Diet

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

Mediterranean diet reduces brain shrinkage in old age

  • The Mediterranean diet is the diet most associated with cognitive and health benefits in older adults.
  • A new study has found larger brain volumes among those following this sort of diet, equivalent to that of brains five years younger.
  • Much of this was associated with two components of the diet in particular: eating fish regularly, and eating less meat.

Another study adds to the growing evidence that a Mediterranean diet is good for the aging brain.

The New York study used data from 674 non-demented older adults (average age 80). It found that those who closely followed such a diet showed significantly less brain shrinkage. Specifically, total brain volume was an average 13.11 milliliters greater, with grey matter volume 5 millilitres greater, and white matter 6.4 millilitres greater.

Eating at least five of the recommended Mediterranean diet components was associated with benefits equivalent to five years of age. By far the most important of these components was regular fish and reduced meat intake — at least 3 to 5 ounces of fish weekly; no more than 3.5 ounces of meat daily.

This is consistent with a considerable amount of research indicating the benefits of fish in fighting age-related cognitive decline.

http://www.theguardian.com/lifeandstyle/2015/oct/21/mediterranean-diet-may-slow-the-ageing-process-by-five-years

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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

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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

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