Brain health is whole-person health. The idea that focusing on only one aspect of health, like diet or exercise, will result in a healthy older brain is naïve. We need to make sustained efforts across all aspects of wellness to remain cognitively vibrant into old age.
The healthier the diet, rich in fruits, veggies, whole grains, and oily fish, will enlarge the brain’s memory center. Healthful eating is among the best ways to protect your aging brain against slippage. Conversely, a diet that skimps on fruits, vegetables, whole grains, nuts and fish and includes lots of fried foods, red meat and alcohol is highly likely to pave a road to cognitive ruin. Don’t worry about pesticides.
Rush University Medical Center: do not add unhealthy (Western Diet) foods to the MIND diet.
This study of 960 older adults who were free of dementia on enrollment showed that the MIND diet (similar to a plant-based diet) found to reduce the risk of cardiovascular conditions, such as hypertension, heart attack, and stroke, as well as cognitive decline.
The MIND diet works independently of other brain pathologies.
The Mayo Clinic recommends the MIND diet or the Mediterranean diet to avoid dementia. But in this study of 28,000 people from Sweden with an average age of 58, researchers did not find a link between following either a conventional diet or the Mediterranean diet and a reduced risk of dementia.
The MIND diet or the Mediterranean diet has been associated with fewer Alzheimer’s disease plaques and tangles.
The MIND die may not be so great after all.
The Mediterranean diet had a significant effect in the studies cited by Dr. Gil Carvalho here.
Those who eat plant-based are unlikely to consume much saturated fat, which may decrease motivation to exercise. Motivation to exercise is linked to the microbiome. A plant-based diet may my exercise easier. Here is why: two bacterial species closely tied to better performance, Eubacterium rectale and Coprococcus eutactus, produce metabolites known as fatty
This Chinese Longitudinal Health Longevity Study (CLHLS) touts veggies and beans. Beans feature soluble fiber, which increases short-chain fatty acids, which interfere with protein-protein interactions between amyloid-β peptides (Aβ), thereby disrupting their assembly into neurotoxic oligomers, the main toxins responsible for synapse dysfunction and cognitive deficits in AD.
Per Dr. Gil Carvalho, as presented in this video, soaking beans breaks down the phytates. Most phytates are gone after one day of soaking, but breakdown continues to happen for up to 3 days. Sprouting beans also eliminates phytates. and makes other nutrients more absorbable. Soaking beans also decreases the gas-causing ologosccharides. 10 minutes of cooking also reduces lectin activity to zero. For those still concerned about gas, Beano works quite well.
This study of 2613 men and women showed the protective effects of fruit and vegetable intake.
This study of 3,718 participants, aged 65 years and older showed the protective effects of fruit and vegetable intake.
This study of 13,388 women showed the protective effects of fruit and vegetable intake.
This systematic review of nine studies featuring 44,004 participants showed the protective effects of fruit and vegetable intake.
This study of 27,842 men with a mean age of 51 years in 1986 showed the protective effects of fruit and vegetable intake.
This study of 6,911 residents aged 65 or older found that lower intakes of vegetables and legumes were associated with cognitive decline.
Shown by a study of 139,000 older Australians.
This study of 1,059 people in Greece with an average age of 73 who did not have dementia showed that people who consumed an anti-inflammatory diet that includes more fruits, vegetables, beans, and tea or coffee, had a lower risk of developing dementia later in life.
A Healthy Diet for a Healthy Life” (plant-based), was carried out over 12 years with the participation of 842 people aged over 65 revealed a protective association between metabolites derived from cocoa, coffee, mushrooms and red wine, microbial metabolism of polyphenol-rich foods (apple, cocoa, green tea, blueberries, oranges or pomegranates) and cognitive impairment in the elderly.
This cross-sectional study included 635 community-dwelling people aged 69–71 years showed that a diet with high intakes of vegetables, soy products, fruit, and fish may have a beneficial effect on cognitive function in older Japanese people.
The AD-stimulating pathway begins inside of us—in our GI-tract microbiome—and therefore is very “locally sourced” and active throughout our lives. The highly potent neurotoxin Bacteroides fragilis – lipopolysaccharide (BF-LPS) is a natural by-product of GI-tract-based microbial metabolism. Bacteroides fragilis abundance in the microbiome, which is the source of the neurotoxin BF-LPS, can be regulated by dietary fiber intake.
All of the foods that are highest in antioxidants are plant foods. Foods rich in antioxidants may reduce the chance of Alzheimer’s disease. Plant foods provide neuroprotective effects by assisting with antioxidant defense.
A purely plant-based diet will minimize pesticide consumption resulting in less chance of cognitive decline.
A purely plant-based diet will minimize the threat of pork tape worms.
Lipoic acid is a critical component of the antioxidant network. R-Lipoic acid—as a micronutrient and a therapeutic agent—stimulated interest in clinical research because of its therapeutic implications for the metabolic syndrome, diabetic polyneuropathies, and neurodegenerative diseases such as Alzheimer’s disease.
People with the highest levels of the antioxidants lutein and zeaxanthin and beta-cryptoxanthin in their blood were less likely to develop dementia decades later than people with lower levels of the antioxidants.
In scientific studies, zeaxanthin and lutein are often described together due to their overlapping functions in the eye, but also because the human body can convert lutein into zeaxanthin (3Trusted Source).
Zeaxanthin is concentrated in the center of the retina, while lutein is found in the peripheral regions of the retina. Together, they form the macular pigment of the eye.
Lutein and zeaxanthin are found in green, leafy vegetables such as kale, spinach, broccoli and peas. Beta-cryptoxanthin is found in fruits such as oranges, papaya, tangerines and persimmons. Even lutein and zeaxanthin supplements improved cognitive function in community-dwelling, older men and women. Dark leafy greens are powerful medicine.
Cerebrovascular resistance index is the ratio of blood pressure to blood flow in the brain. Increased cerebrovascular stiffening, endothelial dysfunction may drive or operate in parallel to these cerebrovascular abnormalities. This study of 232 older adults showed diminished inferior parietal and temporal cerebral blood flow for patients with Alzheimer’s disease. Cerebrovascular resistance index was significantly elevated in amyloid-positive versus amyloid-negative cases, with additional elevation in patients with Alzheimer’s disease.
High levels of nitrates are found in foods such as beets, celery, cabbage, spinach, and other leafy green vegetables can increase blood flow to the frontal lobe of the brain, improving cognitive function and protecting against cognitive decline.
Betalains have been proven to eliminate oxidative and nitrative stress by scavenging DPPH, preventing DNA damage, and reducing LDL. It also has been found to exert antitumor activity by inhibiting cell proliferation, angiogenesis, inducing cell apoptosis, and autophagy. Betalains are found in beets and beet root powder. Bulk supplements is a good source for beet root powder.
Apigenin improves neuron formation and strengthens the connections between brain cells.
Apigenin may have neuroprotective/disease-modifying properties in various neurodegenerative disorders, including Alzheimer’s disease.
Apigenin is found in parsley, chamomile, celery, vine-spinach, artichokes, and oregano.
Apples can contain quercetin which appears to protect brain cells against oxidative stress, a tissue-damaging process associated with Alzheimer’s and other neurodegenerative disorders.
Apples always feature polyphenols and other phytochemicals. Exposure to apples and apple products has been associated with beneficial effects on risk, markers, and etiology of cancer, cardiovascular disease, asthma, and Alzheimer’s disease.
In vivo, anatabine significantly lowers brain soluble Aβ₁₋₄₀ and Aβ₁₋₄₂ levels in a transgenic mouse model of Alzheimer’s disease. In another study, anatabine reduced β-amyloidosis, neuroinflammation and alleviates some behavioral deficits in mice. Anatabine is found in green peppers, eggplant, tobacco and tomatoes.
Anthocyanins, a type of polyphenol, from dark foods such a purple grapes and blueberries support memory acquisition and consolidation via improving the flexiblity of blood vessels and blood flow to the brain. Anthocyanins are mostly from colorful fruits and veggies. Black rice is also a rich source of anthocyanins.
Anthocyanins achieve a therapeutic purpose with neurodegenerative diseases (NDs) by regulating intestinal microflora and certain metabolites (protocateic acid, vanillic acid, etc.). In particular, the inhibitory effect of tryptophan metabolism on some neurotransmitters and the induction of blood-brain barrier permeability by butyrate production has a preventive effect on NDs.
The anthocyanins in red cabbage resulted in greater protection from the A-beta-induced toxicity in cell culture.
Berries are high in flavonoids, especially anthocyanidins, and improve cognition in experimental studies.
Berries can lower oxidative stress and inflammation or directly by altering the signaling involved in neuronal communication, calcium buffering ability, neuroprotective stress shock proteins, plasticity, and stress signaling pathways.
Blueberries, or any berries are neuroprotective.
This study of 16,010 participants, aged ≥70 years showed that higher intake of flavonoids, particularly from berries, appears to reduce rates of cognitive decline in older adults.
Blueberries may slow brain ageing. This study of 26 healthy adults aged 65-77 who drank concentrated blueberry juice every day showed improvements in cognitive function, blood flow to the brain and activation of the brain while carrying out cognitive tests.
Blueberries promote hippocampal plasticity.
Blueberries increase brain blood flow.
This study of nine older adults with early memory changes showed that moderate-term blueberry supplementation can confer neurocognitive benefit.
Blueberries may even counter radiation damage.
Take some blueberry extract if one cannot/will not consume blueberries.
Blueberries work via pterostilbene.
In rats, pterostilbene was effective in reversing cognitive behavioral deficits, as well as dopamine release, and working memory was correlated with pterostilbene levels in the hippocampus.
In rats, pterostilbene treatment attenuated glutamate-induced oxidative stress injury in neuronal cells via the Nrf2 signaling pathway.
All berries will slow cognitive decline:
This study of 16,010 participants, aged ≥70 years showed that higher intake of flavonoids, particularly from berries, appears to reduce rates of cognitive decline in older adults.
60 cognitively healthy participants consumed freeze-dried cranberry powder, equivalent to a cup or 100 grams of fresh cranberries, daily. The results showed that consuming cranberries significantly improved the participants’ memory of everyday events (visual episodic memory), neural functioning, and delivery of blood to the brain (brain perfusion).
This study of rats showed that blueberry, spinach, or strawberry dietary supplementation provides phytochemicals that may be beneficial in reversing the course of neuronal and behavioral aging.
Berries are best when consumed without milk.
Butyrate in mice was associated with an increase in the pleiotropic and prolongevity hormone fibroblast growth factor 21 (FGF21). An increase in FGF21 correlated with increased AMPK and SIRT-1 activation and reduced mTOR signaling. Butyrate increases in ones digestive tract from consuming soluble (fermentable) fiber.
Here is how butyrate is used by neurons.
This study featured a median 19.7-year follow-up in which a total of 670 cases of disabling dementia developed. Dietary fiber intake was inversely associated with risk of dementia. The inverse association was more evident for soluble fiber intake and was confined to dementia without a history of stroke.
Carotenoids play a pivotal role in prevention of many degenerative diseases mediated by oxidative stress including neurodegenerative diseases like Alzheimer’s Disease (AD). Reduced carotenoid levels have been associated with dementia.
The value of carotenoids for keeping one’s marbles was demonstrated in a study of 2983 middle aged adults.
Cruciferous and dark green leafy veggies get special mention here.
The Nrf2 pathway is being increasingly considered a therapeutic target for neurodegenerative disorders.
While oxidative stress alone is able to activate Nrf2, its effect is greatly enhanced by the presence of certain chemical compounds. The simplest of these compounds were identified as 1,4-benzenediol (hydroquinone), tert-butylhydroquinone, and 1,2-benzendiol (catechol), and more complex examples include the isothiocyanate sulforaphane from broccoli seed extract, curcumin from the turmeric plant and carotenoids such as zeaxanthin and lutein (from dark green leafy veggies).
Broccoli sprouts contain 10–100 times higher levels of sulforaphane than mature plants. Radish sprouts may be more potently anti-cancer than broccoli sprouts. The addition of radish, rocket and rape sprouts to broccoli sprouts could promote the hydrolysis of the glucoraphanin to anticancer effective sulforaphane to 2.03, 2.32 and 1.95-fold, respectively, compared to single broccoli sprouts.
Excess oxidative stress is increasingly appreciated to participate in the pathophysiology of brain disorders, and decreases in the major antioxidant, glutathione (GSH), have been reported in multiple studies. In a preclinical model of GSH deficiency, we found a correlation between whole brain and peripheral GSH levels. We found that the naturally occurring isothiocyanate sulforaphane increased blood GSH levels in healthy human subjects following 7 days of daily oral administration. In parallel, we explored the potential influence of sulforaphane on brain GSH levels in the anterior cingulate cortex, hippocampus, and thalamus via 7-T magnetic resonance spectroscopy. A significant positive correlation between blood and thalamic GSH post- and pre-sulforaphane treatment ratios was observed, in addition to a consistent increase in brain GSH levels in response to treatment.
Fisetin may reduce the age-related decline in brain function.
Fisetin has now been shown in preclinical models to be effective at preventing the development and/or progression of multiple neurological disorders including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, stroke (both ischemic and hemorrhagic) and traumatic brain injury as well as to reduce age-associated changes in the brain.
The neuroprotective effects of fisetin have been shown in several in vitro and in vivo models of neurological disorders due to its actions on multiple pathways associated with different neurological disorders.
Oral administration of fisetin to mice from 3 to 12 months of age prevents the development of learning and memory deficits.
Orally administered fisetin crosses the blood–brain barrier and promotes synaptic functions in the hippocampus.
Fisetin can inhibit the aggregation of the amyloid beta protein (Abeta) that may cause the progressive neuronal loss in Alzheimer’s disease.
Blood and brain levels of sugars affixed to proteins known as advanced glycation end-products-or AGEs-were reduced in fisetin-treated compared to untreated mice. These decreases were accompanied by increased activity of the enzyme glyoxalase 1, which promotes removal of toxic AGE precursors.
|Mechanism of Action||Potential Disease Relevance|
|Antioxidant and chelating activity||AD; PD; HD; ALS; stroke; TBI|
|Maintenance of GSH||AD; PD; stroke; TBI|
|Neurotrophic factor signaling pathways||AD; PD; HD; TBI|
|Anti-inflammatory activity||AD; PD; ALS; stroke; TBI|
|Modulation of protein aggregation and stability||AD; PD; HD; ALS|
|Inhibition of oxytosis/ferroptosis||AD; PD; HD; ALS; stroke; TBI|
|Modulation of gut microbiome||AD; PD; stroke; TBI|
|Senolytic activity||AD; PD; ALS|
Fisetin: is found especially in strawberries, also in mangoes, grapes, tomatoes, onion, cucumber, apples, and peaches.
There are more than 5000 types of flavonoid, and they are found almost ubiquitously in plants and thus are widely available in the human diet. The six main subclasses of flavonoids are: anthocyanidins, flavones, isoflavones, flavonols, flavanones, and flavan-3-ols (flavanols). There is now a substantial and growing body of evidence supporting the ability of flavonoids to interfere in AD-related pathways.
Flavonoids exert a multiplicity of neuroprotective actions within the brain, including a potential to protect neurons against injury induced by neurotoxins, an ability to suppress neuroinflammation, and the potential to promote memory, learning and cognitive function.
Flavonoids may cause a rise in BNDF as shown in these two randomised, controlled trials. Here are other foods and lifesyles that may increase BDNF. BDNF is an excellent example of a signalling molecule that is intimately related to both energy metabolism and synaptic plasticity: it can engage metabolic signals to affect cognitive function32. BDNF is most abundant in brain areas that are associated with cognitive and metabolic regulation: the hippocampus and the hypothalamus, respectively33.
Dietary flavonoids were shown effective in a study of 1,640 subjects.
A study of 49,493 women and 27,842 men showed that higher intake of total flavonoids was associated with lower odds of subjective cognitive decline.
Higher dietary flavonoid intake is associated with slower rates of cognitive decline and dementia. And foods rich in anthocyanins and proanthocyanidins, which give berries their red, blue, or purple color, have been found to improve cognition.
An epidemiological study of 2,800 people aged 50 and older showed that those who consumed only small amounts of flavonoid-rich foods, such as berries, apples and tea, were two to four times more likely to develop Alzheimer’s disease and related dementias over 20 years compared with people whose intake was higher.
A 12-week parallel randomised placebo-controlled trial of freeze-dried cranberry powder (high in flavonoids) was conducted in 60 older adults aged between 50 and 80 years. Half of the participants consumed freeze-dried cranberry powder, equivalent to a cup or 100g of fresh cranberries, daily. The other half consumed a placebo. Results are that daily cranberry supplementation (equivalent to 1 small cup of cranberries) over a 12-week period improves episodic memory performance and neural functioning, providing a basis for future investigations to determine efficacy in the context of neurological disease.
Folate and folic acid
Folate increased the expression of Notch1, Hes1, and Hes5 and the number of the newborn hippocampal rat neurons.
Red Blood Cell folate is directly associated with cognitive function scores and is inversely associated with dementia in elderly Latinos despite folic acid fortification.
Here is the problem with folic acid supplements:
Almost all of the folate you ingest from foods gets broken down and converted into its active form in your gut before being absorbed into your bloodstream. In contrast, a much smaller percentage of the folic acid you get from fortified foods or supplements gets turned into its active form in your gut. The rest requires the help of your liver and other tissues to get converted via a slow and inefficient process.
Folic acid supplements or fortified foods may cause unmetabolized folic acid (UMFA) to accumulate in your blood — something that doesn’t happen when you eat high folate foods. This is concerning because high levels of UMFA appear to be linked to various health concerns. Excess folic acid intake may speed age-related mental decline, particularly in people with low vitamin B12 levels.
Excessive folic acid supplement intake may increase cancer cells’ ability to grow and spread, though more research is needed. This may be particularly detrimental to people with a history of cancer.
There is no substitute for a healthy diet.
Inulin is a prebiotic that improved the gut microbiome of middle-aged mice to resemble that of younger mice. Inulin is found onions, garlic, leeks, jerusalem artichoke, chicory, asparagus, and bananas.
The hazard of too much dietary iron
Older adults with high dietary intake of nutrients commonly found in nuts, soybeans, olive oils, and fish (such as vitamin E, lysine, DHA omega-3 and LA omega-6 PUFA) tended to have lower brain iron and better working memory performance than expected for their age. Too much iron in the brain is hazardous.
AD can be prevented by: (1) limiting the dietary supply of trivalent iron contained in red and processed meat; (2) increasing the intake of chlorophyll-derived magnesium; and (3) consumption of foods rich in polyphenolic substances .
Thymoquinone in black cumin (Nigella sativa) prevents β-amyloid neurotoxicity in cultured cerebellar neurons.
Thymoquinone protects cultured rat primary hippocampal neurons against α-synuclein-induced synaptic toxicity. This may apply to Parkinson’s disease.
The use of antioxidants as dietary supplements is common, but little is known of their effects on stem cells. This new research shows that large doses of antioxidants may be harmful to neural stem cells.
There is a large body of evidence that maintaining healthy vitamin C levels can have a protective function against age-related cognitive decline and Alzheimer’s disease, but avoiding vitamin C deficiency is likely to be more beneficial than taking supplements on top of a normal, healthy diet. Here are food sources of vitamin C.
Maintaining healthy vitamin C levels can have a protective function against age-related cognitive decline and Alzheimer’s disease. Vitamin C might help dissolve amyloid β. Ascorbate is transported into the brain and neurons via the Sodium-dependent Vitamin C Transporter-2 (SVCT2), which causes accumulation of ascorbate within cells against a concentration gradient.
Hesperidin and other citrus flavonoids
Hesperidin is a flavanone glycoside found abundantly in the rinds of citrus fruit, has been reported to have antioxidant, hypolipidaemic, analgesic and anti-hypertensive activity. Hand-squeezed citrus juices contain no hesperidin.
Hesperidin and other flavonoids (polyphenols) can protect vascular health.
Hesperidin can effectively protect neurons from damages induced by oxidative or nitrosative stress. Moreover, it enhances cognitive functions through various mechanisms such as elevating BDNF and reversing the disruptive effect of global cerebral I/R on memory.
Hesperidin is able to improve memory in healthy adult mice by two main mechanisms: directly, by inducing synapse formation and function between hippocampal and cortical neurons; and indirectly, by enhancing the synaptogenic ability of cortical astrocytes mainly due to increased secretion of transforming growth factor beta-1 (TGF-β1) by these cells.
Pretreatment of hesperidin (100 and 200 mg/kg body weight orally once daily for 15 days) to Swiss male albino mice has prevented the cognitive impairment that would have been caused by giving single intracerebroventricular-streptozotocin (ICV-STZ) injection (2.57 mg/kg body weight each side) bilaterally.
Naringenin targets several inflammatory signals involved in the neuroinflammation. Pre-treatment with naringenin significantly attenuated neuroapoptosis and cognitive dysfunction in rats.Naringenin is a multi-target flavonoid, possessing promising neuroprotective effects, through targeting multiple therapeutic targets and signaling pathways.
Naringenin improved memory deficits and caused reductions in amyloid and tau proteins in mice.
Preclinical studies have demonstrated the neuroprotective potential of citrus flavonoids and have highlighted both the well established (anti-inflammatory and anti-oxidative properties), and newly emerging (influence upon blood-brain barrier function/integrity) mechanistic actions by which these neurological effects are mediated.
A plant-based diet for a healthier gut microbiome (important): The brain microbiome is the same as the gut microbiome. The elevated presence of pro-inflammatory bacterial strains and the decreased presence of anti-inflammatory strains in the microbiomes of the gut had a positive correlation with a heightened inflammatory state. Higher levels of cognitive impairment and a greater concentration of amyloid deposition in the brain. Meat causes inflammation due to bacterial endotoxins combined the the saturated fat. Saturated fat injures via changed gut bacteria.
Bacteria in the brain are the same as in the gut.
Dietary vitamin K: kale and other dark green leafy veggies are a source:
Vitamin K is a fat-soluble vitamin is essential for forming sphingolipids, a type of fat that’s densely packed into brain cells.
This study of 192 consecutive participants ≥65 years showed that higher dietary phylloquinone (vitamin K) intake was associated with better cognition and behavior among older adults.
Vitamin K2: There is a growing body of evidence demonstrating that vitamin K2 has the potential to slow the progression of AD and contribute to its prevention. (Some K2 is made in the body from vitamin K, natto has lots, the rest of us have to supplement vitamin K2 MK7). Vitamin K2 demonstrated very promising impact in hindering aging-related behavioral, functional, biochemical and histopathological changes in the senile aging rat brain.
Pretreatment of hippocampal cultures with lipoic acid significantly protected against amyloid beta-peptide and iron/hydrogen peroxide toxicity.
Luteolin may have neuroprotective/disease-modifying properties in various neurodegenerative disorders, including Alzheimer’s disease.
Luteolin is effective against amyloid beta(25-35) peptide-induced toxicity in mice.
Luteolin reduces age-related inflammation in the brain and related memory deficits by directly inhibiting the release of inflammatory molecules in the brain.
The flavone luteolin has numerous useful actions that include: anti-oxidant, anti-inflammatory, microglia inhibition, neuroprotection, and memory increase.
Lycopene vs. cerebral oxidative stress.
Lycopene vs. mitochonrial oxidative stress.
Lycopene may protect hippocampal neurons.
The best source lycopene is cooked tomatoes.
Brain lutein preserves P3 amplitude which is a metric of cognitive function in decision making processes.
Lutein works via grey matter thickness of the right parahippocampal cortex.
Lutein and zeaxanthin may boost brain function in older people.
Lutein and zeaxanthin in neural tissue may have biological effects that include antioxidation, antiinflammation, and structural actions. In adults, higher lutein status is related to better cognitive performance.
This study of 59 young (18-25 yrs.), healthy subjects showed that dietary carotenoids lutein and zeaxanthin increqased brain-derived neurotrophic factor (BDNF) and anti-oxidant capacity. For cognitive measures, scores for composite memory, verbal memory, sustained attention, psychomotor speed, and processing speed all improved significantly.
Magnesium supports the amyloid-beta protein precursor (AbetaPP) alpha-secretase cleavage pathway.
Magnesium helps maintain the plasticity of synapses.
Magnesium is abundant in a carefully chosen plant-based diet
But not too much
Dietary polyphenols exhibit a strong potential to promote brain health due to their efficacy in protecting neurons against oxidative stress-induced injury, suppressing neuroinflammation and in ameliorating cardiovascular risk factor control and cardiovascular function thus counteracting neurotoxicity and neurodegeneration.
Pre-conditioning with phenolic sulfates improved cellular responses to oxidative, excitotoxicity and inflammatory injuries and this attenuation of neuroinflammation was achieved via modulation of NF-κB pathway. These small molecules, derived from dietary polyphenols may cross the BBB, reach brain cells, modulate microglia-mediated inflammation and exert neuroprotective effects, with potential for alleviation of neurodegenerative diseases.
Four meta-analyses and thirteen systematic reviews published between 2017–2020 showed that there is support for an association between polyphenol consumption and cognitive benefits.
Polyphenols with notable radical-scavenging activity include curcumin from turmeric and EGCG from green tea. In addition to their antioxidant and anti-inflammatory activity, polyphenols have been coupled with the increased expression of BDNF, assisting in the reversal of neuronal atrophy and behavior deficits.
This systematic review of 48 studies found strong indications that polyphenols tend to have a positive effect on BDNF concentrations.
This randomized, double-blind, parallel-group study was performed in 60 healthy volunteers between 50 and 75 years old who consumed a cocoa powder, a red berries mixture or a combination of both for 12 weeks. All groups did better on a neurocognitive test known as the Tower of London.
This review of 29 published human studies concluded that consumption of sweet or tart cherries can promote health by preventing or decreasing oxidative stress and inflammation.
In this French cohort of 1,329 older adults without dementia, a polyphenol pattern provided by a diet containing specific plant products (nuts, citrus, berries, leafy vegetables, soy, cereals, olive oil) accompanied by red wine and tea was associated with lower dementia risk.
Polyphenols decrease oxidative/inflammatory stress signaling, increase protective signaling and have neurohormetic effects leading to the expression of genes that encode antioxidant enzymes, phase-2 enzymes, neurotrophic factors, and cytoprotective proteins.
Polyphenols may increase cellular signaling and neuronal communication.
Polyphenols can reverse age-related declines in neuronal signal transduction as well as cognitive and motor deficits.
Polyphenols protect the brain by inhibition of apoptosis triggered by neurotoxic species and to a promotion of neuronal survival and synaptic plasticity.
Polyphenols induce beneficial effects on the vascular system, leading to changes in cerebrovascular blood flow capable of causing enhance vascularisation and neurogenesis.
Polyphenols show benefit in the mouse model of Alzheimer’s.
The neuroprotective effect of dietary polyphenols was clearly shown in this systematic review of 24 studies.
Concord grape juice supplementation produced significant improvements in immediate spatial memory and driving performance in 25 healthy women.
Polyphenols are widely distributed in plants.
Phytochemicals are not listed in the “Nutrition Facts” label.
Leaky gut is a cognitive hazard. Here is information on leaky gut. Chronic stress and obesity can cause leaky gut. A polyphenol-rich plant-based diet versus leaky gut syndrome. Fish oil→higher intestinal alkaline posphatase (IAP)→less leaky gut→lower lipopolysccharides. Lipopolysccharides in circulation can damage the blood-brain barrier and enter the brain, causing inflammation, depression, and neurological problems. Insulin resistance may also increase. Epigenetic aging may also accelerate.
Leaky gut is also called intestinal permeability.
Ferrulic acid exhibits wide variety of biological activities such as antioxidant, antiinflammatory, antimicrobial, antiallergic, hepatoprotective, anticarcinogenic, antithrombotic, increase sperm viability, antiviral and vasodilatory actions, metal chelation, modulation of enzyme activity, activation of transcriptional factors, gene expression and signal transduction.
Oral ferrulic acid treatment for 6 months reversed transgene-associated behavioral deficits including defective: hyperactivity, object recognition, and spatial working and reference memory. Furthermore, brain parenchymal and cerebral vascular β-amyloid deposits as well as abundance of various Aβ species including oligomers were decreased.
Ferulic acid has low toxicity and possesses many physiological functions, including anti-inflammatory, antimicrobial, anticancer (for instance lung, breast, colon and skin cancer), anti-arrhythmic, and antithrombotic activity, and it also demonstrated antidiabetic effects and immunostimulant properties, and it reduces nerve cell damage and may help to repair damaged cells.
Ferrulic acid given to diabetic rats resulted in a decrease in the levels of glucose, TBARS, hydroperoxides, FFA and an increase in reduced glutathione.
Oral administration of ferrulic acid appears beneficial in improving hypertension and hyperlipidemia in rats.
A plant-based diet overcomes the ApoE4 genetic Alzheimer’s susceptibility gene.
A quality plant-based diet helps to prevent brain shinkage.
A western diet that is veggie-poor is a cognitive hazard
There is strong evidence for a western diet promoting Alzheimer’s in Japan.
A poor diet caused Alzheimer’s and Parkinson’s in rats.
A poor diet can damage perineuronal nets.
A western diet produced systemic oxidant stress along with evidence of activation of Na,K-ATPase (the sodium–potassium pump enzyme) signaling within both mouse brain and peripheral tissues. This diet caused increases in circulating inflammatory cytokines as well as behavioral, and brain biochemical changes consistent with neurodegeneration.
Just one salad per day may delay brain ageing by 11 years.
Onion extract and quercetin protected against Ischemic neuronal damage in the gerbil hippocampus.
When a plant-based diet is combined with fried food, sweets, refined grains, red meat and processed meat, benefits are diminished.
All diets, including the plant-based diet can have drawbacks. A plant-based diet will not give one license to ignore cholesterol, blood pressure, etc.