Diet

You can help your brain, especially as it ages, by eating and drinking right

Exercise reduces Alzheimer's damage in brain

August, 2012

A mouse study provides more support for the value of exercise in preventing Alzheimer’s disease, and shows one of the ways in which it does so.

A study designed to compare the relative benefits of exercise and diet control on Alzheimer’s pathology and cognitive performance has revealed that while both are beneficial, exercise is of greater benefit in reducing Alzheimer’s pathology and cognitive impairment.

The study involved mice genetically engineered with a mutation in the APP gene (a familial risk factor for Alzheimer’s), who were given either a standard diet or a high-fat diet (60% fat, 20% carbohydrate, 20% protein vs 10% fat, 70% carbohydrate, 20% protein) for 20 weeks (from 2-3 to 7-8 months of age). Some of the mice on the high-fat diet spent the second half of that 20 weeks in an environmentally enriched cage (more than twice as large as the standard cage, and supplied with a running wheel and other objects). Others on the high-fat diet were put back on a standard diet in the second 10 weeks. Yet another group were put on a standard diet and given an enriched cage in the second 10 weeks.

Unsurprisingly, those on the high-fat diet gained significantly more weight than those on the standard diet, and exercise reduced that gain — but not as much as diet control (i.e., returning to a standard diet) did. Interestingly, this was not the result of changes in food intake, which either stayed the same or slightly increased.

More importantly, exercise and diet control were roughly equal in reversing glucose intolerance, but exercise was more effective than diet control in ameliorating cognitive impairment. Similarly, while amyloid-beta pathology was significantly reduced in both exercise and diet-control conditions, exercise produced the greater reduction in amyloid-beta deposits and level of amyloid-beta oligomers.

It seems that diet control improves metabolic disorders induced by a high-fat diet — conditions such as obesity, hyperinsulinemia and hypercholesterolemia — which affects the production of amyloid-beta. However exercise is more effective in tackling brain pathology directly implicated in dementia and cognitive decline, because it strengthens the activity of an enzyme that decreases the level of amyloid-beta.

Interestingly, and somewhat surprisingly, the combination of exercise and diet control did not have a significantly better effect than exercise alone.

The finding adds to the growing pile of evidence for the value of exercise in maintaining a healthy brain in later life, and helps explain why. Of course, as I’ve discussed on several occasions, we already know other mechanisms by which exercise improves cognition, such as boosting neurogenesis.

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High-fructose diet directly impairs brain function

June, 2012

A rat study shows how high-fructose corn syrup hurts memory, and that omega-3 oils can counteract the effect.

A rat study has shown how a diet high in fructose (from corn syrup, not the natural levels that occur in fruit) impairs brain connections and hurts memory and learning — and how omega-3 fatty acids can reduce the damage.

We know that these unnaturally high levels of fructose can hurt the brain indirectly through their role in diabetes and obesity, but this new study demonstrates that it also damages the brain directly.

In the study, two groups of rats consumed a fructose solution as drinking water for six weeks. One of these groups also received omega-3 fatty acids in the form of flaxseed oil and DHA. Both groups trained on a maze twice daily for five days before starting the experimental diet. After the six weeks of the diet, the rats were put in the maze again.

Those who didn’t receive the omega-3 oils navigated the maze much more slowly than the second group, and their brains showed a decline in synaptic activity. They also showed signs of resistance to insulin. Indications were that insulin had lost much of its power to regulate synaptic function.

It’s suggested that too much fructose could block insulin's ability to regulate how cells use and store sugar for the energy required for processing information.

It’s estimated that the average American consumes more than 40 pounds of high-fructose corn syrup per year.

The findings are consistent with research showing an association between metabolic syndrome and poorer cognitive function, and help explain the mechanism. They also support the consumption of omega-3 fatty acids as a preventative or ameliorative strategy.

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Type of fat, not amount of fat, linked to cognitive decline in old age

June, 2012

A large four-year study of older women has found high amounts of saturated fat were associated with greater cognitive decline, while higher amounts of monounsaturated fat were associated with better performance.

Data from the Women's Health Study, involving 6,183 older women (65+), has found that it isn’t the amount of fat but the type of fat that is associated with cognitive decline. The women were given three cognitive function tests at two-yearly intervals, and filled out very detailed food frequency surveys at the beginning of the study.

Women who consumed the highest amounts of saturated fat (such as that from animals) had significantly poorer cognitive function compared to those who consumed the lowest amounts. Women who instead had a high intake of monounsaturated fats (such as olive oil) had better cognitive scores over time. Total fat, polyunsaturated fat, and trans fat, were not associated with cognitive performance.

The findings are consistent with research associating the Mediterranean diet (high in olive oil) with lower Alzheimer’s risk, and studies linking diets high in saturated fats with greater cognitive decline.

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Why eating less may keep the brain young

February, 2012

Two animal studies add to our understanding of why calorie restriction might help prevent cognitive impairment and dementia and how to accrue cognitive benefits from it. A human study adds to the evidence for the benefits of eating less.

I have reported often on studies pointing to obesity as increasing your risk of developing dementia, and on the smaller evidence that calorie restriction may help fight age-related cognitive decline and dementia (and help you live longer). A new mouse study helps explain why eating less might help the brain.

It turns out that a molecule called CREB-1 is triggered by calorie restriction (defined as only 70% of normal consumption). cAMP Response Element Binding (CREB) protein is an essential component of long-term memory formation, and abnormalities in the expression of CREB have been reported in the brains of Alzheimer’s patients. Restoring CREB to Alzheimer’s mice has been shown to improve learning and memory impairment.

Animal models have also indicated a role for CREB in the improvements in learning and memory brought about by physical exercise. CREB seems to be vital for adult neurogenesis.

The current study found that, when CREB1 was missing (in mice genetically engineered to lack this molecule), calorie restriction had no cognitive benefits. CREB deficiency in turn drastically reduced the expression of Sirt-1. These proteins have been implicated in cardiac function, DNA repair and genomic stability (hence the connection to longevity). More recently, Sirt-1 has also been found to modulate synaptic plasticity and memory formation — an effect mediated by CREB. This role in regulating normal brain function appears to be quite separate from its cell survival functions.

The findings identify a target for drugs that could produce the same cognitive (and longevity) benefits without the need for such strict food reduction.

Reducing your eating and drinking to 70% of normal intake is a severe reduction. Recently, researchers at the National Institute on Ageing in Baltimore have suggested that the best way to cut calories to achieve cognitive benefits was to virtually fast (down to around 500 calories) for two days a week, while eating as much as you want on the other days. Their animal experiments indicate that timing is a crucial element if cognitive benefits are to accrue.

Another preliminary report, this time from the long-running Mayo Clinic study of aging, adds to the evidence that lower consumption reduces the risk of serious cognitive impairment. The first analysis of data has revealed that the risk of developing mild cognitive impairment more than doubled for those in the highest food consumption group (daily calorie consumption between 2,143 and 6,000) compared to those in the lowest (between 600 and 1,526 calories).

Calorie consumption was taken from food questionnaires in which respondents described their diets over the previous year, so must be taken with a grain of salt. Additionally, the analysis didn’t take into account types of food and beverages, or other lifestyle factors, such as exercise. Further analysis will investigate these matters in more depth.

The study involved 1,233 older adults, aged 70 to 89. Of these, 163 were found to have MCI.

None of this should be taken as a recommendation for severely restricting your diet. Certainly such behavior should not be undertaken without the approval of your doctor, but in any case, calorie restriction is only part of a much more complex issue concerning diet. I look forward to hearing more from the Mayo Clinic study regarding types of foods and interacting factors.

Reference: 

[2681] Fusco, S., Ripoli C., Podda M V., Ranieri S C., Leone L., Toietta G., et al.
(2012).  A role for neuronal cAMP responsive-element binding (CREB)-1 in brain responses to calorie restriction.
Proceedings of the National Academy of Sciences. 109(2), 621 - 626.

The findings from the National Institute on Aging were presented at the annual meeting of the American Association for the Advancement of Science in Vancouver.

Geda, Y., Ragossnig, M., Roberts, L.K., Roberts, R., Pankratz, V., Christianson, T., Mielke, M., Boeve, B., Tangalos, E. & Petersen, R. 2012. Caloric Intake, Aging, and Mild Cognitive Impairment: A Population-Based Study. To be presented April 25 at the American Academy of Neurology's 64th Annual Meeting in New Orleans.

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Diet linked to brain atrophy in old age

January, 2012
  • A more rigorous measurement of diet finds that dietary factors account for nearly as much brain shrinkage as age, education, APOE genotype, depression and high blood pressure combined.

The study involved 104 healthy older adults (average age 87) participating in the Oregon Brain Aging Study. Analysis of the nutrient biomarkers in their blood revealed 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, while those with diets high in trans fats were more likely to score more poorly on cognitive tests.

These were dose-dependent, with each standard deviation increase in the vitamin BCDE score ssociated with a 0.28 SD increase in global cognitive score, and each SD increase in the trans fat score associated with a 0.30 SD decrease in global cognitive score.

Trans fats are primarily found in packaged, fast, fried and frozen food, baked goods and margarine spreads.

Brain scans of 42 of the participants found that those with diets high in vitamins BCDE and omega 3 fatty acids were also less likely to have the brain shrinkage associated with Alzheimer's, while those with high trans fats were more likely to show such brain atrophy.

Those with higher omega-3 scores also had fewer white matter hyperintensities. However, this association became weaker once depression and hypertension were taken into account.

Overall, the participants had good nutritional status, but 7% were deficient in vitamin B12 (I’m surprised it’s so low, but bear in mind that these are already a select group, being healthy at such an advanced age) and 25% were deficient in vitamin D.

The nutrient biomarkers accounted for 17% of the variation in cognitive performance, while age, education, APOE genotype (presence or absence of the ‘Alzheimer’s gene’), depression and high blood pressure together accounted for 46%. Diet was more important for brain atrophy: here, the nutrient biomarkers accounted for 37% of the variation, while the other factors accounted for 40% (meaning that diet was nearly as important as all these other factors combined!).

The findings add to the growing evidence that diet has a significant role in determining whether or not, and when, you develop Alzheimer’s disease.

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Why diabetes is linked to cognitive impairment in older adults

January, 2012
  • The link between diabetes and cognitive impairment in older adults seems to be mediated by the release of molecules that increase inflammation, leading to constricted blood vessels, thus reduced blood flow, and finally loss of gray matter.

Why is diabetes associated with cognitive impairment and even dementia in older adults? New research pinpoints two molecules that trigger a cascade of events that end in poor blood flow and brain atrophy.

The study involved 147 older adults (average age 65), of whom 71 had type 2 diabetes and had been taking medication to manage it for at least five years. Brain scans showed that the diabetic patients had greater blood vessel constriction than the age- and sex-matched controls, and more brain atrophy. The reduction in brain tissue was most marked in the grey matter in the parietal and occipital lobes and cerebellum. Research has found that, at this age, while the average brain shrinks by about 1% annually, a diabetic brain might shrink by as much as 15%. Diabetics also had more white matter hyperintensities in the temporal, parietal and occipital lobes.

Behaviorally, the diabetics also had greater depression, slower walking, and executive dysfunction.

The reduced performance of blood vessels (greater vasoconstriction, blunted vasodilatation), and increased brain atrophy in the frontal, temporal, and parietal lobes, was associated with two adhesion molecules – sVCAM and sICAM. White matter hyperintensities were not associated with the adhesion molecules, inflammatory markers, or blood vessel changes.

It seems that the release of these molecules, probably brought about by chronic hyperglycemia and insulin resistance, produces chronic inflammation, which in turn brings about constricted blood vessels, reduced blood flow, and finally loss of neurons. The blood vessel constriction and the brain atrophy were also linked to higher glucose levels.

The findings suggest that these adhesion molecules provide two biomarkers of vascular health that could enable clinicians to recognize impending brain damage, that could then perhaps be prevented.

The findings also add weight to the growing evidence that diabetes management is crucial in preventing cognitive decline.

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How neighborhood status affects cognitive function in older adults

November, 2011

New research confirms the correlation between lower neighborhood socioeconomic status and lower cognitive function in older adults, and accounts for most of it through vascular health, lifestyle, and psychosocial factors.

In the last five years, three studies have linked lower neighborhood socioeconomic status to lower cognitive function in older adults. Neighborhood has also been linked to self-rated health, cardiovascular disease, and mortality. Such links between health and neighborhood may come about through exposure to pollutants or other environmental stressors, access to alcohol and cigarettes, barriers to physical activity, reduced social support, and reduced access to good health and social services.

Data from the large Women’s Health Initiative Memory Study has now been analyzed to assess whether the relationship between neighborhood socioeconomic status can be explained by various risk and protective factors for poor cognitive function.

Results confirmed that higher neighborhood socioeconomic status was associated with higher cognitive function, even after individual factors such as age, ethnicity, income, education, and marital status have been taken into account. A good deal of this was explained by vascular factors (coronary heart disease, diabetes, stroke, hypertension), health behaviors (amount of alcohol consumed, smoking, physical activity), and psychosocial factors (depression, social support). Nevertheless, the association was still (barely) significant after these factors were taken account of, suggesting some other factors may also be involved. Potential factors include cognitive activity, diet, and access to health services.

In contradiction of earlier research, the association appeared to be stronger among younger women. Consistent with other research, the association was stronger for non-White women.

Data from 7,479 older women (65-81) was included in the analysis. Cognitive function was assessed by the Modified MMSE (3MSE). Neighborhood socioeconomic status was assessed on the basis of: percentage of adults over 25 with less than a high school education, percentage of male unemployment, percentage of households below the poverty line, percentage of households receiving public assistance, percentage of female-headed households with children, and median household income. Around 87% of participants were White, 7% Black, 3% Hispanic, and 3% other. Some 92% had graduated high school, and around 70% had at least some college.

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[2523] Shih, R. A., Ghosh-Dastidar B., Margolis K. L., Slaughter M. E., Jewell A., Bird C. E., et al.
(2011).  Neighborhood Socioeconomic Status and Cognitive Function in Women.
Am J Public Health. 101(9), 1721 - 1728.

Previous:

Lang IA, Llewellyn DJ, Langa KM, Wallace RB, Huppert FA, Melzer D. 2008. Neighborhood deprivation, individual socioeconomic status, and cognitive function in older people: analyses from the English Longitudinal Study of Ageing. J Am Geriatr Soc., 56(2), 191-198.

Sheffield KM, Peek MK. 2009. Neighborhood context and cognitive decline in older Mexican Americans: results from the Hispanic Established Populations for Epidemiologic Studies of the Elderly. Am J Epidemiol., 169(9), 1092-1101.

Wight RG, Aneshensel CS, Miller-Martinez D, et al. 2006. Urban neighborhood context, educational attainment, and cognitive function among older adults. Am J Epidemiol., 163(12), 1071-1078.

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Diabetes & Cognition

Older news items (pre-2010) brought over from the old website

Diabetic episodes affect memory

A study involving 62 children with type 1 diabetes, of whom 33 had experienced diabetic ketoacidosis, has found those with such experience performed significantly worse on a memory test that tested their ability to recall events in association with specific details. The finding points to the importance of avoiding diabetic ketoacidosis, which is avoidable in those known to have diabetes.

[1384] Ghetti, S., Lee J. K., Sims C. E., DeMaster D. M., & Glaser N. S.
(2010).  Diabetic Ketoacidosis and Memory Dysfunction in Children with Type 1 Diabetes.
The Journal of Pediatrics. 156(1), 109 - 114.

http://www.eurekalert.org/pub_releases/2009-10/uoc--dea101909.php

Poor glucose control linked to cognitive impairment in diabetics

The ongoing Memory in Diabetes (MIND) study, involving some 3,000 type 2 diabetics 55 years and older, has found that cognitive functioning abilities drop as average blood sugar levels rise. However, there was no connection between daily blood glucose levels and cognitive performance. The study adds to growing evidence that poorer blood glucose control is strongly associated with poorer memory function, that may eventually lead to mild cognitive impairment, vascular dementia and Alzheimer's disease. It is also possible that people with impaired cognitive ability are less compliant in taking medications and controlling their diabetes. Further research will test the hypothesis that improving glucose control results in improved cognitive function.

[797] Marcovina, S. M., Launer L. J., Cukierman-Yaffe T., Gerstein H. C., Williamson J. D., Lazar R. M., et al.
(2009).  Relationship Between Baseline Glycemic Control and Cognitive Function in Individuals With Type 2 Diabetes and Other Cardiovascular Risk Factors.
Diabetes Care. 32(2), 221 - 226.

http://www.eurekalert.org/pub_releases/2009-02/wfub-hbs021109.php

Adult-onset diabetes slows mental functioning in several ways, with deficits appearing early

A comparison of 41 adults with diabetes and 424 adults in good health, aged between 53 and 90, has revealed that healthy adults performed significantly better than adults with diabetes on two of the five domains tested: executive functioning and speed of processing. There were no significant differences on tests of episodic and semantic memory, verbal fluency, reaction time and perceptual speed. The effect remained even when only the younger group (those below 70) were analyzed, indicating that the diabetes-linked cognitive deficits appear early and remain stable.

[796] Yeung, S. E., Fischer A. L., & Dixon R. A.
(2009).  Exploring effects of type 2 diabetes on cognitive functioning in older adults.
Neuropsychology. 23(1), 1 - 9.

http://www.eurekalert.org/pub_releases/2009-01/apa-ads123008.php

Blood sugar linked to normal cognitive aging

Following research showing that decreasing brain function in the area of the hippocampus called the dentate gyrus is a main contributor of normal age-related cognitive decline, an imaging study has been investigating the cause of this decreasing function by looking at measures that typically change during aging, like rising blood sugar, body mass index, cholesterol and insulin levels. The study of 240 community-based nondemented elders (average age 80 years), of whom 60 had type 2 diabetes, found that decreasing activity in the dentate gyrus only correlated with levels of blood glucose. The same association was also found in aging rhesus monkeys and in mice. The finding suggests that maintaining blood sugar levels, even in the absence of diabetes, could help maintain aspects of cognitive health. It also suggests that one reason why physical exercise benefits memory may be its effect on lowering glucose levels.

[830] Mayeux, R., Vannucci S. J., Small S. A., Wu W., Brickman A. M., Luchsinger J., et al.
(2008).  The brain in the age of old: The hippocampal formation is targeted differentially by diseases of late life.
Annals of Neurology. 64(6), 698 - 706.

http://www.eurekalert.org/pub_releases/2008-12/cumc-rac121508.php

Diabetic seniors may experience memory declines after eating high-fat food

Growing evidence links diabetes to cognitive impairment. Now a small study of 16 adults (aged 50 years and older) with type 2 diabetes compared their cognitive performance on three separate occasions, fifteen minutes after consuming different meals. One meal consisted of high fat products – a danish pastry, cheddar cheese and yogurt with added whipped cream; the second meal was only water; and the third was the high-fat meal plus high doses of vitamins C (1000 mg) and E (800 IU) tablets. Researchers found that vitamin supplementation consistently improved recall scores relative to the meal alone, while those who ate the high fat meal without vitamin supplements showed significantly more forgetfulness of words and paragraph information in immediate and time delay recall tests. Those on water meal and meal with vitamins showed similar levels in cognitive performance. The finding indicates not only that diabetics can temporarily further worsen already underlying memory problems associated with the disease by consuming unhealthy meals, but also that this can be remedied by taking high doses of antioxidant vitamins C and E with the meal, suggesting that the effect of high-fat foods is to cause oxidative stress. However, this is hardly a recommended course of action, and the real importance of this finding is that it emphasizes the need for diabetics to consume healthy foods high in antioxidants, like fruits and vegetables. Of course, this is a very small study, and further replication is needed.

[1094] Chui, M., & Greenwood C.
(2008).  Antioxidant vitamins reduce acute meal-induced memory deficits in adults with type 2 diabetes.
Nutrition Research. 28(7), 423 - 429.

http://www.eurekalert.org/pub_releases/2008-06/bcfg-swt062408.php

Stress hormone impacts memory, learning in diabetic rodents

A rodent study sheds light on why diabetes can impair cognitive function. The study found that increased levels of a stress hormone (called cortisol in humans) in diabetic rats impaired synaptic plasticity and reduced neurogenesis in the hippocampus. When levels returned to normal, the hippocampus recovered. Cortisol production is controlled by the hypothalamic-pituitary axis (HPA). People with poorly controlled diabetes often have an overactive HPA axis and excessive cortisol.

[1050] Stranahan, A. M., Arumugam T. V., Cutler R. G., Lee K., Egan J. M., & Mattson M. P.
(2008).  Diabetes impairs hippocampal function through glucocorticoid-mediated effects on new and mature neurons.
Nature Neuroscience. 11(3), 309 - 317.

http://www.eurekalert.org/pub_releases/2008-02/nioa-shi021508.php

Tight diabetes control does not impact cognitive ability in type 1 diabetes

A long-running study involving 1,441 type 1 diabetics, aged 13 to 39, has demonstrated that multiple episodes of severe hypoglycaemia, though they can cause confusion, irrational behavior, convulsions and unconsciousness, do not lead to long-term loss of cognitive ability.

[1120] The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications(DCCT/EDIC) Study Research
(2007).  Long-Term Effect of Diabetes and Its Treatment on Cognitive Function.
N Engl J Med. 356(18), 1842 - 1852.

http://www.eurekalert.org/pub_releases/2007-05/jdc-sst050107.php

Brain function not impaired by tight diabetes control and hypoglycemia

Previous research had indicated that tight blood glucose control -- achieved by taking three or more insulin injections daily – meant type 1 diabetics were three times as likely to suffer episodes of severe hypoglycemia, raising the fear that it might lead to a long-term loss of cognitive ability. Now a follow-up study provides the reassuring news that there was no link between multiple severe hypoglycemic reactions and impaired cognitive function in people with type 1 diabetes.

Jacobson, A.M. et al. 2006. Effects of Intensive and Conventional Treatment on Cognitive Function Twelve Years after the Completion of the Diabetes Control and Complications Trial (DCCT). Abstract Number 750232, presented at the American Diabetes Association's 66th Annual Scientific Sessions held in Washington, D.C, June 9—13.

http://www.eurekalert.org/pub_releases/2006-06/jdc-lss060806.php

Fat hormone linked to learning and memory

A new study reveals why obese patients who have diabetes also may have problems with their long-term memory. Leptin — the so-called ‘fat’ hormone — doesn't cross into the brain to help regulate appetite in obese people. Leptin also acts in the hippocampus, suggesting that leptin plays a role in learning and memory. The new study supports this by demonstrating that mice navigated a maze better after they received leptin. Moreover, mice with elevated levels of amyloid-beta plaques (characteristic of Alzheimer's) were particularly sensitive to leptin.

[2400] Farr, S. A., Banks W. A., & Morley J. E.
(2006).  Effects of leptin on memory processing.
Peptides. 27(6), 1420 - 1425.

http://www.sciencedaily.com/releases/2006/06/060614090511.htm
http://www.eurekalert.org/pub_releases/2006-06/slu-alb061306.php

Age-related vision problems may be associated with cognitive impairment

Age-related macular degeneration (AMD) develops when the macula, the portion of the eye that allows people to see in detail, deteriorates. An investigation into the relationship between vision problems and cognitive impairment in 2,946 patients has been carried out by The Age-Related Eye Disease Study (AREDS) Research Group. Tests were carried out every year for four years. Those who had more severe AMD had poorer average scores on cognitive tests, an association that remained even after researchers considered other factors, including age, sex, race, education, smoking, diabetes, use of cholesterol-lowering medications and high blood pressure. Average scores also decreased as vision decreased. It’s possible that there is a biological reason for the association; it is also possible that visual impairment reduces a person’s capacity to develop and maintain relationships and to participate in stimulating activities.

Chaves, P.H.M. et al. 2006. Association Between Mild Age-Related Eye Disease Study Research Group. 2006. Cognitive Impairment in the Age-Related Eye Disease Study: AREDS Report No. 16. Archives of Ophthalmology,124, 537-543.

http://www.eurekalert.org/pub_releases/2006-04/jaaj-avp040606.php

Review supports link between lifestyle factors and cognitive function in older adults

A review of 96 papers involving 36 very large, ongoing epidemiological studies in North America and Europe looking at factors involved in maintaining cognitive and emotional health in adults as they age has concluded that controlling cardiovascular risk factors, such as reducing blood pressure, reducing weight, reducing cholesterol, treating (or preferably avoiding) diabetes, and not smoking, is important for maintaining brain health as we age. The link between hypertension and cognitive decline was the most robust across studies. They also found a consistent close correlation between physical activity and brain health. However, they caution that more research is needed before specific recommendations can be made about which types of exercise and how much exercise are beneficial. They also found protective factors most consistently reported for cognitive health included higher education level, higher socio-economic status, emotional support, better initial performance on cognitive tests, better lung capacity, more physical exercise, moderate alcohol use, and use of vitamin supplements. Psychosocial factors, such as social disengagement and depressed mood, are associated with both poorer cognitive and emotional health in late life. Increased mental activity throughout life, such as learning new things, may also benefit brain health.

Wagster M, Hendrie H, Albert M, Butters M, Gao S, Knopman DS, Launer L, Yaffe K, Cuthbert B, Edwards E. The NIH Cognitive and Emotional Health ProjectReport of the Critical Evaluation Study Committee. Alzheimer's and Dementia [Internet]. 2006 ;2(1):12 - 32. Available from: http://www.alzheimersanddementia.com/article/S1552-5260(05)00503-0/abstract?articleId=&articleTitle=&citedBy=false&medlinePmidWithoutMDLNPrefix=&overridingDateRestriction=&related=false&restrictdesc_author=&restrictDescription=&restrictName.jalz=jalz&rest

http://www.eurekalert.org/pub_releases/2006-02/aa-nss021606.php

Risk for lowered cognitive performance greater in people at high risk for stroke

A new large-scale study supports earlier suggestions that those with a high risk for stroke within 10 years are also at risk for lowered cognitive function and show a pattern of deficits similar to that seen in mild vascular cognitive impairment. It is speculated that the reason may lie in structural and functional changes in the brain that do not rise to the level of clinical detection, and this is supported by a recent brain imaging study showing that abnormal brain atrophy is related both to higher risk of stroke and poorer cognitive ability. The probability of experiencing stroke within 10 years was calculated using weighted combinations of age, systolic blood-pressure, presence of diabetes, cigarette smoking, history of cardiovascular disease, treatment for hypertension and atrial fibrillation.

[1422] Elias, M. F., Sullivan L. M., D'Agostino R. B., Elias P. K., Beiser A., Au R., et al.
(2004).  Framingham stroke risk profile and lowered cognitive performance.
Stroke; a Journal of Cerebral Circulation. 35(2), 404 - 409.

http://www.eurekalert.org/pub_releases/2004-01/ama-rfl010804.php

Age-related changes in the brain's white matter affect cognitive function

From around age 60, "white-matter lesions" appear in the brain, significantly affecting cognitive function. But without cognitive data from childhood, it is hard to know how much of the difference in cognitive abilities between elderly individuals is due to aging. A longitudinal study has been made possible by the Scottish Mental Survey of 1932, which gave 11-year-olds a validated cognitive test. Scottish researchers have tracked down healthy living men and women who took part in this Survey and retested 83 participants. Testing took place in 1999, when most participants were 78 years old.
It was found that the amount of white-matter lesions made a significant contribution to general cognitive ability differences in old age, independent of prior ability. The amount of white-matter lesions contributed 14.4% of the variance in cognitive scores; early IQ scores contributed 13.7%. The two factors were independent.
Although white-matter lesions are viewed as a normal part of aging, they are linked with other health problems, in particular to circulatory problems (including hypertension, diabetes, heart disease and cardiovascular risk factors).

[442] Deary, I. J., Leaper S. A., Murray A. D., Staff R. T., & Whalley L. J.
(2003).  Cerebral white matter abnormalities and lifetime cognitive change: a 67-year follow-up of the Scottish Mental Survey of 1932.
Psychology and Aging. 18(1), 140 - 148.

http://www.eurekalert.org/pub_releases/2003-03/apa-aci031703.php

High sugar blood levels linked to poor memory

A new study takes an important step in explaining cognitive impairment in diabetics, and suggests a possible cause for some age-related memory impairment. The study assessed non-diabetic middle-aged and elderly people. Those with impaired glucose tolerance (a pre-diabetic condition) had a smaller hippocampus and scored worse on tests for recent memory. These results were independent of age or overall cognitive performance. The brain uses glucose almost exclusively as a fuel source. The ability to get glucose from the blood is reduced in diabetes. The study raises the possibility that exercise and weight loss, which help control blood sugar levels, may be able to reverse some of the memory loss that accompanies aging.

[543] Convit, A., Wolf O. T., Tarshish C., & de Leon M. J.
(2003).  Reduced glucose tolerance is associated with poor memory performance and hippocampal atrophy among normal elderly.
Proceedings of the National Academy of Sciences of the United States of America. 100(4), 2019 - 2022.

http://www.eurekalert.org/pub_releases/2003-02/nyum-hsb013003.php

Diabetes and high blood pressure linked to decline in mental ability

A large-scale six-year study of people aged 40 to 70 years old found that people with diabetes and high blood pressure are more likely to experience cognitive decline. Diabetes was associated with greater cognitive decline for those younger than 58 as well as those older than 58, but high blood pressure was a risk factor only for the 58 and older group.

[2534] Knopman, D. S., Boland L. L., Mosley T., Howard G., Liao D., Szklo M., et al.
(2001).  Cardiovascular risk factors and cognitive decline in middle-aged adults.
Neurology. 56(1), 42 - 48.

http://www.eurekalert.org/pub_releases/2001-01/MC-Nsld-0701101.php
http://www.eurekalert.org/pub_releases/2001-01/AAoN-Dahb-0801101.php

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More evidence of the benefits of B vitamins in fighting cognitive decline

September, 2011
  • High daily doses of B-vitamins significantly slowed cognitive decline and brain atrophy in those with MCI, especially if they had high levels of homocysteine.

In a small study, 266 older adults with mild cognitive impairment (aged 70+) received a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B12 and 20 mg vitamin B6 or a placebo for two years. Those treated with B vitamins had significantly lower levels of homocysteine at the end of the trial (high homocysteine is a known risk factor for age-related cognitive decline and dementia). Moreover, this was associated with a significantly slower rate of brain shrinkage.

However, while there were significant effects on homocysteine level, brain atrophy, and executive function, it wasn’t until results were separated on the basis of baseline homocysteine levels that we get really dramatic results.

It was the group with high homocysteine levels at the start of the study who really benefited from the high doses of B vitamins. For them, brain atrophy was cut by half, and there were clear benefits in episodic memory, semantic memory, and global cognitive function, not just executive function. Among those with high baseline homocysteine who received the placebo, significant cognitive decline occurred.

The level of B vitamins in the supplements was considerably greater than the recommended standard. However, caution must be taken in dosing yourself with supplements, because folic acid can have negative effects. Better to try and get your diet right first.

A longer and larger follow-up study is now planned, and hopefully that will tell us if such treatment can keep MCI developing into Alzheimer’s.

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Vitamins & minerals

B vitamins

Vitamin C

The newborn brain may be particularly vulnerable to vitamin C deficiency, which has been found in rodent studies to lead to a marked decrease in the number of brain cells in the hippocampus. Although there is no clear evidence that vitamin C supplements on their own improve memory or brain function in adults, two large studies of older adults have found that taking both vitamin C and vitamin E supplements significantly reduced the risk of Alzheimer's. Other indications suggest the efficacy of these vitamins may depend on whether they are taken in through food or through supplements (food is better), and whether the individual has the "Alzheimer's gene" (better not to).

Vitamin D

Vitamin E

It's been proposed that vitamin E might help prevent Alzheimer's, because of the role that oxidative stress plays in the development of the disease. Vitamin E is an antioxidant. It has been found in cultured cell studies that vitamin E does help protect against the effects of oxidative stress, and results in significantly fewer neurons dying. At the level of the organism, results are not so clearcut. One study of older adults found those eating the most vitamin E-rich foods had a lower risk of developing Alzheimer's, provided they didn't have the 'Alzheimer's gene'. Supplements did not have the same effect. Another, larger, study found that those with high intakes of vitamins E and C were less likely to develop Alzheimer's, regardless of gene status. This was especially true for smokers.

Choline

Research indicates that choline is a crucial ingredient in a pregnant woman's diet, for brain development in the fetus. 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. A choline food database is available at: www.nal.usda.gov/fnic/foodcomp

Iron

Magnesium

Research with rats indicates that increasing magnesium levels in the brain improves learning and memory, apparently through its effects on synaptic density and plasticity. Unfortunately, traditional supplements have little effect on magnesium levels in the brain, but the researchers developed a new compound that was effective. Magnesium deficits are common in the population of industrialized countries, and increase with age. Good sources of magnesium are dark green leafy vegetables (such as spinach), some nuts (almonds and cashews are particularly good), beans, seeds and whole unrefined grains (especially buckwheat). See here for a list of magnesium-rich foods.

Zinc

Zinc has been linked to cognitive and motor function in very young children and adults, and one small study has found zinc supplements improved cognition, especially attention, in adolescents, who are particularly at risk of zinc deficiency. Red meats, fish and grains are good sources of zinc.

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