Diet linked to brain atrophy in old age

 

 

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.

Mounting evidence emphasizes the health benefits of a Mediterranean diet. New research suggests that the healthful diet helps to preserve brain volume in elderly adults.

A new study suggests that a Mediterranean diet could protect against certain changes to the brain in older age.

More and more studies seem to suggest that components of the Mediterranean diet, either in isolation or taken together, can have a beneficial effect on various aspects of human health.
The "traditional" Mediterranean diet - consisting of large amounts of fruits and vegetables, whole grains, olive oil, a moderate amount of fish, dairy, and wine, as well as a limited intake of red meat - has been shown to improve cardiometabolic health.
Research ranging from observational studies to randomized trials has shown the diet to reduce the risk of type 2 diabetes and obesity, aid weight loss, and contribute to the prevention of cardiovascular disease.
Other studies have suggested that the diet helps to keep mental and physical health well into old age and can reduce the risk of premature death.
New research published in Neurology, the medical journal of the American Academy of Neurology, looks specifically at the benefits of the Mediterranean diet on brain health in elderly adults.

Examining link between diet and brain volume in elderly people

Researchers led by Michelle Luciano, Ph.D. - from the University of Edinburgh in Scotland - looked at the effects of the Mediterranean diet (MeDi) on total brain volume, gray matter volume, and the thickness of the cortex.
The authors explain that, with age, the human brain shrinks, and more and more of its cells die. This may cause problems with learning and memory.
The study followed 967 people aged between 73 and 76 years, who lived in Scotland and who did not have dementia, over a period of 3 years.
The 967 participants were asked to complete food questionnaires when they were 70 years old - 3 years prior to collecting data on their brain volume.
Then, 562 of these people had a magnetic resonance imaging brain scan at the age of 73, in order to measure total brain volume, gray matter volume, and cortical thickness. Of these, 401 people had a second brain scan at age 76.
People's dietary habits were calculated using a food frequency questionnaire. The brain measurements were compared with how well the participants adhered to the MeDi during the 3-year period.

Mediterranean diet accounts for 0.5 percent of total brain volume change

The scientists found an association between MeDi adherence and brain volume.
Participants who did not follow the diet closely were likely to develop brain atrophy over the 3-year interval.
More specifically, poor adherence to the diet was associated with a 0.5 percent greater reduction in total brain volume than those who had followed the diet closely.
A 0.5 percent decrease in brain volume is half the size of what is considered a normal decrease due to the natural aging process.
Researchers adjusted for variables that might have influenced the changes in brain volume, including age, education, and health conditions such as diabetes or hypertension.
The study found no association between the diet and gray matter volume or thickness of the cortex.
Contrary to previous studies, this research did not find a relationship between fish and meat consumption and changes in brain volume. This suggests that other individual components of the diet - or all of its components taken in combination - might be responsible for the association.
Additionally, unlike previous research - which measured the brain at one point in time - this study examined changes in brain volume over time.

"In our study, eating habits were measured before brain volume was, which suggests that the diet may be able to provide long-term protection to the brain. Still, larger studies are needed to confirm these results."

Michelle Luciano, Ph.D.

Learn how a Mediterranean diet may slow cognitive decline and prevent Alzheimer's.

Written by Ana Sandoiu

Like your stash of leftover Halloween candy and your reserve of willpower for the day, there are a few things in life you really don't want to run out of.
Also at the top of that list: your gray (and white) matter. Obviously, your capacity to remember things and process information—abilities bestowed upon us by the robustness of our physical brains—holds a prize spot way higher up than those fun-size Snickers (at least, let's hope).

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For a while now, researchers have known that following a Mediterranean diet—one heavy on whole grains, fresh produce, and fatty fish and low in red meat and dairy—seems to ward off signs of looming cognitive decline. But in a new study published in the journal Neurology, researchers examined the effect of the diet "on the brain itself," says lead author Yian Gu, PhD, assistant professor of neuropsychology at Columbia University, "rather than clinical symptoms." (Boost your memory and age-proof your mind with these natural solutions.)
MORE: 9 Power Foods That Boost Immunity
Gu and her colleagues wanted to find out how the Mediterranean diet confers its cognitive benefits, and their research showed that the eating plan seems to be linked with a physically bigger brain. So much bigger, in fact, that sticking to the diet prevents the amount of decline researchers would expect to see naturally occur with 5 years of aging. (Here are 5 foods that are hurting your brain.)

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The researchers analyzed food questionnaires from 674 adults, ages 65 and older, without dementia who were part of ongoing aging research. Each person was scored on their intake of these components of the Mediterranean diet: veggies, legumes, whole grains, fish, fruit, nuts, monounsaturated fats, little red meat, little dairy, and moderate alcohol consumption. They were awarded 1 point for each component if they ate more of the good stuff or less of the bad stuff than the average person.
Brain MRIs showed that the 304 people who scored from 5 to 9 on the questionnaire had more brain volume than the 370 who scored from 0 to 4. Those Mediterranean eaters had on average 13.11 milliliter larger total brain volume, 5 milliliter larger volume of gray matter (the part of our brains that contains all our synapses), and 6.41 milliliter larger volume of white matter (which connects different areas of gray matter).
MORE: 11 Eating Rules To Rev Your Metabolism All Day Long
"Age so far is the most important factor contributing to brain shrinkage in older people," Gu says. "The difference between the high- and low-scoring Mediterranean diet groups is similar to the brain size difference between a 70-year-old and a 75-year-old."

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Even just eating 3 to 5 ounces of fish a week (choose from one of these 10 healthiest fish on the planet) and lowering red meat intake to 100 grams (roughly a quarter-pounder) a day or less offered a protective effect to the tune of 3 to 4 years of aging. "When gray and white matter shrinks, you basically can't process information, you get more forgetful, memory starts to become impaired," says cardiologist Michael Ozner, author of The Complete Mediterranean Diet. "As a result, your risk of Alzheimer's disease increases."
The Mediterranean way of eating is in stark contrast to the more traditional American diet. "I call it the 'toxic American diet'—highly processed, calorie-dense, and nutrient-depleted," Ozner says. While red meat's not completely off the table in Mediterranean eating, he says, it should probably be reserved for special occasions. (Here are healthy ways to eat red meat.) The traditional Mediterranean diet was low in red meat not because our ancestors knew one day it would be added to the World Health Organization's list of carcinogens, but simply because they couldn't afford it. "They'd have veal or lamb on birthdays or at weddings," he says.
MORE: 7 Weird Reasons You're Gaining Weight
We don't entirely understand how the Mediterranean diet might stop this kind of brain shrinkage, Gu says, but it's probably a melting pot of anti-inflammatory and antioxidant superpowers from the wide range of nutrients you'll get by eating more fish and more produce. (Here's how to pick perfect produce every shopping trip.) We also can't definitively say that the Mediterranean diet caused these larger brain sizes, according to the study authors. But the ever-growing wealth of scientific evidence favoring the Mediterranean diet makes it pretty much a, er, no-brainer, Ozner says. "We should be shouting this from the rooftops." Emphasizing nonprocessed meats, nonrefined carbohydrates, and unsaturated fats could not only keep our minds sharp, but could also help many of us avoid interventions like cardiac stents and bypass surgeries and meds like statins, he says. "Leave these things for people who absolutely need it. Everybody shouldn't have to have them."

  People who eat a diet rich in fish, fruits and vegetables but low in meat may lose fewer brain cells as they age, according to a new study.In the study of 674 older adults, the researchers looked at whether the participants' diets during the past year included the following nine components of the so-called Mediterranean diet: eating lots of vegetables, legumes, cereals, fish, fruits and nuts; consuming healthy monosaturated fats like olive oil but avoiding saturated fats; drinking moderate amounts of alcohol; and eating low amounts of meat and dairy products. The average age of the people in the study was 80.
The researchers scanned the participants' brains, and found that those whose diets included at least five of these nine components had brain volumes that measured 13.11 milliliters larger on the scans, on average, compared with the brain volumes of the people whose diets included fewer than five components.
This difference in brain volume between the two groups is equivalent to the amount of shrinkage that happens over five years of aging, the researchers said.
"These results are exciting, as they raise the possibility that people may potentially prevent brain shrinking and the effects of aging on the brain simply by following a healthy diet," study author Yian Gu, of Columbia University in New York, said in a statement.
When the researchers took a closer look at the relationship between brain shrinkage and the Mediterranean diet, they found that the diet's protective effect was driven to the greatest extent by two components: eating more fish and eating less meat.
This finding suggests that "eating at least 3 to 5 ounces of fish weekly or eating no more than 3.5 ounces of meat daily may provide considerable protection against loss of brain cells equal to about three to four years of aging," Gu said. [7 Ways the Mind and Body Change With Age]
None of the people in the new study had dementia. The researchers noted, however, that greater amounts of brain shrinkage have been linkedto a greater risk of cognitive decline.
The new study was observational, and more research is needed to examine the relationship between the Mediterranean diet and brain structure, Gu told Live Science. The new study does not prove that following the Mediterranean diet prevents brain shrinkage; rather, it shows there is a link between the two, she said.
The mechanism between the Mediterranean diet and a greater brain volume is not clear, but it may have something to do with the beneficial effects of nutrients present in the foods, the researchers said. For example, the omega-3 fats as well as vitamins B and D in fish have been shown to promote the growth of neurons and slow brain shrinkage, they said.
The new study was published today (Oct. 21) in the journal Neurology.

Cerebral atrophy is a common feature of many of the diseases that affect the brain.^[1] Atrophy of any tissue means a decrement in the size of the cell, which can be due to progressive loss of cytoplasmic proteins. In brain tissue, atrophy describes a loss of neurons and the connections between them. Atrophy can be generalized, which means that all of the brain has shrunk; or it can be focal, affecting only a limited area of the brain and resulting in a decrease of the functions that area of the brain controls. If the cerebral hemispheres (the two lobes of the brain that form the cerebrum) are affected, conscious thought and voluntary processes may be impaired.
Some degree of cerebral shrinkage occurs naturally with age; after the brain completes growth and attains its maximum mass at around age 25^{[citation needed]}, it gradually loses mass with each decade of life, although the rate of loss is comparatively tiny until the age of 60, when approximately .5 to 1% of brain volume is lost per year. By age 75, the brain is an average of 15% smaller than it was at 25. Some areas of the brain such as short-term memory are affected more than others and men lose more brain mass overall than women.^{[citation needed]}
Brain atrophy does not affect all regions with the same intensity as shown by neuroimaging.^[2]

Possible Causes and Associated Diseases and Disorders

The pattern and rate of progression of cerebral atrophy depends on the disease involved.

Injury

• Stroke, loss of brain function due to a sudden interruption of blood supply in the brain
• Traumatic brain injury
• Corticosteroid Use (There appears to be correlations between degree of dosing with corticosteroids and cerebral atrophy)^[3]

Diseases/Disorders

Pick's Disease showing brain atrophy,

• Alzheimer's disease (High resolution MRI scans have shown the progression of cerebral atrophy in Alzheimer's disease) ^[4]
• Cerebral palsy, in which lesions (damaged areas) may impair motor coordination
• Senile dementia, fronto-temporal dementia, and vascular dementia
• Pick’s disease, causes progressive destruction of nerve cells in the brain
• Huntington's disease, and other genetic disorders that cause build-up of toxic levels of proteins in neurons
• Leukodystrophies, such as Krabbe disease, which destroy the myelin sheath that protects axons
• Multiple sclerosis, which causes inflammation, myelin damage, and lesions in cerebral tissue
• Epilepsy, in which lesions cause abnormal electrochemical discharges that result in seizures
• Anorexia nervosa, bulimia nervosa, and other eating disorders
• Malnutrition, caused by lack or excess of nutrition from foods
• Type II Diabetes, where the body does not use insulin properly resulting in high blood sugar
• Mitochondrial encephalomyopathies, such as Kearns-Sayre syndrome, which interfere with the basic functions of neurons

Infections

Where an infectious agent or the inflammatory reaction to it destroys neurons and their axons, these include...

• Encephalitis, acute inflammation in the brain
• Neurosyphilis, an infection in the brain or spinal chord
• AIDS, disease of the immune system

Drug induced

• Neuroleptics

Symptoms

Many diseases that cause cerebral atrophy are associated with dementia, seizures, and a group of language disorders called the aphasias. Dementia is characterized by a progressive impairment of memory and intellectual function that is severe enough to interfere with social and work skills. Memory, orientation, abstraction, ability to learn, visual-spatial perception, and higher executive functions such as planning, organizing and sequencing may also be impaired. Seizures can take different forms, appearing as disorientation, strange repetitive movements, loss of consciousness, or convulsions. Aphasias are a group of disorders characterized by disturbances in speaking and understanding language. Receptive aphasia causes impaired comprehension. Expressive aphasia is reflected in odd choices of words, the use of partial phrases, disjointed clauses, and incomplete sentences.

Reducing the Risk and Treatment

Unfortunately, cerebral atrophy is not usually preventable, however there are steps that can be taken to reduce the risks such as controlling your blood pressure, eating a healthy balanced diet including omega-3's and antioxidants, and staying active mentally, physically, and socially.^[5]
While most cerebral atrophy is said to be irreversible there are some recent studies that show this is not always the case. A child who was treated with ACTH originally showed atrophy, but four months after treatment the brain was seemingly normal again.^[6]

Cerebral atrophy

Cerebral atrophy is a common complication of anorexia nervosa, a sequela of severe weight loss and lower body fat.  In brain tissue, atrophy describes the loss of neurons and neural pathways, negatively affecting conscious thought and voluntary processes. Cerebral atrophy affects memory, orientation, abstraction, ability to learn, and executive functions such as planning, organizing and sequencing. This complication leads to the erratic thoughts and behaviors of undernourished patients. Recent studies have demonstrated total brain volume increases significantly after patients are sustained at healthy weight.
 The Cognitive Function Test is a free online screening test that checks four key types of cognitive ability that decline in dementia.
If your score isn’t great you’ll get a letter to take to your GP recommending homocysteine testing. If your homocysteine level is above 10mcmol/l you’ll be advised to supplement with B vitamins. Homocysteine testing can be carried out by your doctor. You can also do it privately through many laboratories, or with a home test kit from www.yorktest.com.

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You can also start to follow our '6 Alzheimer's Prevention Steps' which are outlined below:

The 6 Alzheimer's Prevention Steps

Eating one serving of oily fish a week is associated with halving the risk of Alzheimer’s.[1] Supplements of one kind of omega 3 fish oil, called DHA, have been shown to enhance memory in adults[2] who don’t eat fish, and to prevent memory loss in those in the early stages of memory decline.[3] But it’s not just oily fish. The more fish you eat, the better your memory test performance. Fish is also an excellent source of vitamins B12[4][5], D and choline, all essential for the brain. Chia and flax seeds are also an excellent source of omega 3. Back to 6 steps

The more fruit and vegetables you eat the lower is your risk of cognitive decline[6] with vegetables being particularly protective.[7] The best kinds of vegetables are carrots, cauliflower, broccoli, Brussels sprouts, cabbage, spinach and mushrooms. The best fruits are berries, especially blueberries and strawberries.[8] Flavonoids and polyphenols, found not only in fruit and vegetables, but also in tea, red wine and dark chocolate, are associated with preserving memory[9]and a number of mechanisms exist to explain their positive actions on cognitive performance.[27] The most protective effect is found eating six servings (500g) a day of fruit and vegetables.[7] Supplementing both vitamin C (1g) and vitamin E combined is associated with halving the risk of Alzheimer’s disease.[10] Back to 6 steps

Keeping your blood sugar level down, which also means you make less insulin, preserves your memory.[11] That means avoiding sugar as much as possible and eating slow-releasing ‘whole’ carbohydrate foods such as wholegrain bread or pasta and oat cakes. Eating white bread is associated with a poorer cognitive test performance, whereas high fibre bread is associated with better performance.[7] Eating carbohydrate foods with protein, for example brown rice with fish, or porridge oats with seeds, further reduces the glycemic load (GL) of a meal. Best fruits in this respect are berries, cherries and plums while grapes, raisins and bananas are high GL. These kinds of foods are consistent with a Mediterranean diet which has also been shown to reduce risk.[12] Eat your fruit, don’t drink it. Fruit juice has a lot of sugar in it. Back to 6 steps

Having a higher intake and blood level of vitamin B12 and folic acid is associated with a quarter of the risk of developing Alzheimer’s.[13] Vitamin B6, B12 and folic acid, especially in combination, lower blood levels of homocysteine, which is a key predictor of risk. [14]Lowering your homocysteine, if above 10mcmol/l, by supplementing high dose B6 (20mg), folic acid (800mcg) and B12 (500mcg) has been shown to greatly reduce the rate of brain shrinkage[15] and memory loss[16] in those at risk of Alzheimer’s. That is why it is VITAL to check your homocysteine level and, if above 10, speak with your doctor about supplementing high doses of B vitamins. Otherwise, supplement a daily multivitamin or B complex. B12 absorption can greatly worsen with age, and is inhibited by the diabetes drug metformin[17], and antacid ‘proton-pump inhibitor’ (PPI) medication[18]. If you are taking these be sure your GP checks your homocysteine level. Back to 6 steps

While there is inconsistent evidence linking coffee with more or less risk, drinking lots of coffee both raises homocysteine levels[19] and promotes the excretion of protective B vitamins.[20] For example, two cups of coffee raises homocysteine by 11% in 4 hours.[21] Green tea on the other hand, is associated with a lower risk of cognitive impairment. [22]Ordinary tea drinking is also associated with better cognition.[23] Our advice is to limit coffee to one a day and drink tea, ideally green, instead. Back to 6 steps

Keeping fit,[24] learning new things to stimulate your mind and staying in touch with friends and family all help to reduce your risk. If you don’t use it you lose it. There may also be a benefit in exercises that require more mind-body coordination, such as t’ai chi[25] or yoga, and exercising outdoors – we make vitamin D in the presence of sunlight. These activities also help to reduce stress, which is another prevention step in the right direction, as is keeping your blood pressure down.[26] Back to 6 steps

 

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Food for the Brain seeks to increase funding for research on prevention of Alzheimer's disease, with the aim of vastly reducing the numbers of people having to endure this disease. This statement, signed by over 100 scientists from 136 countries, calls upon the governments of the G8 countries to make prevention of dementia one of their major health aims; it was written by the Head of Food for the Brain's Scientific Advisory Board, Professor David Smith, and published in the Journal of Alzheimer's Disease in December, 2013. Dementia (Including Alzheimer’s Disease) can be Prevented: Statement Supported by International Experts.

Ageing causes changes to the brain size, vasculature, and cognition. The brain shrinks with increasing age and there are changes at all levels from molecules to morphology. Incidence of stroke, white matter lesions, and dementia also rise with age, as does level of memory impairment and there are changes in levels of neurotransmitters and hormones. Protective factors that reduce cardiovascular risk, namely regular exercise, a healthy diet, and low to moderate alcohol intake, seem to aid the ageing brain as does increased cognitive effort in the form of education or occupational attainment. A healthy life both physically and mentally may be the best defence against the changes of an ageing brain. Additional measures to prevent cardiovascular disease may also be important.

Keywords: ageing, brain, cognition

The effects of ageing on the brain and cognition are widespread and have multiple aetiologies. Ageing has its effects on the molecules, cells, vasculature, gross morphology, and cognition. As we age our brains shrink in volume, particularly in the frontal cortex. As our vasculature ages and our blood pressure rises the possibility of stroke and ischaemia increases and our white matter develops lesions. Memory decline also occurs with ageing and brain activation becomes more bilateral for memory tasks. This may be an attempt to compensate and recruit additional networks or because specific areas are no longer easily accessed. Genetics, neurotransmitters, hormones, and experience all have a part to play in brain ageing. But, it is not all negative, higher levels of education or occupational attainment may act as a protective factor. Also protective are a healthy diet, low to moderate alcohol intake, and regular exercise. Biological ageing is not tied absolutely to chronological ageing and it may be possible to slow biological ageing and even reduce the possibility of suffering from age related diseases such as dementia.

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Physical changes

It has been widely found that the volume of the brain and/or its weight declines with age at a rate of around 5% per decade after age 40¹ with the actual rate of decline possibly increasing with age particularly over age 70.² The manner in which this occurs is less clear. The shrinking of the grey matter is frequently reported to stem from neuronal cell death^3,4,5 but whether this is solely responsible or even the primary finding is not entirely clear.⁶ It has been suggested that a decline in neuronal volume rather than number contributes to the changes in an ageing brain and that it may be related to sex with different areas most affected in men and women.⁷ Additionly, there may be changes in dentritic arbour, spines, and synapses. Dendritic sprouting may occur thus maintaining a similar number of synapses⁵ and compensating for any cell death.⁴ Conversely a decrease in dendritic synapses or loss of synaptic plasticity has also been described.⁸ Functional organisational change may occur and compensate in a similar way to that found in patients after recovery from moderate traumatic brain injury.⁹ However research in the latter area suffers from small numbers of cases. The role of white matter in the ageing brain also needs to be considered.³ White matter may decline with age, the myelin sheath deteriorating after around the age of 40 even in normal ageing and it has been suggested that the late myelinating regions of the frontal lobes are most affected by white matter lesions (WML)^10,11,12) although not all studies support this view.¹³ Leukoariosis/WML increase with age and may indicate subclinical ischaemia. They will be discussed in more detail below.

Brain changes do not occur to the same extent in all brain regions.⁶ That these brain changes are not uniform is supported by a longitudinal study, using two MRI scans separated by around one or two years,² and by a review of cross sectional studies. The latter included only those studies that compared younger (aged less than 30) and older (greater than 60) groups to compare wider age ranges and in contrast with much of the other work in this area. The review looked at volume and found that the prefrontal cortex was the most affected. The striatum came second with the analysis including over seven studies. The temporal lobe, cerebellar vermis, cerebellar hemispheres, and hippocampus also reduced volume with between 8 and 18 studies and the prefrontal white matter also showed a reduction (five studies). The occipital cortex was the least affected (five studies).³ The finding that the prefrontal cortex is most affected and the occipital least, fits well with the cognitive changes seen in ageing, although some studies also suggest that ageing has the greatest effect in the hippocampus.^4,8 Men and women may also differ with frontal and temporal lobes most affected in men compared with the hippocampus and parietal lobes in women.^7,14 Finally the rate of reduction in brain volume may increase with age particularly over 70 although numbers studied are very small.² Because of the individual differences seen in brain development and ageing¹⁵ mapping structure to function and change because of ageing is a complex task,¹⁶ however there are studies that show links between volume and neuropsychological function. A study looking at cortical volume and white matter hyperintensity volume in 140 people aged 50 to 81 years pre‐screened for dementia and depression, found an association between increasing age, a reduction in prefrontal cortical volume, increased subcortical white matter lesions, and an increase in perseverative behaviour (decreased executive function).¹⁷

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Cognitive change

The most widely seen cognitive change associated with ageing is that of memory. Memory function can be broadly divided into four sections, episodic memory, semantic memory, procedural memory, and working memory.¹⁸ The first two of these are most important with regard to ageing. Episodic memory is defined as “a form of memory in which information is stored with ‘mental tags', about where, when and how the information was picked up”.¹⁹ An example of an episodic memory would be a memory of your first day at school, the important meeting you attended last week, or the lesson where you learnt that Paris is the capital of France. Episodic memory performance is thought to decline from middle age onwards. This is particularly true for recall in normal ageing and less so for recognition.²⁰ It is also a characteristic of the memory loss seen in Alzheimer's disease (AD).¹⁸

Semantic memory is defined as “memory for meanings”, for example, knowing that Paris is the capital of France, that 10 millimetres make up a centimetre, or that Mozart composed the Magic Flute.¹⁹ Semantic memory increases gradually from middle age to the young elderly but then declines in the very elderly.²⁰ It is not yet clear why these changes occur and it has been hypothesised that the very elderly have less resources to draw on and that their performance may be affected in some tasks by slower reaction times, lower attentional levels, slower processing speeds, detriments in sensory and or perceptual functions, or potentially a lesser ability to use strategies.^20,21,22,23

There have been studies investigating different types of memory in ageing using neuropsychological testing and neuroimaging. However, it must be pointed out that it is sometimes methodologically difficult to separate some of these functions, for example episodic memory encoding and semantic memory retrieval.²⁴ Despite this studies are beginning to examine performance on memory tasks with ageing and by neuroimaging. A review article focusing in this area highlighted the changes in regional brain activation.²⁴ Older brains tend to show more symmetrical activation, either because they have increased activation in a hemisphere that is less activated than in younger adults or because they show reduced activation in the areas most activated in younger adults. This has been shown for visual perception and in memory tasks.²⁴ The observed changes in activation in the left and right prefrontal cortex are in keeping with changes in memory performance, particularly episodic memory, as this is thought to be based in this area.²⁴ It has also been suggested that the actual level of brain activation, as shown in neuroimaging, may be related more directly to the levels of memory performance.²⁵ A review of studies using electroencephalograms to examine event related potentials in response to stimuli also contribute some support for increased symmetry in brain activation with age.²⁶

The increased symmetrical hemispheric activation is a robust finding and has been referred to as HAROLD or hemispheric asymmetry reduction in older adults. It is not clear whether this change is an attenuation of the response seen in younger subjects, an inability to recruit specific areas, or an attempt to compensate for the ageing process.^21,23,25 This change in activation occurring in the frontal lobes fits with changes in memory performance and with the possible white matter changes referred to above, however, other factors such as changes in neurotransmitter or hormone levels also require consideration.

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Mechanisms of change

The neurotransmitters most often discussed with regard to ageing are dopamine and serotonin. Dopamine levels decline by around 10% per decade from early adulthood and have been associated with declines in cognitive and motor performance.^20,27 It may be that the dopaminergic pathways between the frontal cortex and the striatum decline with increasing age, or that levels of dopamine itself decline, synapses/receptors are reduced or binding to receptors is reduced.²⁰ Serotonin and brain derived neurotrophic factor levels also fall with increasing age and may be implicated in the regulation of synaptic plasticity and neurogenesis in the adult brain²⁸ A substance related to neurotransmitter levels, monoamine oxidase, increases with age and may liberate free radicals from reactions that exceed the inherent antioxidant reserves.²⁹ Other factors that have been implicated in the ageing brain include calcium dysregulation,³⁰ mitochondrial dysfunction, and the production of reactive oxygen species.³¹

Another factor to consider with regard to the ageing brain and its cognitive performance is hormonal influence. It is known that sex hormones can affect cognitive processes in adulthood and that changes in sex hormones occur in ageing particularly in women at menopause. Women also have a higher incidence of AD even when longer life expectancy is taken into account.¹⁴ AD is characterised by failing memory and there has been a suggestion that oestrogen therapy may increase dopaminergic responsivity³² and play a protective part in AD.^33,34 It must be remembered though that the use of HRT has recently been shown to have cancer risks.³⁵ Growth hormone levels also decline with age and may be associated with cognitive performance although the evidence is far from clear.³⁶

The ageing brain may also suffer from impaired glucose metabolism²⁰ or a reduced input of glucose or oxygen as cerebrovascular efficiency falls, although reduction in glucose may partly be attributable to atrophy rather than any change in glucose metabolism.³⁷ Change in vasculature is important and another common finding in elderly brains related to ischaemia are white matter lesions and stroke.

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Vascular factors and dementia

WML, strokes, and dementia increase with increasing age.^10,12,38,39 WML show levels of heritability,⁴⁰ are common in the elderly even when asymptomatic and are not the benign finding they were once thought to be.^11,41 For a review see Hsu‐Ko.⁴² WML or hyperintensities are related to increased cardiovascular risk^13,42 and a reduction in cerebral blood flow, cerebral reactivity,⁴³ and vascular density although it is unclear if the WML prompt the vessel loss or vice versa.⁴⁴ They may also associated with further tissue changes in grey matter visible when using magnetisation transfer magnetic resonance imaging.⁴⁵ WML are found more in frontal rather than posterior brain regions in keeping with cognitive and morphological findings discussed above^10,12) and the fact that WML are related to poor cognition has been shown.^13,41,46 Other damage associated with ageing and related to blood pressure and vascular factors include strokes and small vessel disease. Moderate to high 24 hour ambulatory blood pressure has been related to increased brain atrophy as has increased variability of systolic blood pressure.⁴⁷ In Japanese subjects raised systolic blood pressure was related to grey matter volume loss in a cross sectional study⁴⁸ and in the Framingham offspring cohort an increased 10 year risk of first stroke was associated with decrements in cognitive function.³⁸ The authors suggest that this may be attributable to cerebrovascular related injuries, accelerated atrophy, white matter abnormalities, or asymptomatic infarcts.³⁸ That cerebral vasculature could be related to cognitive function is not surprising because microvasculature ability to respond to metabolic demand falls with increasing age and moreover functional adult neurogenesis^49,50 may be related to good capilliary growth. For reviews see Lie et al and Riddle et al.^51,52 In addition to this there have been many links made between dementia, even AD, and vascular risk factors.^53,54,55

Increasing evidence points to vascular factors not only contributing to cognitive problems in ageing but also to the two most common dementias seen in this population. The prevalence of dementia increases almost exponentially with increasing age with around 20% of those aged 80 affected rising to 40% of those aged 90.³⁹

The dementia types seen most frequently in the elderly are AD accounting for around 40%–70% of dementias, and vascular dementia (VaD) 15%–30%.^39,56 In recent years, it has seemed increasingly likely that there is an overlap between these two dementias⁵⁷ and there have been calls for AD to be reclassified as a vascular disorder⁵⁸ or for dementia to become a multifactorial disorder⁵⁹ A postmortem study found that 77% of VaD cases showed AD pathology⁶⁰ and high blood pressure has been associated with increased neurofibrilliary tangles characteristic of AD.⁶¹ Multiple types of vascular pathology have been associated with AD including microvascular degeneration, disorders of the blood‐brain barrier, WML, microinfarctions, and cerebral haemorrhages.⁶² It has been suggested that large vessel factors, for example, atherosclerosis, increase the risk of AD⁶³ and may play a part in cerebral vessel amyloid deposition.⁶⁴ AD patients do show significantly higher levels of cerebrovascular pathology when compared with controls at postmortem examination⁶⁵ although this did not correlate with severity of cognitive decline. A similar finding, that small infarcts in AD do not affect the rate of cognitive decline,⁶⁶ suggests that vascular factors may unmask or magnify underlying AD pathology,^62,67 or shorten the pre‐clinical phase of AD, at least in Western populations.⁶⁸ Alternatively multiple risk factors may be acting together.^69,70 The characteristic neurofibrilliary tangles and plaques found in AD are also evident to some degree in most elderly brains at postmortem examination even those without symptoms, as are white matter lesions.⁷¹

The issue of normal ageing is a difficult one because there are studies that show cognitively intact adults aged 100,^72,73 and yet a high percentage suffer from dementia and the line between mild cognitive impairment and normal memory changes⁷⁴ is still a little blurred.^75,76 What is in no doubt is that changes in brain vasculature, WML and intra/extra cellular changes are likely to begin in midlife.⁷¹ There are many influences on the ageing brain, genetics, biological, and environmental influences all of which contribute to the physiological and cognitive changes^77,78; Mattson⁷⁹ provided a review.

Risk factors that have been put forward with regard to ageing and development of dementia include hypertension, diabetes, hyperhomocysteinaemia, and a high cholesterol although the evidence for all but hypertension is far from clear.^{80,81,82,83,84,85,86,87} Protective factors include diet, alcohol, exercise, and intellectual pursuits.

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Protective factors

That diet may have a part to play in biological ageing and the development of cognitive decline is raised by studies showing that a diet higher in energy and lower in antioxidants is a risk factor⁸⁸ alongside studies showing that energy restriction may prolong life,^79,89 reduce oxidative damage,⁹⁰ or ameliorate/protect against cognitive decline.^79,89,91 Increased consumption of fish and seafood, even only once a month, may be protective and reduce stroke.⁹² Consumption of antioxidant supplements⁹³ may be protective although the evidence for other preparations purported to aid cognitive function, such as ginkgo biloba or piracetam is mixed.⁹⁴ In addition to a healthy diet, low to moderate alcohol intake may reduce cardiovascular risk and may stimulate the hippocampus. Alcohol seems to show a U or J shaped curve such that teetotal people or heavy drinkers are disadvantaged whereas moderate drinkers show reduced WML, infarcts, and even dementia.^95,96,97,98 Exercise is also beneficial and studies have shown increasing executive functioning and even reduction in the ageing expected decline of white and grey tissue density with increased fitness.^99,100 As is shown by the studies mentioned above, biological age is not always synchronised with chronological age particularly with regard to cardiovascular risk factors.¹⁰¹ Lower cardiovascular risk may be linked to lower biological age and vice versa. Another factor to consider with regard to cognitive decline is the effect of intelligence and environmental factors such as schooling and occupation contributing to a cognitive reserve that protects against decline despite neuropathology^{22,102,103,104} although there is not total support for this theory.¹⁰⁵

Epidemiological evidence linking diet, one of the most important modifiable environmental factors, and risk of Alzheimer's disease (AD) is rapidly increasing. Several studies have shown that higher adherence to a Mediterranean diet (MeDi) is associated with reduced risk of AD. This study examines the associations between high vs. lower adherence to a MeDi and structural MRI-based brain atrophy in key regions for AD in cognitively normal (NL) individuals with and without risk factors for AD.

DESIGN:

Cross-sectional study.

SETTING:

Manhattan (broader area).

PARTICIPANTS:

Fifty-two NL individuals (age 54+12 y, 70% women) with complete dietary information and cross-sectional, 3D T1-weighted MRI scans were examined.

MEASUREMENTS:

Subjects were dichotomized into those showing higher vs. lower adherences to the MeDi using published protocols. Estimates of cortical thickness for entorhinal cortex (EC), inferior parietal lobe, middle temporal gyrus, orbitofrontal cortex (OFC) and posterior cingulate cortex (PCC) were obtained by use of automated segmentation tools (FreeSurfer). Multivariate general linear models and linear regressions assessed the associations of MeDi with MRI measures.

RESULTS:

Of the 52 participants, 20 (39%) showed higher MeDi adherence (MeDi+) and 32 (61%) showed lower adherence (MeDi-). Groups were comparable for clinical, neuropsychological measures, presence of a family history of AD (FH), and frequency of Apolipoprotein E (APOE) ε4 genotype. With and without controlling for age and total intracranial volume, MeDi+ subjects showed greater thickness of AD-vulnerable ROIs as compared to MeDi- subjects (Wilk's Lambda p=0.026). Group differences were most pronounced in OFC (p=0.001), EC (p=0.03) and PCC (p=0.04) of the left hemisphere. Adjusting for gender, education, FH, APOE status, BMI, insulin resistance scores and presence of hypertension did not attenuate the relationship.

CONCLUSION:

NL individuals showing lower adherence to the MeDi had cortical thinning in the same brain regions as clinical AD patients compared to those showing higher adherence. These data indicate that the MeDi may have a protective effect against tissue loss, and suggest that dietary interventions may play a role in the prevention of AD.

Even if you seem perfectly healthy, you may be losing as much as 0.4% of your brain mass every year.^1,2 The rate of brain shrinkage increases with age and is a major factor in early cognitive decline and premature death.^2-7
Studies show that older adults with significant brain shrinkage are much more likely to have cognitive and movement disorders than similarly aged people with normal brain size. They are also at an increased risk of vascular death and ischemic stroke.^4,8-10
In addition, atrophy of specific brain regions has been associated with a variety of cognitive, behavioral, and mental health problems. Shrinkage of the temporal lobes, for example, is associated with a 181% increase in the risk of major depression.⁷
Perhaps most alarmingly, brain shrinkage sharply increases risk of early death:

• Younger individuals with overall brain shrinkage have as much as a 70% increase in the chance of dying,⁵
• In a study of people aged 85, temporal lobe atrophy is associated with a 60% increase in the risk of dying,²
• Severe atrophy of the frontal lobe (behind the forehead) increases the risk of death by 30%.²

Brains also shrink from the inside out, resulting in enlargement of the fluid-filled ventricles, or hollow spaces on the interior of the brain; such shrinkage has its own modest effect on early death.²
Even though brain shrinkage is progressive, a growing number of neuroscientists believe that brain shrinkage can be slowed or even reversed.^11-13 In this article, we will share with you how lifestyle changes and proper supplementation can help prevent this devastating cause of cognitive decline and premature death.

 

Brain Shrinkage Is Not Inevitable

Like so many of the symptoms of aging, brain shrinkage was long thought to be simply an inevitable consequence of growing older. However, we are learning that brain atrophy is by no means inevitable. A host of conditions—from cardiovascular disease and diabetes to sleep and anxiety disorders to lifestyle choices—have been associated with brain shrinkage. Since many of these are reversible or at least preventable, it’s important to understand their impact on brain shrinkage, cognition, and life span.

What you need to know

Protect Against Brain Shrinkage

• Your brain is shrinking as you age, costing you memories and mental sharpness.
• Worse, brain shrinkage has been directly associated with premature death.
• Causes of brain shrinkage are closely related to symptoms of aging, including cardiovascular disease, obesity, diabetes, and even poor sleep habits and distress.
• You may be able to prevent brain shrinkage by adopting healthy lifestyle habits and using supplements that target your own aging body’s vulnerabilities.
• Supplements that reduce your cardiovascular risk, lower your blood sugar, or improve your sleep, for example, may do double duty in slowing or stopping brain shrinkage and improving your chances for a long, mentally fit life.

The Connection Between Cardiovascular Disease And Brain Shrinkage

 

Although we don’t often hear about this, there is a strong connection between cardiovascular disease and brain shrinkage.
Perhaps the most obvious connection is the one between blood vessel disease (atherosclerosis) and brain volume. Atherosclerosis occurs when plaque builds up inside your arteries and restricts blood flow throughout the body. Although we typically think of the negative effect atherosclerosis has on the heart, its effect on your brain can be equally devastating.
When blood flow to the brain is restricted, your brain receives less oxygen and fewer nutrients, causing it to shrink. Studies show that people with lower levels of blood flow to the brain have smaller total brain volumes and total thickness of the cortex (the active surface layer of the brain)—resulting in poorer performance on tests of cognitive function.¹⁴
In addition, disease of the coronary arteries (the arteries that feed the heart muscle) is also associated with decreased brain volume. When compared to healthy controls, patients with coronary artery disease had significantly smaller gray matter volume in several regions of their brains.¹⁵ This is especially significant since gray matter is where all thinking, feeling, sensory, and motor function originates.
The relationship between cardiovascular disease and brain volume operates in both directions: People with smaller brain volumes have been found to have a 58% increase in the risk of death from all causes, a 69% increase in risk of vascular death, and a 96% increase in the risk of stroke, compared with those having normal brain volumes.¹⁰
Several other risk factors commonly associated with cardiovascular disease may also predict brain shrinkage. For example, people carrying the ApoE4 gene variant have significantly smaller overall brain size—with a specific decrease in brain areas that process memory and emotion.¹⁶
High levels of the amino acid homocysteine, another risk factor typically associated with heart disease, have now also been connected to brain shrinkage (independent of its impact on cardiovascular disease).
Specifically, studies have shown that people with high levels of homocysteine have smaller volumes of gray matter in the brain—and as a result, have worse scores on many tests of cognitive function.¹⁷
This was especially evident in a study of a group of people who had recently suffered strokes. The researchers found that those with the highest homocysteine levels had a tremendous 8.8-fold increase in risk of brain shrinkage (compared with those having the lowest).¹⁸ Other studies have demonstrated that the higher the level of plasma homocysteine, the greater the rate of brain atrophy and the risk for Parkinson’s and Alzheimer’s diseases.^19-22
A deficiency of B vitamins has also been tied to brain shrinkage. This makes sense, since inadequate amounts of vitamins B6, B12, and folic acid can lead to elevated homocysteine levels. This occurs because these vitamins play a role in converting homocysteine into an important protein building block and when there’s a shortage of B vitamins, that conversion process isn’t as efficient, and homocysteine levels increase.^13,23
Close associations have been found between low levels of folate, for example, and severe gray matter atrophy and atrophy of the hippocampus, a main memory-processing center in the brain.^24,25 Similarly, people with lower vitamin B12 levels have been shown to have progressive brain atrophy, with rates of brain volume loss 517% greater than those with higher levels.^13,26
Remarkably, it has been found that brain shrinkage due to high homocysteine levels must reach a critical level before cognitive decline sets in.²¹ This is another example of the “therapeutic window of opportunity” during which brain shrinkage may be prevented by adequate supplementation, as we’ll see later.²⁷

The Connection Between Diabetes And Brain Shrinkage

 

Diabetes is notorious for causing problems with the peripheral nervous system,²⁸ leading to conditions such as painful diabetic neuropathy and blindness-inducing diabetic retinopathy. New findings suggest that high blood sugar levels—and the advanced glycation end products (AGEs) that they produce—cause damage to the central nervous system as well, specifically neurodegeneration and brain atrophy.^29-31
Studies have shown that, when compared to nondiabetic people of similar age, diabetics have an average of 4% smaller hippocampal volume, a nearly 3% reduction in whole brain volume, and double the risk of mild cognitive impairment.^32,33
In addition to causing brain shrinkage, studies now suggest that diabetes induces toxic, misfolded proteins quite similar to those found in neurodegenerative diseases such as Alzheimer’s, pointing to yet another way that diabetes can damage brain cells.³⁴ Indeed, diabetes and Alzheimer’s disease share many properties, including defective insulin release and signaling, impaired glucose uptake from the blood, increased oxidative stress, stimulation of brain cell death by apoptosis,^35,36 blood vessel abnormalities, and problems with energy production in mitochondria.^37,38

Obesity And Your Brain

Like diabetes, obesity is a known cause of brain atrophy.³⁹ Even in people with normal cognition, higher body mass index (BMI, a measure of obesity) is associated with lower brain volume in obese and overweight people.⁴⁰
Obesity and diabetes share many similar mechanisms, including insulin resistance and oxidative stress, both of which are known to contribute to brain atrophy.^38,41 In addition, fat deposits produce huge amounts of inflammatory signaling molecules (cytokines) that may contribute to brain cell death and brain volume loss.³⁹
Additional links between obesity and brain shrinkage may be even more fundamental. About 46% of Western Europeans and their descendants carry a gene variant called FTO, which is associated with fat mass and obesity. People who carry this gene weigh on average about 2.64 pounds more and have an extra half-inch of waist circumference compared to those who lack the gene variant.⁴² Recent findings show that carriers of the FTO gene variant have approximately 8% smaller frontal lobe volumes, and 12% smaller occipital (back of the brain) volumes than people who don’t carry this gene variant. These changes were not associated with differences in cholesterol levels or blood pressure, suggesting an independent relationship.⁴²

Sleep Disruptions

Sleep disruptions and anxiety also contribute to loss of brain volume. Relatively healthy older adults with short sleep duration have significantly smaller brains than those with longer sleep duration. In addition, for every hour of reduced sleep duration, they experience a 0.59% yearly increase in the size of the blood-filled ventricles, and a 0.67% decrease in cognitive performance.⁴³ Similarly, increases in brain shrinkage are associated with decreased quality of sleep as well.⁴⁴
Poor sleep and anxiety, of course, are related, and one study has shown that middle-aged women who have had longstanding psychological distress (based on a standard questionnaire) are at a 51% increased risk of moderate-to-severe atrophy of the temporal lobes.⁶

Smoking And Drinking

Smoking has been recognized as a cause of brain shrinkage since at least 1987.^45,46 More recent studies have confirmed and extended this association, with evidence that any lifetime history of smoking (even if you currently do not smoke) is associated with faster brain shrinkage in multiple brain regions, compared with people who never smoked.⁴⁷
Chronic alcohol consumption has also been associated with brain shrinkage, but in a dose-dependent way. While light-to-moderate drinkers have larger total brain volume than nondrinkers,⁴⁸ heavy drinkers are 80% more likely than nondrinkers to sustain frontal lobe shrinkage, compared with nondrinkers,⁴⁹ and 32% more likely to have enlargement of the ventricles, indicating shrinkage from within.⁵⁰ (A heavy drinker is defined as someone who consumes more than about 15 ounces of pure alcohol per week. A standard drink is equal to 14.0 grams, or 0.6 ounces, of pure alcohol.)

Natural Supplements That Protect Brain Volume

 

Even though the array of factors that can cause brain shrinkage can be daunting, there is good news. Since brain shrinkage results from the same basic processes that cause other symptoms of aging, it’s likely that brain shrinkage is preventable—especially when caught early enough.
That’s why we want to provide you with information on key nutrients that have been shown to powerfully protect the brain. Here are four of the most potent brain-protecting nutrients.

B Vitamins

B vitamins are essential for supporting normal metabolic function, especially in the regulation of homocysteine⁵¹ (and elevated homocysteine, as we have seen, leads to significant brain shrinkage and dementia, especially when B-vitamins are deficient).^18,27,52,53
Elderly people are now generally advised to maintain optimal B-vitamin status—and for good reason.^13,54 Studies show that people with higher folate levels have slower rates of brain atrophy and a lower rate of conversion from mild cognitive impairment to actual dementia, and those who take folate or B12 have lower grades of brain white matter abnormalities.^53,55
While each of these B vitamins provides its own unique benefits, several recent studies show why it’s beneficial to supplement with a combination of folate, vitamin B6, and vitamin B12. This was clearly seen in a double-blind, placebo-controlled clinical trial in adults over age 70 who had mild cognitive impairment.⁵⁶
For the study, one group of subjects took folate (800 mcg/day), vitamin B12 (500 mcg/day), and vitamin B6 ( 20 mg/day), while the other group took placebo.⁵⁶ After two years, supplemented patients’ brains shrank at an annual rate that was 30% slower than those taking the placebo. Supplemented patients whose homocysteine levels were abnormally high at baseline had a 53% slower brain shrinkage rate than unsupplemented patients, showing that supplementing with B vitamins is especially important in people who have high homocysteine levels.
A follow-up study showed that brain areas most susceptible to atrophy in the early development of Alzheimer’s disease are especially well-protected by the same B-vitamin regimen, with supplemented patients experiencing as much as a 7-fold reduction in shrinkage of those regions.⁵⁷ Another study, using the same doses of B vitamins, found that supplemented patients had 30% lower mean plasma homocysteine levels, and slower rates of cognitive decline on multiple standard tests.⁵⁸

Omega-3 Fatty Acids

 

Omega-3 fatty acids comprise a large and important portion of brain cell membranes, where they participate in a wide variety of cellular functions. Indeed, 30 to 50% of the fatty acids in brain cell membranes are long-chain polyunsaturated fatty acids that include the vital omega-3 group. Brain cell membranes are especially rich in DHA, an essential fatty acid derived only from the diet.^59,60
Omega-3s have many functions that help protect brain cells. Omega-3 fats are known to enhance the brain’s relaxing functions.⁶¹ This protects brain cells from overexcitation, which is a major cause of brain cell damage that occurs with aging.⁶² Omega-3s also help preserve brain cell function by increasing the production of anti-inflammatory signaling molecules in the brain.^59,63 Similarly, omega-3 fats in brain tissue protect cells from damage induced by stress and elevated stress steroids.⁶³
The importance of this protection is especially seen when there’s not enough of this vital nutrient. Indeed, abnormal distributions of fatty acids in brain cells are associated with a variety of mental health disorders, particularly major depression and bipolar disorder.⁶⁴
It is not surprising, then, that age-related changes in brain cell omega-3 fat composition raise the risk of brain abnormalities as people age.⁶⁵ By contrast, studies show that a higher omega-3 index (which is the sum of the omega-3 fats EPA plus DHA), is correlated with larger brain volume.⁶⁶
Unfortunately, aging is associated with a significant decline in DHA levels in the brain, a drop that is sharply worsened in Alzheimer’s disease and possibly other neurodegenerative disorders.^67,68 This highlights the importance of protecting your brain by supplementing with omega-3 fats.

Pomegranate

Pomegranates contain very high levels of polyphenols, which are plant-derived molecules with anti-inflammatory and neuroprotective properties.⁶⁹ Animal studies reveal that supplementing with pomegranate juice slows the development of Alzheimer-like disease, a major cause of brain atrophy.^69-71 This protection may arise from the ability of the polyphenols in pomegranate to slow or stop brain cell death.⁷²
Human studies demonstrate significant improvements in cognition and memory with consumption of 8 ounces of pomegranate juice daily, and lab studies with human brain cells in culture show that pomegranate polyphenols protect cells against changes that occur in other neurodegenerative diseases.^73,74

Resveratrol

 

Resveratrol is a major component of red grapes and certain other dark fruits; it has seen widespread use in preventing aging and age-related cardiovascular and neurologic conditions. Studies in a mouse model of chronic fatigue syndrome (which can produce brain shrinkage) show that four weeks of resveratrol therapy increased the animals’ daily physical activity by more than 20%, possibly as a result of reduced brain cell death.⁷⁵ In addition, the volume of the memory-intensive hippocampus was larger following supplementation.
Researchers are also exploring resveratrol as a potent neuroprotectant against the brain-shrinking effects of obesity and a high-fat diet. In studies of obese animals (obesity is a cause of brain shrinkage), resveratrol protected brain tissue from oxidative damage, a precursor to brain cell death.⁷⁶ And in mice fed a high-fat diet, resveratrol similarly protected against oxidative damage to the vital blood-brain barrier and decreased injury to the endothelial cells in the brain.⁷⁷
These findings in animals may explain the results of a compelling human study in 2014, which demonstrated that, in healthy overweight older adults, supplementing with 200 mg/day of resveratrol improved the functional connections between the hippocampus and the frontal areas of the brain.⁷⁸ Such changes were accompanied by improved memory performance as well as better blood sugar control, again pointing to the complex interactions of metabolism and brain performance.