Diet

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

Alzheimer's disease consists of 3 distinct subtypes

  • A very small study points to three subtypes of Alzheimer's disease, each of which seems to be associated with:
    • different physiological abnormalities
    • different causes and risk factors
    • different symptoms / progression
    • different age-onsets.
  • This suggests that effective treatments need to be tailored to the subtype.

A two-year study which involved metabolic testing of 50 people, suggests that Alzheimer's disease consists of three distinct subtypes, each one of which may need to be treated differently. The finding may help explain why it has been so hard to find effective treatments for the disease.

The subtypes are:

  • Inflammatory, in which markers such as C-reactive protein and serum albumin to globulin ratios are increased.
  • Non-inflammatory, in which these markers are not increased but other metabolic abnormalities (such as insulin resistance, hypovitaminosis D, and hyper-homocysteinemia) are present. This tends to affect slightly older individuals than the first subtype: 80s rather than 70s.
  • Cortical, which affects relatively young individuals (typically 50s- early 70s) and appears more widely distributed across the brain than the other subtypes, showing widespread cortical atrophy rather than marked hippocampal atrophy. It typically presents with language and number difficulties first, rather than memory loss. Typically, there is an impaired ability to hold onto a train of thought. It is often misdiagnosed, typically affects people without a family history of Alzheimer's, who do not have an Alzheimer's-related gene, and is associated with a significant zinc deficiency (Zinc is implicated in multiple Alzheimer's-related metabolic processes, such as insulin resistance, chronic inflammation, ADAM10 proteolytic activity, and hormonal signaling. Zinc deficiency is relatively common, and associated with increasing age.).

The cortical subtype appears to be fundamentally a different condition than the other two.

I note a study I reported on last year, that found different molecular structures of amyloid-beta fibrils in the brains of Alzheimer's patients with different clinical histories and degrees of brain damage. That was a very small study, indicative only. However, I do wonder if there's any connection between these two findings. At the least, I think this approach a promising one.

The idea that there are different types of Alzheimer's disease is of course consistent with the research showing a variety of genetic risk factors, and an earlier study indicating at least two pathways to Alzheimer's.

It's also worth noting that the present study built on an earlier study, which showed that a program of lifestyle, exercise and diet changes designed to improve the body's metabolism reversed cognitive decline within 3-6 months in nine out of 10 patients with early Alzheimer's disease or its precursors. Note that this was a very small pilot program, and needs a proper clinical trial. Nevertheless, it is certainly very interesting.

http://www.eurekalert.org/pub_releases/2015-09/uoc--adc091615.php

Reference: 

Bredesen, D.E. 2015. Metabolic profiling distinguishes three subtypes of Alzheimer's disease. AGING, 7 (8), 595-600. Full text at http://www.impactaging.com/papers/v7/n8/full/100801.html

Bredesen, D.E. 2014. Reversal of cognitive decline: A novel therapeutic program. AGING, Vol 6, No 9 , pp 707-717. Full text at http://www.impactaging.com/papers/v6/n9/full/100690.html

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A diet to delay age-related cognitive decline

More evidence for the benefits of the Mediterranean diet for fighting age-related cognitive decline comes from a large 5-year study. The study involved 960 older adults, whose cognitive change was assessed over 4.7 years. Those who followed the MIND diet more rigorously showed an equivalent of being 7.5 years younger cognitively than those who followed the diet least.

The Mediterranean-DASH Diet Intervention for Neurodegenerative Delay is a hybrid of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets. It requires at least:

  • three servings of whole grains every day
  • a green leafy vegetable and one other vegetable every day
  • a glass of wine
  • snack most days on nuts
  • beans every other day or so
  • poultry at least twice a week
  • fish at least once a week
  • berries at least twice a week (blueberries are particularly recommended)
  • very limited intake of designated unhealthy foods, especially:
    • butter
    • sweets and pastries
    • whole fat cheese
    • fried or fast food

http://www.eurekalert.org/pub_releases/2015-08/rumc-eaa080415.php

http://www.theguardian.com/society/2015/aug/05/diet-high-in-leafy-green-vegetables-may-slow-cognitive-decline-in-elderly-study

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More evidence for a link between type 2 diabetes and Alzheimer’s

Glucose levels linked to cognitive decline in those with MCI

A study involving 264 older adults with mild cognitive impairment has found that those with normal glucose levels (167; 63%) had less cognitive decline over 2 years than those with impaired (high) glucose levels (97; 37%). They also showed less brain shrinkage and were less likely to develop Alzheimer’s. The fasting glucose levels were classified according to the American Diabetes criteria.

[3614] Vos, S JB., Xiong C., Visser P J., Jasielec M. S., Hassenstab J., Grant E. A., et al.
(2013).  Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study.
The Lancet Neurology. 12(10), 957 - 965.

Rat study suggests cognitive decline in diabetics related to amyloid-beta buildup

A rat study supports the growing evidence of a link between type 2 diabetes and Alzheimer’s. In this study, 20 rats were fed a high-fat diet to give them type 2 diabetes. A subsequent test found that the diabetic rats had significantly poorer memories than the control group of rats on a healthy diet (the rats were taught to associate a dark cage with an electric shock; how long the rat continues to remember that the stimulus means a shock — as shown by their frozen reaction — is taken as a measure of how good their memory is; the diabetic rats froze for less than half the time of the controls).

The diabetic rats then had their brains (specifically, the hippocampus) injected with antibodies that disrupt amyloid-beta plaques. This produced no change in their behavior. However, when they were given antibodies that disrupt amyloid-beta oligomers (precursors of the plaques), the memory deficit was reversed, and they behaved the same as the healthy rats.

These findings suggest that the cognitive decline often seen in type 2 diabetes is not due to the disruption in insulin signaling, as thought, but rather the build-up of amyloid oligomers. Previous research has shown that the same enzymes break down both insulin and the oligomers, so when there’s a lot of insulin (which the enzymes prioritize), the enzymes don’t have as much opportunity to work on breaking down the oligomers. The oligomers collect, preventing the insulin from reaching their proper receptors in the hippocampus, which impairs cognitive function.

All this supports the idea that type 2 diabetes may be thought of as early-stage Alzheimer's. Obviously a lot more work needs to be done to confirm this picture, but certainly in the mean time, it can be taken as another reason to take type 2 diabetes very seriously.

www.newscientist.com/article/mg22029453.400-are-alzheimers-and-diabetes-the-same-disease.html

McNay, E.C., Osborne, D., et al. 2014. Preliminary data presented at the Society for Neuroscience meeting in San Diego in November, 2013

High blood sugar makes Alzheimer’s plaque more toxic

A study of cell cultures taken from rodents’ cerebral blood vessels has found that, while cells exposed to either high glucose or amyloid-beta showed no changes in viability, exposure to both decreased cell viability by 40%. Moreover, cells from diabetic mice were more vulnerable to amyloid-beta, even at normal glucose levels.

The findings support evidence pointing to high glucose as a risk factor for vascular damage associated with Alzheimer’s, and adds weight to the view that controlling blood sugar levels is vital for those with diabetes.

http://www.futurity.org/high-blood-sugar-makes-alzheimers-plaque-toxic/

[3558] Carvalho, C., Katz P. S., Dutta S., Katakam P. V. G., Moreira P. I., & Busija D. W.
(2014).  Increased Susceptibility to Amyloid-β Toxicity in Rat Brain Microvascular Endothelial Cells under Hyperglycemic Conditions.
Journal of Alzheimer's Disease. 38(1), 75 - 83.

Mechanism by which diabetes increases Alzheimer's risk revealed

Although it's well-established now that diabetes is a major risk factor for dementia, the reason is still not well understood. To test the hypothesis that epigenetic changes in the brain, affecting synaptic function, may be part of the reason, the brains of diabetics and others were examined post-mortem. Diabetics' brains were found to have significantly higher expression of a class of molecules (histone deacetylases class IIa) and this was associated with impaired expression of synaptic proteins.

This finding was confirmed in mice genetically engineered to develop an Alzheimer’s-type condition, who were induced to develop diabetes. The increase of HDAC IIa was associated with synaptic impairments in the hippocampus, through the work of amyloid oligomers.

Some 60% of Alzheimer's patients have at least one serious medical condition associated with diabetes.

http://www.eurekalert.org/pub_releases/2013-10/tmsh-cie102213.php

[3615] Wang, J., Gong B., Zhao W., Tang C., Varghese M., Nguyen T., et al.
(2014).  Epigenetic Mechanisms Linking Diabetes and Synaptic Impairments.
Diabetes. 63(2), 645 - 654.

High Blood Sugar Linked to Dementia

A seven-year study involving 2,067 older adults (average age 76 at start) has found that those with a high blood glucose level, whether or not they had diabetes, were more likely to develop dementia. Moreover, this was a linear relationship — meaning that the risk steadily increased with higher glucose levels, and decreased the lower it was. Thus, even those with ‘normal’ glucose levels were subject to this relationship, with those whose blood sugar averaged 115 milligrams per deciliter, having an 18% higher risk of dementia than those at 100 mg/dL. Other risk factors, such as high blood pressure, smoking, exercise, and education, were taken into account in the analysis.

The findings add weight to the idea that the brain is a target organ for damage by high blood sugar.

Over the course of the study, a quarter (524) developed dementia of some kind, primarily Alzheimer’s disease or vascular dementia. At the beginning of the study, 232 (11%) had diabetes, and a further 111 developed it by the end of the study. Nearly a third (32%) of those with diabetes at the beginning of the study developed dementia, compared to just under a quarter of those without (24.5%).

http://newoldage.blogs.nytimes.com/2013/08/09/high-blood-sugar-linked-to-dementia/

The journal article is freely available at http://www.nejm.org/doi/full/10.1056/NEJMoa1215740#t=article

[3563] Crane, P. K., Walker R., Hubbard R. A., Li G., Nathan D. M., Zheng H., et al.
(2013).  Glucose Levels and Risk of Dementia.
New England Journal of Medicine. 369(6), 540 - 548.

Undiagnosed pre-diabetes highly prevalent in early Alzheimer's disease

A study involving 128 patients with mild to moderate Alzheimer’s disease, which had specifically excluded those with known diabetes, found that 13% of them did in fact have diabetes, and a further 30% showed glucose intolerance, a pre-diabetic condition.

Turner presented his findings at the Alzheimer's Association International Congress in Boston on July 14.

http://www.eurekalert.org/pub_releases/2013-07/gumc-uph070513.php

Association between hypoglycemia, dementia in older adults with diabetes

A 12-year study involving 783 older adults with diabetes (average age 74) has found that 148 (19%) developed dementia. Those 61 patients (8%) who had a reported hypoglycemic event were twice as likely to develop dementia compared to those who didn’t suffer such an event (34% vs. 17%). Similarly, those with dementia were more likely to experience a severe hypoglycemic event.

The findings suggest some patients risk entering a downward spiral in which hypoglycemia and cognitive impairment fuel one another, leading to worse health

http://www.eurekalert.org/pub_releases/2013-06/tjnj-abh060613.php

http://www.eurekalert.org/pub_releases/2013-06/uoc--aal060613.php

[3622] Yaffe, K., CM F., N H., & et al
(2013).  ASsociation between hypoglycemia and dementia in a biracial cohort of older adults with diabetes mellitus.
JAMA Internal Medicine. 173(14), 1300 - 1306.

Dementia risk greatest for older Native-Americans and African-Americans with diabetes

In the first study to look at racial and ethnic differences in dementia risk among older adults with type 2 diabetes, Native Americans were 64% more likely to develop dementia than Asian-Americans, and African-Americans were 44% more likely. Asian-Americans had the lowest risk, and non-Hispanic whites and Latinos were intermediate.

The study involved 22,171 older adults (60+), of whom 3,796 patients (17%) developed dementia over the 10 years of the study. Almost 20% of the African-Americans and Native Americans developed dementia.

The ethnic differences were not explained by diabetes-related complications, glycemic control or duration of diabetes, or neighborhood deprivation index, body mass index, or hypertension.

http://www.eurekalert.org/pub_releases/2013-12/kp-drg121113.php

[3590] Mayeda, E. R., Karter A. J., Huang E. S., Moffet H. H., Haan M. N., & Whitmer R. A.
(2014).  Racial/Ethnic Differences in Dementia Risk Among Older Type 2 Diabetic Patients: The Diabetes and Aging Study.
Diabetes Care. 37(4), 1009 - 1015.

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Healthy midlife diet may prevent dementia later

Data from the population-based Finnish Cardiovascular Risk Factors, Aging and Incidence of Dementia (CAIDE) study has revealed that healthy dietary choices in midlife may prevent dementia in later years. Out of 2,000 participants, 1,449 took part in the follow-up. The participants were 39 to 64 years old at baseline and 65 to 75 years old at follow-up.

Those who ate the healthiest diet at around age 50 had an almost 90% lower risk of dementia in a 14-year follow-up study than those whose diet was the least healthy.

Healthy foods included vegetables, berries and fruits, fish and unsaturated fats from milk products and spreads; unhealthy foods included sausages, eggs, sweets, sugary drinks, salty fish and saturated fats from milk products and spreads.

Consistent with other research, a high intake of saturated fats was also linked to poorer cognition and an increased risk of mild cognitive impairment 21 years later. A higher saturated fat intake was also associated with an increased risk of dementia among those carrying the “Alzheimer's gene”, ApoE4.

Those consuming 3 to 5 cups of coffee daily had a smaller risk of dementia than those consuming less or more.

http://www.eurekalert.org/pub_releases/2014-03/uoef-hmd031014.php

Reference: 

Eskelinen, Marjo: The effects of midlife diet on late-life cognition: an epidemiological approach. Publications of the University of Eastern Finland. Dissertations in Health Sciences., no 220. http://epublications.uef.fi/pub/urn_isbn_978-952-61-1394-4/

Eskelinen MH, Ngandu T, Helkala E-L, Tuomilehto J, Nissinen A, Soininen H, Kivipelto M. Fat intake at midlife and cognitive impairment later in life: a population-based CAIDE study. Int J Geriatr Psychiatry 23(7): 741, 2008.

Laitinen MH, Ngandu T, Rovio S, Helkala E-L, Uusitalo U, Viitanen M, Nissinen A, Tuomilehto J, Soininen H, Kivipelto M. Fat Intake at Midlife and Risk of Dementia and Alzheimer's Disease: A Population-Based Study. Dement Geriatr Cogn Disord 22(1): 99, 2006.

Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife Coffee and Tea Drinking and the Risk of Late-Life Dementia: A Population-based CAIDE Study. J Alzheimers Dis 16(1): 85-91, 2009.

Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife Healthy Diet Index and Late-Life Dementia and Alzheimer's Disease. Dement Geriatr Cogn Disord Extra 1(1): 103-112, 2011.

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Diet

Older people do seem to be much more vulnerable to deficits in thinking and remembering caused by poor diet.

Low levels of B-12 and folic acid in particular, appear to be involved in age-related cognitive decline.

Green leafy vegetables, citrus fruits and juices, whole wheat bread and dry beans are good sources of folate. Fruit and vegetables, whole grains, beans and other protein sources (nuts, meat, fish) are good sources of the B vitamins.

Experiments with rats suggest sunflower seeds (and other seeds high in linoleic acid) may help against cognitive decline caused by hypertension.

Fruits and vegetables high in antioxidants (for example, spinach, blueberries) may reduce and even reverse age-related impairment to neuron function.

Experiments in rats suggest that two chemicals normally found in the body's cells and available as dietary supplements may also improve memory function and increase energy in older people. One of these substances is found in meat and vegetables, the other in green leafy vegetables.

Carbohydrates, fat, and protein, all seem to have positive effects - different effects - on thinking and remembering. It has been shown that having breakfast has a positive effect on memory in older adults; perhaps low energy intake in general is partly responsible for cognitive decline in some older people.

 

Health news relating to diet

tags lifestyle: 

Calorie Restriction

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

Cognitive benefit of reduced calories for older adults

Recent rat studies have indicated that significant calorie restriction lengthens lives, but the evidence for humans is rather more mixed. Now a German study of 50 healthy but overweight older adults (average age 60) has found that those who were on a balanced but severely restricted diet (reduced by 30%) for 3 months significantly improved their performance on a verbal memory test. Those who didn’t reduce their calorie intake but increased their consumption of unsaturated fatty acids (linked to improved cognition), and those who didn’t change their diets, showed little or no improvement. It’s important to note that the participants were overweight to start with; further research will be needed to see whether the same effect occurs with normal-weight older adults.

[361] Witte, A. V., Fobker M., Gellner R., Knecht S., & Floel A.
(2009).  From the Cover: Caloric restriction improves memory in elderly humans.
Proceedings of the National Academy of Sciences. 106(4), 1255 - 1260.

http://sciencenow.sciencemag.org/cgi/content/full/2009/127/1?etoc

Calorie restriction may help prevent Alzheimer's

A mouse study has found that beta-amyloid peptides can be reduced by restricting calorie intake, primarily through a low carbohydrate diet. Conversely, a high caloric intake based on saturated fat was shown to increase levels of beta-amyloid peptides. This is the first study to suggest that caloric restriction might inhibit the generation of beta-amyloid peptides, but there have been a number of studies providing evidence that high cholesterol, obesity, and other cardiovascular risk factors increase the likelihood of Alzheimer’s.

Qin, W. et al. 2006. Neuronal SIRT1 Activation as a Novel Mechanism Underlying the Prevention of Alzheimer Disease Amyloid Neuropathology by Calorie Restriction. Journal of Biological Chemistry, 281 (31), 21745-21754.

http://www.sciencedaily.com/releases/2006/06/060614113128.htm

Fewer calories may slow Alzheimer's

Restricting the diets of genetically engineered mice by 40% over 4 weeks reduced the build-up of plaques in the brain that are linked to Alzheimer's disease by 50%. It remains to be seen whether such dietary changes would similarly affect humans. Researchers are now looking to isolate the specific factors of the diet restriction which are important.

Patel, N.V., Gordon, M.N., Connor, K.E., Good, R.A., Engelman, R.W., Mason, J., Morgan, D.G., Morgan, T.E. & Finch, C.E. (in press). Caloric restriction attenuates Aβ-deposition in Alzheimer transgenic models. Neurobiology of Aging, In Press, Corrected Proof, Available online 25 November 2004.

http://www.eurekalert.org/pub_releases/2004-12/uosc-fcm121404.php

Calorie restriction leads to some brain benefits but not others in mice

A mouse study has found that although severe calorie restriction prevents certain aging-related changes in the brain, such as the accumulation of free radicals, and impairments in coordination and strength, the reduced diet did not seem to prevent age-related cognitive impairment.

Dugan, L.L. et al. 2004. Presented on Sunday, Oct. 24 at Neuroscience 2004, the Society for Neuroscience's 34th Annual Meeting in San Diego.

http://www.eurekalert.org/pub_releases/2004-10/wuso-crl102204.php

Meal skipping protects the nerve cells of mice

A new mouse study suggests fasting every other day may protect brain neurons as well as or better than either vigorous exercise or caloric restriction. The mice were allowed to eat as much as they wanted on non-fasting days, and did not, overall, eat fewer calories than the control group. Their nerve cells however, proved to be more resistant to neurotoxin injury or death than nerve cells of both the calorie-restricted mice or the control group. Previous research has found that meal-skipping diets can stimulate brain cells in mice to produce a protein called brain-derived neurotrophic factor (BDNF) that promotes the survival and growth of nerve cells. The researchers are now investigating the effects of meal-skipping on the cardiovascular system in laboratory rats.

[1429] Anson, M. R., Guo Z., de Cabo R., Iyun T., Rios M., Hagepanos A., et al.
(2003).  Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake.
Proceedings of the National Academy of Sciences of the United States of America. 100(10), 6216 - 6220.

http://www.eurekalert.org/pub_releases/2003-04/nioa-msh042403.php

Calorie restriction reduces age-related brain cell death

A recent rat study has shown that certain proteins that increase with age and are linked to cell death were significantly reduced in the brains of rats whose calories were limited (but nutritionally dense, to guard against malnutrition). Moreover, the levels of a beneficial protein known to protect against neuron death were twice as high in older rats whose calories were restricted by 40%. This is consistent with a number of studies of other species that have found calorie restriction not only boosts life span and general health but also increases mental capacity.

[552] Shelke, R. R. J., & Leeuwenburgh C.
(2003).  Life-long calorie restriction (CR) increases expression of apoptosis repressor with a caspase recruitment domain (ARC) in the brain.
FASEB J.. 02-0803fje - 02-0803fje.

http://www.eurekalert.org/pub_releases/2003-01/uof-usc010903.php

tags lifestyle: 

Sugar

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

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

Right breakfast bread keeps blood sugar in check all day

A doctoral study has found that those given low glycemic index breakfasts could concentrate better and had a better working memory. Moreover, healthy individuals with low glucose tolerance (higher than average rises in blood sugar following a meal) generally performed less well. The study also found that eating the right whole-grains for breakfast didn’t simply regulate blood-sugar levels all morning, but all day — some ten hours. Experiments also showed that the blood sugar increase following breakfast can be moderated in a similar way by eating the right grain products the night before. Great variations in levels of blood sugar are being associated more and more with the risk of old-age diabetes, obesity, and cardiovascular diseases.

Nilsson, A. 2007. Effects of Indigestible Carbohydrates and GI of Cereal Products on Glucose Metabolism, Satiety and Cognitive Function in Healthy Subjects; Emphasising mechanisms for glycaemic regulation at the acute, second and third meal. Division of Applied Nutrition and Food Chemistry, Lund University, P.O Box 124, 221 00 Lund.

http://www.eurekalert.org/pub_releases/2007-09/src-rbb090507.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

Energy consumption improves memory performance in the elderly

On four occasions, a small group of older people ( 61–79 years) were given, after the night's fast, either a drink containing protein (whey), carbohydrate (glucose), fat (safflower oil), or a nonenergy placebo. Cognitive tests were given 15 and 60 minutes later. Only the carbohydrate drink increased blood glucose levels, but all 3 of the energy drinks improved memory for paragraphs. Other memory improvements were specific to the type of drink. For example, fat was the only one that enhanced attention. In general, improvement was greater 60 minutes after drinking than 15 minutes after.

[1210] Kaplan, R. J., Greenwood C. E., Winocur G., & Wolever T MS.
(2001).  Dietary protein, carbohydrate, and fat enhance memory performance in the healthy elderly.
Am J Clin Nutr. 74(5), 687 - 693.

http://www.eurekalert.org/pub_releases/2001-10/ajoc-ecr101901.php

A good breakfast improves memory function in older adults

A study of 41 healthy seniors aged 60 to 84 found that memory function was improved after a breakfast of wholegrain unsweetened cereal, milk, and juice (compared to no breakfast). This improvement was greatest for those with memory problems and those with early signs of adult-onset diabetes. The study was carried out by researchers at the Baycrest Centre for Geriatric Care at the University of Toronto.

Findings were presented to the Society for Neurosciences 2000 annual meeting in New Orleans.

http://www.baycrest.org/news_archive_2001_breakfast_memory.htm

 

tags lifestyle: 

Vitamin D

Vitamin D is now known to be important in brain development and brain function. There is a wide distribution of vitamin D receptors in the brain, and many are directly involved in learning and memory, as well as motor control. A large study of older men suggests attention and speed of processing may be particularly affected by vitamin D deficits. Infants and the elderly, and those with darker skin living at northern latitudes, are particularly at risk of vitamin D deficiency. Vitamin D is received mostly from sunlight, but can also be found in some foods such as oily fish.

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Iron

A number of studies have found that iron deficiency in children and adolescents is associated with lower scores of cognitive tests. Moreover, there is some evidence that iron deficiency during infancy has persistent effects on cognition that are still evident in adolescence. This may be exacerbated for those with poor family conditions.

While iron deficiency was once presumed to exert most of its deleterious effects only if it reached the level of anemia, it has more recently become recognized that many organs show negative changes in functioning before there is any drop in iron hemoglobin concentration. A large U.S. national study found iron deficiency in 3% of children (6-16), and 8.7% of girls aged 12 to 16.

There has been less research done on the effects of iron deficiency on cognition in adults, but there are indications that iron deficiency is associated with poorer attention and working memory in both young and older women.

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

Iron supplements might harm infants who have enough

U.S. infant formulas typically come fortified with 12 mg/L of iron to prevent iron-deficiency anemia, although Europe generally uses a lower amount. A study of 494 Chilean children has now showed that those who received iron fortified formula in infancy at the 12 mg level used in the U.S. lagged behind those who received low-iron formula in cognitive and visual-motor development by age 10 years. While most children who received the higher level formula did not show lower scores, the 5% with the highest hemoglobin levels at 6 months showed the poorest outcome. Adversely affected children scored 11 points lower in IQ and 12 points lower in visual-motor integration. This suggests that those who are not deficient in iron are adversely affected by giving them too much. It seems likely that more than 5% of U.S. infants will have high hemoglobin levels. More research is needed to confirm this finding.

Castillo, M. & Smith, J.B. 2008. Poorer developmental outcome at 10 years with 12 mg/L iron-fortified formula in infancy. Paper presented May 5 at the Pediatric Academic Societies annual meeting in Honolulu.

http://www.eurekalert.org/pub_releases/2008-05/uom-ism043008.php

Iron-deficient infants have lower cognitive scores at 19, especially in lower socioeconomic levels

Another study has come out finding that teenagers who were iron-deficient as infants continue to lag behind their peers in cognitive test scores, with a wider gap for children at lower socioeconomic levels. The study of 185 children from an urban area in Costa Rica, found that among children from middle-class families, initial scores on cognitive tests were eight points apart, 101.2 for those with iron deficiency and 109.3 for those with sufficient iron levels, and this gap remained at eight or nine points through 19 years. However, for those in lower socio-economic classes, initial scores that were ten points apart (93.1 for iron-deficient infants and 102.8 for those with normal iron levels) had widened by 19 years to 25 points (70.4 vs. 95.3). The finding points to the snowball effect of early failure.

[1145] Lozoff, B., Jimenez E., & Smith J. B.
(2006).  Double Burden of Iron Deficiency in Infancy and Low Socioeconomic Status: A Longitudinal Analysis of Cognitive Test Scores to Age 19 Years.
Arch Pediatr Adolesc Med. 160(11), 1108 - 1113.

http://www.eurekalert.org/pub_releases/2006-11/jaaj-idi110206.php

Impact of iron deficiency in infancy continues into adolescence

A new study has found that teens who suffered iron deficiency as infants are likely to score lower on cognitive and motor tests, even if that iron deficiency was identified and treated in infancy. The study followed 191 children. Those who were diagnosed with severe, chronic iron deficiency when they were 12-23 months old and were treated with iron supplements, lagged behind their peers in both motor and mental measures. The difference, moreover, actually increased over time. The iron-deficient infants scored about six points lower on cognitive tests at age 1-2 years, and 11 points lower at age 15-18 years. The gap was even more pronounced for children of families with low socioeconomic status, lower stimulation in the home or mothers lower in IQ. For children with good iron status, family conditions did not seem to affect their cognitive test scores. The researcher stressed that the children were not generally malnourished. Moreover, it must be emphasized that these children received treatment for their iron deficiency, yet still showed continuing ill effects, pointing to the need to prevent the deficiency occurring in the first place.

Lozoff, B. 2004. Longitudinal Analysis of Cognitive and Motor Effects of Iron Deficiency in Infancy. Presented at the Pediatric Academic Societies' annual meeting in San Francisco May 3.

http://www.eurekalert.org/pub_releases/2004-05/uom-iis050404.htm

American Academy of Pediatrics information on iron intake for infants: http://aappolicy.aappublications.org/cgi/content/full/pediatrics;104/1/119

Even moderate iron deficiency affects cognitive performance

A new study involving 149 young women (aged 18 to 35, average age 21), has found that iron supplementation significantly improved attention, short-term and long-term memory, and performance on cognitive tasks in those who were deficient in iron, even if not classified as anemic. On the baseline test, women who were iron deficient but not anemic completed the tasks in the same amount of time as iron sufficient women of the same age, but they performed significantly worse. Women who were anemic both performed significantly worse and took longer, with length of time increasing with degree of anemia. However, 16 weeks of iron supplementation markedly improved both scores and time to complete the task.
While iron deficiency was once presumed to exert most of its deleterious effects only if it had reached the level of anemia, it has more recently become recognized that many organs show negative changes in functioning before there is any drop in iron hemoglobin concentration. Iron deficiency is thought to occur in 9 – 11% of women of reproductive age and 25% of pregnant women. In non-industrialized countries, the prevalence of anemia is over 40% in non-pregnant women and over 50% for pregnant women and children aged five to 14.

Murray-Kolb, L., Beard, J. & Whitfield, K. 2004. presented at Experimental Biology 2004, in the American Society of Nutritional Sciences' scientific program.

http://www.eurekalert.org/pub_releases/2004-04/foas-mid040404.php

U.N. prescribes nutrient-fortified foods

A new U.N. survey says the brainpower of many developing countries has diminished because of a shortage of the right vitamins. To fight the problem, the United Nations is prescribing artificially fortified foods: soy sauce laced with zinc, "super salt" spiked with iron, cooking oil fortified with vitamin A. The report claimed a lack of iron lowered children's IQs by an average five to seven points, while a deficiency in iodine cuts it 13 more points. The report was produced by the Micronutrient Initiative and the United Nations Children's Fund.
http://www.micronutrient.org/

Iron deficiency may affect maths achievement in children and teens

A U.S. national study of 5,398 children aged 6 to 16 found iron deficiency in 3% of the children overall, and 8.7% of girls aged 12 to 16 (7% without anemia). Average math scores for iron-deficient children with or without anemia were about six points lower than those with normal iron levels. Among adolescent girls, the difference in scores was more than eight points. Previous research has linked iron-deficiency anemia with lower developmental test scores in young children, but there is less information on older children and on iron deficiency without anemia. It is suggested that this finding may help explain why the female superiority in maths at younger ages reverses itself in adolescence.

Halterman, J.S., Kaczorowski, J.M., Aligne, C.A., Auinger, P. & Szilagyi, P.G. 2001. Iron Deficiency and Cognitive Achievement Among School-Aged Children and Adolescents in the United States. Pediatrics, 107 (6), 1381-1386.

http://www.pediatrics.org/cgi/content/abstract/107/6/1381

Anemia linked to impaired thinking in older adults

For older adults, anemia has long been linked to fatigue, muscle weakness and other physical ailments. But a new study suggests it may also be an independent risk factor for executive-function impairment. The study examined 364 women between 70 and 80 years old, of whom some 10% had mild anemia. Those with anemia were four to five times more likely to perform worst on the executive function tests.

[708] Chaves, P. H. M., Carlson M. C., Ferrucci L., Guralnik J. M., Semba R., & Fried L. P.
(2006).  Association Between Mild Anemia and Executive Function Impairment in Community-Dwelling Older Women: The Women's Health and Aging Study II.
Journal of the American Geriatrics Society. 54(9), 1429 - 1435.

http://www.eurekalert.org/pub_releases/2006-09/jhmi-aab091306.php

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B Vitamins & Folate

Much of the research into the importance of folate and B12 levels has centered on seniors, and there is now quite a lot of research pointing to the need for adequate levels of these vitamins for maintaining cognitive functioning as you get older. In particular, high levels of homocysteine increase the risk of developing Alzheimer’s, and these go hand-in-hand with low levels of B12 and folate. Homocysteine is produced by the breakdown of a dietary protein called methionine, and B-vitamins are required to convert homocysteine back to methionine. Mouse research indicates that increased levels of homocysteine impair cognition through microvascular changes in the hippocampus. Greater brain atrophy is also found in those with high levels of homocysteine.

Elevated levels of homocysteine are not only associated with a significantly greater risk of developing Alzheimer's, they also dramatically increase the risk for stroke and vascular dementia.

Excitingly, though, a study found that vitamin B supplements markedly reduced brain atrophy in older adults with mild cognitive impairment, offering hope that they may be effective in delaying the development of Alzheimer’s. The benefits were greatest for those with the highest levels of homocysteine.

Higher levels of homocysteine are also linked with smoking.

Folic acid levels are of course also regarded as crucial when the brain is developing, which is why pregnant women are urged to take supplements, and why some countries fortify their bread with it.

There has been much less research on the effects of B-vitamins outside of the areas of prenatal development and age-related cognitive impairment and dementia. However, one study, carried out in a country which doesn't fortify its flour with folic acid, found significant academic achievement between those in the top third of folic acid intake and those in the bottom third.

Although the evidence for the age-related cognitive benefits of B12 and folate is greater than for any other supplement, not all studies have come out proclaiming their value. The inconsistencies may be explained by a finding that seniors with normal levels of vitamin B12 performed better if folate level was high, but when vitamin B12 was low, high levels of folate were associated with poor cognitive performance, as well as a greater probability of anemia.

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. Vitamin B12 is often deficient in older people.

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

Vitamin B12 may protect the brain in old age

A five-year study of 107 older adults (61—87) has found that those who had higher vitamin B12 levels were six times less likely to experience brain shrinkage compared with those who had lower levels of the vitamin in their blood, even though none of them had vitamin B12 deficiency. Vitamin B12 is found in meat, fish and milk, and is often deficient in older people.

[516] Vogiatzoglou, A., Refsum H., Johnston C., Smith S. M., Bradley K. M., de Jager C. A., et al.
(2008).  Vitamin B12 status and rate of brain volume loss in community-dwelling elderly.
Neurology. 71(11), 826 - 832.

http://www.eurekalert.org/pub_releases/2008-09/aaon-vbm090208.php

B-vitamin deficiency may cause vascular cognitive impairment

A new mouse study helps clarify the association between homocysteine, folate & B12, and cognitive impairment. The study found that mice fed a diet deficient in folate and vitamins B12 and B6 demonstrated significant deficits in spatial learning and memory compared with normal mice, developed plasma homocysteine concentrations that were seven-fold higher, and showed smaller capillary length and density in blood vessels in the hippocampus. Homocysteine is produced by the breakdown of a dietary protein called methionine; B-vitamins are required to convert homocysteine back to methionine. A third group of mice were fed a diet enriched with methionine. These mice showed similar, but less pronounced effects. The findings indicate that increased levels of homocysteine, produced by low intake of folate and B vitamins, impairs cognition through microvascular changes.

[1025] Troen, A. M., Shea-Budgell M., Shukitt-Hale B., Smith D. E., Selhub J., & Rosenberg I. H.
(2008).  B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice.
Proceedings of the National Academy of Sciences. 105(34), 12474 - 12479.

Full text is available at http://www.pnas.org/content/105/34/12474.abstract
http://www.physorg.com/news139574626.html

How food affects the brain

I’ve reported on quite a lot of studies finding beneficial effects of one food or another on the brain. Now a researcher has analyzed more than 160 studies about food's effect on the brain, and here’s the bottom line. He comes out for omega-3 fatty acids, as both improving synaptic plasticity and the expression of several molecules proteins to learning and memory, as well as protecting against attention-deficit disorder, dyslexia, dementia, depression, bipolar disorder and schizophrenia. He suggests it’s better to get it from food than supplements (which is always recommended). Salmon, walnuts and kiwi fruit are all good sources. They’re still working out which fatty acids are most important, but one is definitely docosahexaenoic acid, or DHA — which like vitamin C we’re not good at making for ourselves; we have to ingest it. He also concludes that diets high in trans fats and saturated fats are bad for cognition.
Studies also support the need for folic acid (found in spinach, orange juice and yeast), which is essential for brain function, and appears to reduce age-related cognitive decline and dementia. And BDNF, important for learning and memory as well as metabolic regulation (so there’s a connection there with obesity), is helped by omega-3 fatty acids and the curry spice curcumin, and also, it seems, smaller food portions.

[1293] Gómez-Pinilla, F.
(2008).  Brain foods: the effects of nutrients on brain function.
Nat Rev Neurosci. 9(7), 568 - 578.

Full text is available online at www.nature.com/nrn/journal/v9/n7/abs/nrn2421.html
http://www.eurekalert.org/pub_releases/2008-07/uoc--slh070908.php

Vitamin B12, folate, and cognitive function

Confirming earlier studies, a large epidemiological study has found that older people with normal vitamin B12 status and high levels of folate had higher scores on a test of cognitive function. The study clarifies some inconsistencies in earlier research by disentangling the interaction between these factors. It appears seniors with normal levels of vitamin B12 perform better if folate level is high, but when vitamin B12 is low, high levels of folate are associated with poor cognitive performance, as well as a greater probability of anemia. There are also indications that the combination might be a factor in some other diseases.

[1443] Morris, M S., Jacques P. F., Rosenberg I. H., & Selhub J.
(2007).  Folate and vitamin B-12 status in relation to anemia, macrocytosis, and cognitive impairment in older Americans in the age of folic acid fortification.
Am J Clin Nutr. 85(1), 193 - 200.

http://www.eurekalert.org/pub_releases/2007-02/tu-fab020907.php

Folic acid supplementation may improve cognitive performance

A study involving 818 older adults with raised homocysteine levels and normal vitamin B12 levels found that those given daily folic acid supplements (800 micrograms) for 3 years had lower homocysteine levels and improved cognitive performance compared to those given a placebo.

[443] Durga, J., van Boxtel M. P. J., Schouten E. G., Kok F. J., Jolles J., Katan M. B., et al.
(2007).  Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomised, double blind, controlled trial.
Lancet. 369(9557), 208 - 216.

http://www.eurekalert.org/pub_releases/2007-01/l-fas011707.php

More evidence for value of folate for aging brains

Confirming a growing body of evidence, a study of 50-85 year old Boston-area men (members of the ongoing Normative Aging Study) found that men who obtained more folate in their diets showed significantly less of a decline in verbal fluency skills over the course of three years than did men with lower dietary folate intake. High folate levels also appeared protective against declines in spatial copying. The effects of folate were independent of its impact on homocysteine, which turned out to be more strongly associated with tests of memory. Folate is a B vitamin found particularly in leafy green vegetables and citrus fruit.

[888] Tucker, K. L., Qiao N., Scott T., Rosenberg I., & Spiro A.
(2005).  High homocysteine and low B vitamins predict cognitive decline in aging men: the Veterans Affairs Normative Aging Study.
Am J Clin Nutr. 82(3), 627 - 635.

http://www.eurekalert.org/pub_releases/2005-09/tu-lgv092205.php

Preventing high levels of homocysteine may protect against age-related cognitive impairment

Previous studies have found a link between high levels of homocysteine and poor cognitive performance, but it has been difficult to work out just what the association is, in view of confounding factors such as cardiovascular risk factors and levels of folate, B12, and B6, all of which play a role in high levels of homocysteine. A new analysis has disentangled these factors, and has found that, in people over 60 (but not those under 60), higher levels of homocysteine are independently associated with lower levels of cognitive performance. Similarly, higher levels of vitamin B12 are associated with higher levels of cognitive performance. The researchers suggest vitamins B12, B6, and folate taken before 60 could help protect against later cognitive impairment.

[839] Wolf, P. A., Elias M. F., Sullivan L. M., D'Agostino R. B., Elias P. K., Jacques P. F., et al.
(2005).  Homocysteine and Cognitive Performance in the Framingham Offspring Study: Age Is Important.
Am. J. Epidemiol.. 162(7), 644 - 653.

http://www.eurekalert.org/pub_releases/2005-09/bu-atp092705.php

Folates more effective in limiting Alzheimer's disease risk than antioxidants, other nutrients

Analysis of data from the Baltimore Longitudinal Study of Aging has revealed that those with higher intake of folates, vitamin E and vitamin B6 had a lower risk of developing Alzheimer’s. When the three vitamins were analyzed together, only folates were associated with a significantly decreased risk. 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. No association was found between vitamin C, carotenoids (such as beta-carotene) or vitamin B-12 intake and decreased Alzheimer's risk.

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.

http://www.eurekalert.org/pub_releases/2005-08/uoc--fme081105.php

Moderately high homocysteine linked to Alzheimer’s risk

A study of 83 Alzheimer’s patients, 78 patients with vascular dementia, 64 stroke patients, and 71 healthy controls, found that elevated levels of homocysteine were associated with a more than five-fold increase in the risk for stroke, a nearly five-fold risk for vascualr dementia, and almost triple the risk for Alzheimer's disease. High blood levels of homocysteine have been found to be associated with an increased heart attack risk in several studies. High levels of homocysteine have been found to be associated with deficiencies in vitamin B12 and folate, and also with smoking.

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.

http://www.eurekalert.org/pub_releases/2002-10/aha-mhh092602.php

Study links high levels of homocysteine, and folic acid or vitamin B-12 deficiencies to cognitive decline

Current estimates suggest that more than one million elderly in Europe and about 750,000 elderly in North America become cognitively impaired each year. Recent research suggests that deficiencies of folate or vitamin B-12 and elevations of plasma homocysteine (tHcy) may be partly responsible. A British study of 331 participants in a longitudinal survey found significant negative effects on cognition in the elderly subjects who had deficiencies of folic acid or vitamin B-12 and elevated tHcy. In the older group (aged 76-78), increased levels of tHcy correlated both with lower serum folate and vitamin B-12 concentrations and with lower cognitive test scores. In the younger group (aged 61-63),higher folate concentrations correlated with higher scores on one of the assessment tests, but otherwise no effects of B vitamins or tHcy were apparent.
Green leafy vegetables, citrus fruits and juices, whole wheat bread and dry beans are good sources of folate.

[899] Duthie, S. J., Whalley L. J., Collins A. R., Leaper S., Berger K., & Deary I. J.
(2002).  Homocysteine, B vitamin status, and cognitive function in the elderly.
Am J Clin Nutr. 75(5), 908 - 913.

Smith, A.D. 2002. Homocysteine, B vitamins and cognitive deficit in the elderly. American Journal of Clinical Nutrition, 75,785-6.

http://www.eurekalert.org/pub_releases/2002-04/ajoc-nsa041902.php

Folic acid possibly a key factor in preventing Alzheimer's disease

Experiments with mice bred with mutant genes that cause Alzheimer's disease found that those mice fed on a diet deficient in folate had fewer neurons in the hippocampus ( a brain region critical for learning and memory that is destroyed as plaques accumulate during Alzheimer’s disease), and elevated levels of homocysteine. Researchers suspect that increased levels of homocysteine in the brain caused damage to the DNA of nerve cells in the hippocampus. In the mice fed an adequate amount of folate, nerve cells in this brain region were able to repair the damage. But in those mice fed a folate-deficient diet, nerve cells were unable to repair this damage. A human study is being planned.
Green leafy vegetables, citrus fruits and juices, whole wheat bread and dry beans are good sources of folate. In the U.S., since 1998, the Food and Drug Administration has required the addition of folic acid to enriched breads, cereals, flours, corn meals, pastas, rice, and other grain products.

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.

http://www.eurekalert.org/pub_releases/2002-03/nioa-fap030102.php

High homocysteine levels may double Alzheimer's risk

Findings from the long-running Framingham study found people with elevated levels of homocysteine in the blood had nearly double the risk of developing Alzheimer’s disease (AD). This study is the first to tie homocysteine levels measured several years before with later diagnosis of AD and other dementias, and provides the most powerful evidence yet of the link between high homocysteine levels and AD.

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.

http://www.eurekalert.org/pub_releases/2002-02/nioa-hhl021202.php

Research ties vitamin B12 and folate deficiencies with Alzheimer's disease

People with low levels of B12 or folate may have a higher risk of developing Alzheimer's disease. A 3-year Swedish study of 370 people 75-years-old and older found that more than half (46 out of 78) of those diagnosed with dementia during the timeframe of the study had both low levels of vitamin B12 or folate and Alzheimer's type dementia. Low vitamin B12 and folate levels have long been observed in elderly people, and it has been theorized that this vitamin deficiency might be tied to neurological or psychiatric disorders. This study breaks new ground by connecting these deficiencies with Alzheimer's disease.
Vitamins B12 and folate (a form of water-soluble vitamin B) are found in common foods. Vitamin B12 is naturally found in animal foods including fish, milk and milk products, eggs, meat, and poultry. Leafy greens such as spinach and turnip greens, dry beans and peas, fortified cereals and grain products, and some fruits and vegetables are rich food sources of folate.

[2416] Wang, H. - X., Wahlin Å., Basun H., Fastbom J., Winblad B., & Fratiglioni L.
(2001).  Vitamin B12 and folate in relation to the development of Alzheimer’s disease.
Neurology. 56(9), 1188 - 1194.

http://www.eurekalert.org/pub_releases/2001-05/AAoN-RtvB-0705101.php

High homocysteine levels are associated with decreased memory capability after age 60

Recent studies have linked Alzheimer disease and dementia after multiple strokes to extremely high serum homocysteine concentrations. A survey of 1299 men and women aged 60 and over, none of who had previously had a stroke, found an independent relationship between very high homocysteine levels and poor performance on cognitive tests. The folate status of the participants was checked as folate has been shown to significantly modify homocysteine levels. Story recall was worse among subjects with a combination of low folate and high homocysteine than in those whose homocysteine levels were normal or low. Homocysteine levels increased with age and were accompanied by a comparable decline in folate status. The researchers found independent associations between the highest levels of homocysteine and poorer recall. Among subjects with the highest level of homocysteine, the odds of passing a word delayed-recall test were identical whether their folate status was high or low.

[2415] Morris, M S., Jacques P. F., Rosenberg I. H., & Selhub J.
(2001).  Hyperhomocysteinemia associated with poor recall in the third National Health and Nutrition Examination Survey.
The American Journal of Clinical Nutrition. 73(5), 927 - 933.

http://www.eurekalert.org/pub_releases/2001-04/AJoC-Hhla-2504101.php

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