to sing normally – but only if exposure to birdsong occurs within the first 30-100 days of their life; after that, the window of opportunity is closed.  

And sensitive periods don’t only apply to hearing and producing sounds: vision has a sensitive period too. Human infants born with cataracts blocking their vision in one eye will see normally if corrective surgery is performed within a few months of birth, but if the surgery is delayed a few years, normal vision never develops.  Apparently, within the first few months of life, the brain learns how to see — how to interpret information coming from the eyes — and if that learning isn’t set up early in life, the window of opportunity closes.  

In all these examples, the message is the same: early learning is easy and natural; later learning may be harder if not impossible.

But newer research, while not overturning the idea of sensitive periods, is challenging the idea that they are immutable.  The truth may be more subtle.  Although adults may have more trouble than children in mastering the sounds of a new language, many can learn to speak a new language quite fluently. And the adults may learn faster – even if their final level of proficiency is not as high as someone who learned the language as a child.  Language is a complex phenomenon that may require many subskills – some of which may have sensitive periods that “close” later than others, and some of which may never close at all.  

Perhaps the best news of all is that, although language learning is harder after childhood, there is no good evidence that the ability to learn a new language drops off significantly after that.  In language learning as with anything else, it appears that you can teach a new dog new tricks… it just takes a little longer.

 

Further reading on sensitive periods:

M. Thomas and M. Johnson (2008). “New advances in understanding sensitive periods in brain development.” In, Current Directions in Psychological Science, vol. 17, pp. 1-5.

The Brain of the World’s Oldest Woman

For most of human history, it has been assumed that senility is a normal consequence of growing old.  (At least as far back as Shakespeare, old age was considered to entail losing one’s mind as well as one’s teeth and eyesight.)

But current research is suggesting the opposite: Some researchers go so far as to suggest that there is no reason why minds should decay simply because we age, and that any appreciable loss of cognitive function is therefore a symptom of some disease or disorder.  On this extreme view, the fact that elderly individuals, on average, score worse than younger adults on tests of memory and other cognitive functions merely reflects the fact that elderly individuals are statistically more likely than youngsters to develop a number of conditions (such as Alzheimer’s disease, vascular dementia, or diabetes) that damage the brain.

A recent study in the Netherlands examined the brain of a woman who died of cancer at age 115. (At the time, she was the world’s oldest woman.) Two years before she died, she’d completed extensive neuropsychological testing, and had performed extremely well. After her death, the researchers examined her brain and concluded that it was free of any obvious pathology, and (at least in the areas examined) contained as many neurons as would be expected in “healthy people of 60-80 years old.” There was little evidence of abnormalities, such as the plaques and tangles which accumulate in the brains of patients with Alzheimer’s disease, nor of the small brain infarcts that appear in the brains of many aged individuals.  In other words, although this woman lived well beyond her 60s, her brain didn’t appear to have accumulated damage through those extra decades.

Why was this woman so lucky, when others are less so?  That remains an open question, although genes probably play a role (this woman’s mother died at age 100, and her maternal grandparents and siblings all lived past 70).  Cardiovascular health may be relevant too: the scientists who examined the woman’s brain also examined her body and found a striking absence of atherosclerosis – the “hardening of the arteries” associated with high levels of LDL or “bad” cholesterol. 

Whatever the reason, the encouraging bottom line here is that – although many elderly individuals will develop cognitive impairments due to underlying brain pathology – decline is not inevitable.  As the case of the world’s oldest woman shows, it is clearly possible to live to a ripe old age with a healthy brain and the mental acuity to match.

 

Further reading:

Wilfred den Dunnen and others. (2008) “No disease in the brain of a 115-year-old woman.” In Neurobiology of Aging, vol 29, pp. 1127-1132.

Memory In the Lab… and In the World

The overwhelming majority of psychological research takes place in university psychology laboratories.  The reasons for this are largely the same as the reason that chemistry research and physics research take place in chemistry and physics labs: to do careful, reliable science, it’s best to work under controlled conditions, where experimenters can identify the one variable they wish to manipulate and carefully rule out other factors that could be affecting the data.

But memory studied in the lab may not be exactly the same as memory experienced in real life.  For example, typical laboratory tests of people’s verbal memory involve having a participant listen to a list of words, or a short story, and then asking the participant to repeat that list or story from memory, verbatim, after a predetermined delay.  This allows researchers to calculate a convenient, easy-to-understand memory score, based on the number of items correctly recalled.  But how often in real life are any of us required to recall random word lists from memory?  People who complain of memory problems are much more likely to cite examples such as forgetting where they left the car keys, difficulties remembering acquaintances’ names, or walking into a room and being unable to remember what errand they meant to complete there.  These memory lapses are not so easy to measure (or even observe) in a laboratory setting – and yet they are the kind of “real world” tasks against which we all evaluate our memory ability every day.

A group of researchers at Purdue University have been thinking carefully about the effects that real-world relevance might have on memory: specifically, about the idea that our memories evolved to help us survive – and that our memories might therefore be especially good at remembering not random word lists but ideas and concepts that might have helped our long-ago ancestors find food and evade predators.  As one example, in a recent study, the researchers used the familiar technique of showing participants a list of words and asking them to recall those words from memory later.  The twist was that, while studying the words, the researchers instructed some participants to imagine how relevant each word would be if you were stranded in the wilderness, and needed to find food, water, and shelter.  Other participants were instructed to imagine how relevant each word would be if you were planning to move to a new home in a foreign land, and needed to find and purchase a new home and transport your belongings.  Both scenarios are challenging, but only one involves the kind of basic survival challenges faced by our long-ago ancestors.  The results?  At test, particicpants given the survival scenario recalled significantly more words than participants given the moving-home scenario.

One interpretation of these results is that our memories are optimized for certain kinds of information – and these may not always be closely related to the kinds of information involved in standard laboratory tests of memory.  There are other interpretations too:  for example, it’s possible that (even in participants’ imagination) the survival scenario was more stressful than the moving-home scenario; heightened stress often helps us fix information more strongly in memory.  As another possible interpretation, modern-day humans may have more experience moving home than surviving in the wilderness, and so they had to think harder to imagine in the latter scenario; heightened concentration also often helps us fix information in memory.

Nevertheless, this type of research study reminds us that real-world influences strongly impact memory, and that a person’s performance in the highly artificial world of a psychology laboratory may tell us something about that person’s memory ability – but it certainly does not tell us everything about how that person’s memory functions in the real world.

 

For further reading on how imagining “survival situations” affects memory:

JA Nairne and others, 2008, “Adaptive memory: The comparative value of survival processing.” In, Psychological Science, vol. 19, pp. 176-180.

JS Nairne and others, 2007, “Adaptive memory: Survival processing enhances retention.” In, Journal of Experimental Psychology: Learning, Memory and Cognition, vol. 33, pp. 263-273. 

No Good News for Chocaholics

Evidence is accumulating that some compounds found in everyday foods can have beneficial effects on memory and brain health.  Some of the most interesting of these compounds are antioxidants, so called because they interfere with the chemical process of oxidation that, some scientists believe, may cause much of the cell damage that accompanies normal aging of our bodies and brains.

Antioxidants occur naturally in many fruits and vegetables and also in black and green tea.  For this reason, many brain researchers advocate ingesting these foods as protection for the aging brain. (See also prior post on this site, “Brain-Boosting Berries.”)

Another food that’s rich in antioxidants is chocolate – specifically dark chocolate and cocoa. (Milk chocolate is much less rich in antioxidants.) Dark chocolate and cocoa also contain substances called phytochemicals that may have further protective effects on brain cells. This has led to the delightful prospect that a daily dose of chocolate could actually be good for your brain, as well as your tastebuds.

Alas, this does not seem to be the case.  A new study tested the beneficial effects of chocolate on cognition in a hundred healthy older adults.  Half of the participants were assigned the onerous duty of eating one bar of dark chocolate and drinking one serving of cocoa daily for six weeks.  The other half received “placebo” products that were similar in appearance and in taste, but that did not contain the critical chemical compounds. 

At the end of the study, there were no significant differences between the groups on any of a wide range of measures cognitive ability.  In other words, the folks who’d been responsibly eating chocolate showed no benefits, compared to the group who’d abstained.

The results aren’t completely definitive.  A questionnaire, administered after the study, showed at more than half of the volunteers knew whether they had been consuming “real” chocolate or the placebo products.  This could contaminate the results, although one might ordinarily expect that the contamination would skew the results toward – not away from – showing benefits of chocolate. The study authors note that another contamination could have arisen if the participants in the placebo group were getting their antioxidants from other parts of their diet – for example, by eating berries. And the study only lasted six weeks; it is possible that the cumulative effects of antioxidant ingestion become apparent only over longer periods – months, perhaps, or even years.

But the failure to find any beneficial effect of dark chocolate and cocoa in elderly adults replicates an earlier study, in which cocoa consumption was found to increase blood flow in healthy young adults, but not to significantly improve their performance on a cognitive task.  In other words, to date, there is no evidence in favor of the idea that dark chocolate benefits the brain, in either youngsters or the elderly.

 

 

Further reading on chocolate and cognition:

 

W. Crews and others (2008). “A double-blind, placebo-controlled, randomized trial of the effects of dark chocolate and cocoa on variables associated with neuropsychological functioning and cardiovascular health: Clinical findings from a sample of healthy, cognitively intact older adults.” In, American Journal of Clinical Nutrition, vol. 87, pp. 872-880.

 

S. Francis and others (2006). “The effect of flavanol-rich cocoa on the fMRI response to a cognitive task in healthy young people. In, Journal of Cardiovascular Pharmacology, vol. 47(supplement), pp. S215-S220.