The information and study references in this article are from my book Natural Brain Support: Preventing and Treating Alzheimer’s and Dementia and Other Related Diseases Naturally, published in 2021, and dives into peer-reviewed, researched, natural approaches for both helping reduce the risk of onset of Alzheimer’s disease and other types of dementia as well as ways to naturally help maintain and even improve healthy brain function. The article will be discussing many of the possible underlying causes or contributing factors that need to be considered as part of any treatment protocol, but also identifies essential nutrients and antioxidants found to be deficient in the brains of Alzheimer’s and other patients suffering from dementia, as well as dietary and lifestyle considerations and critical foods to both eat and to avoid that contribute to either brain health or disease.
This article will focus on Alzheimer’s disease (AD), being it is the most common form of dementia and the statistically fastest growing. As of 2019, an estimated 5.6 million Americans had Alzheimer’s disease; and fourteen percent of those over seventy have some form of dementia. It is the sixth leading cause of death, with one out of three seniors dying from AD or another form of dementia. One in 10 people, age 65 and older (10%), has Alzheimer’s dementia. AD and dementia cost society 19-times more when compared with age-matched people without dementia, estimated to be around $290 billion in 2019.
Yet there is much that can be done to reduce the risk of AD and even treat it naturally. The onset of dementia is connected to the health of the whole body. For example, studies have shown that illnesses such as anemia, diabetes mellitus, and cardiovascular disease as well as people with fewer teeth (often related to poor health habits) all increase the risk of dementia.
The conventional treatment approach focuses primarily on preventing acetylcholine breakdown by inhibiting acetylcholinesterase and reducing excess glutamine, both critical neurotransmitters essential for healthy brain function. It is recognized that AD patients have excessive build-up of beta amyloid in the brain as well as intracellular neurofibrillary tangles (NFTs) consisting primarily of tau protein, which in normal levels provides essential functions for brain health, but excessive growth destroys healthy brain cells.
But what is the underlying cause of these build-ups and what can be done naturally to both prevent this from happening as well as reversing them naturally? This article will discuss the many variables that contribute to or may cause these excessive build-ups, as well as result in apoptosis (cell death), mitochondrial dysfunction, and excessive free radical and reactive oxygen species (ROS) exposure, as well as the effects of chronic stress and inflammation on the brain, environmental exposure to toxins, brain plasticity, neurogenesis, breakdown of the blood-brain barrier, effects of emotional imbalances, effects on emotions and socialization, and more.
A whole-body approach is needed to be more effective in preventing, managing, and treating AD. For example, the foods we eat and the health of our gastrointestinal system play a major role in our brain health because although the brain is only one to two percent of our body weight, it utilizes twenty percent of our body’s energy, so any impairment in this system will effect the health of one’s brain over time.
Underlying Causes or Contributing Factors
Lifestyle considerations play a critical role in our brain’s health and its ability to function well. Some genetic factors can play a role in higher risk of AD onset, so does how we live our lives though maintaining a healthy diet, exercising regularly, maintaining a positive outlook on life, and tending to one’s emotional well-being, including managing excessive anger, resentment, and the effects of chronic stress.
Aging and Circulation. Aging is associated with a reduction of blood flow to the brain, which contributes to adverse changes in cognitive function. A significant body of evidence points to diminished cerebral circulation as a precursor to both vascular and Alzheimer’s dementia. With aging, one loses some brain plasticity, which results in a loss of cognitive function. That’s why a young person, with an active, flexible brain, easily latches on to new ideas and simply thinks faster than an older person whose brain has lost plasticity and is more fixed in its patterns. Loss of resilience can, for example, be counteracted by regular physical activity. Brain plasticity refers to the process through which patterns of synaptic activity stimulate changes at synapses. Patterns of synaptic activity or inactivity regulate the amount of communication at the synapse. Synapses can change and the degree of change depends on how much they are used.
Self-Help: Keep doing regular exercise and eat an alkaline diet, which includes avoiding most sugar and refined carbohydrates (see more on diet below). Nutrients that help improve circulation include bilberry, Gingko biloba, vinpocetine, lutein, zeaxanthin, saffron, nattokinase.
Free Radicals. Free radicals are considered a key factor in the aging of brain cells (as well as overall aging). In the central nervous system (CNS), cellular damage due to free radicals may be responsible for neurodegeneration.
Free radicals exist throughout one’s body and are a natural part of physiological activity. They contain an extra electron on their outer orbit, so seek to steal an electron from a healthy cell, resulting in cell damage and cell death. The body produces some of its own antioxidants that neutralize free radicals before they destroy healthy cells, but it also needs antioxidants from food. If antioxidants are missing in the diet, then higher levels of oxidative stress exist within the brain.
Stress. Healthy stress reactions help one deal with emergency situations, allowing us to spring into action. Once over, the body returns to homeostasis. This is often referred to as the “flight and fight mode,” resulting in allostatic overload. In modern life, the daily challenges often leave one in a constant state of flight and fight mode, ultimately causing a variety of health issues, including having damaging effects on the brain.
Studies have shown that stress can cause functional and structural changes in the hippocampus, including atrophy and neurogenesis disorders. Chronic stress and, consequently, an increase in plasma cortisol, leads to a reduction in the number of dendritic branches, and neurons, structural changes in synaptic terminals, and decreased neurogenesis in hippocampus tissue.
When chronic stress is experienced, the body makes more cortisol than it has a chance to release, which can over time wear down the brain, disrupt synapse regulation, kill brain cells, and actually shrink the size of the brain.
Chronic stress causes an increase in excitatory amino acids, particularly glutamate, which play a key role in structural as well as functional changes in the brain. Glutamate is the major excitatory transmitter; excess glutamate causes damage and inflammation. Chronic stress results in immune suppression,, as well as many other health conditions, including high blood pressure and digestive disorders.
Chronic stress can negatively affect different parts of the brain, including the amygdala which helps us manage our so-called “fight or flight” response, as well as regulate emotions such as fear and aggression. It ties our emotional meaning to our memories. reward processing, and decision-making.24 The effects of acute and chronic stress on the amygdala can result in stress-induced loss of spines25 and shrinkage of dendrites.26 Spines are neuronal protrusions and are essential for synaptic function and plasticity. They function to obtain information from other cells and carry that information to the cell body. Dendrites are critical for synapsis, the transmission of nerve impulses between neurons.
Two other hormones essential for memory and normal brain function are noradrenaline, which is both a hormone and neurotransmitter, creating emotional aspects of memories stored in the basolateral amygdala area, and corticosteroids that facilitate the memory process. If high levels of chronic stress cause excessive release of corticosteroids, noradrenaline effectiveness is suppressed causing a negative effect on memory formation in the amygdala. Glucocorticoids are hormones secreted by the adrenal glands (also called glucocorticosteroids, corticosteroids or steroids) and are present in almost all organs and tissues, including brain. They affect homeostasis, the body’s ability to adapt to stress, and mediate hormonal activity through the stimulation or suppression of target gene transcription. This increase in glucocorticoids is postulated to be a key step in the irreversible activation of the cascade leading to Alzheimer’s disease, involving inactivation of the adaptive insulin receptor mechanism.
Glucocorticoids can diffuse through the blood-brain barrier and exert long-term effects on processing and cognition. Excess chronic stress causes the increased release of glucocorticoids, which in turn causes changes seen in AD patients in glutamate neurotransmission in the prefrontal cortex and the hippocampus, thereby influencing some aspects of cognitive processing.
A decrease in the secretion of glucocorticosteroids causes preservation of spatial memory in adults and has also been shown to have neuroprotective effects. Lifelong corticosterone levels determine age-related decline in neurogenesis and memory.
Chronic Inflammation. In AD, damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide stimuli for inflammation, which then exacerbates more deposits and tangles resulting in a degenerative cycle. Exaggerated oxidative stress in AD      leads to overproduction of amyloid beta protein-associated free radical production and cell death,  causing yet more oxidative stress–a dangerous cycle.
Inflammation in the brain causes shrinkage, decreased neurogenesis, and neurodegeneration in pathologically vulnerable regions of the brain, as in AD.   Chronic intestinal inflammation is associated with decreased neurogenesis in the subgranular region of the hippocampus, which is responsible for learning, memory, and mood control.
Many studies have shown a connection between inflammation and Alzheimer’s, dementia, and cognitive decline, including circulating inflammatory markers.    Inflammation in AD pathology is linked to activated inflammatory cells (microglia and astrocytes) and inflammatory proteins (e.g. cytokines), which surround amyloid plaque and neurofibrillary tangles.
Chronic inflammation and oxidative stress  are prominent issues related to contributing nerve damage and the onset of AD, and may play a role in other forms of dementia. 
Neuroinflammation has been tied to disease progression and severity in AD, where misfolded and aggregated proteins trigger an immune response resulting in neuronal death and progressive cognitive decline.  
Microglia are a collective type of neuroglia (glial cell) located throughout the brain and spinal cord. Microglia account for ten to fifteen percent of all cells found within the brain. In normal conditions microglia perform significant functions in maintaining healthy brain functions, including disposing of dead neurons, breaking down amyloid beta plaque (a causative factor in AD), and disposing of other brain debris. A hallmark of brain damage is an increased inflammatory response capable of activating microglial cells. Microglial activation has also been linked with brain diseases.
Many studies have proposed that inflammatory dysfunctions are associated with psychiatric disorders and neurodegeneration in both animal models and human patients. 
Self-Help: A strong alkaline, anti-inflammatory diet is critical as part of an overall treatment strategy.
Neurogenesis and Brain Plasticity. The human brain is capable of forming new connections between neurons. When we take in new information, an electro-chemical signal is sent across the space between neurons (called the synaptic space). This ability of the brain to form new connections or neural pathways to communicate with each other is often referred to as brain plasticity. Brain plasticity is now understood to be the very foundation of learning and memory.
Neurogenesis is the brain’s ability to product new brain cells. Researchers noted in the 90s that neurogenesis decreases with aging. But the number and type of stem cells in the neurogenic region of the hippocampus apparently does not decrease with aging, rather they become inactive or dormant. Neurogenesis occurs through stem cells that can differentiate into many other types of cells, including nerve cells.
Neurotrophic factors are molecules produced by the body (biomolecules), mostly peptides and proteins. The three known neurotrophins are brain-derived: neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and nerve growth factor (NGF). Loss of neurotrophins cause impaired brain plasticity, which results in loss of cognitive capacity expressed in conditions like Alzheimer’s disease. These growth factors are responsible for the ability to utilize and put into action essential proteins in the brainand thepromotion of health and re-growth of neurons.
Neurotrophic factors keep the brain nourished. When they are working well, our ability to think and process information stays healthy. When their action is impaired, learning and remembering becomes more difficult, and the brain actually withers and shrinks over time. Neurotrophic factors are positively affected by having a healthy diet, being emotionally balanced, managing stress, and exercising regularly. Negative influences include an unhealthy diet, sedentary lifestyle, tobacco and alcohol use, mood disorders, oxidative stress, emotional imbalances such as excessive fear or anger, chronic pain, deficiencies in certain essential vitamins, and some medications.
Brain derived neurotropic factor (BDNF) regulates hippocampal neurogenesis.  It is required for the development of the nervous system, proper cognitive function, and memory formation, and is known to be critical for the development of the brain, neuron survival,  neuronal regeneration, and synaptic plasticity.    When BDNF levels are irregular or declining, neurological diseases such as Alzheimer’s, Parkinson’s, Huntington’s disease, and amyotrophic lateral sclerosis can develop.
Nerve growth factors (NGF) have been shown to improve neural regeneration in neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s disease. Neurotrophins have also been found to be located in adult stem cells niches and therefore may promote tissue regeneration outside of the nervous system.
Microglia. Microglia are the resident macrophages (large cells) and primary immune cells of the brain, and they have a multitude of functions, including attacking and consuming bacteria (phagocytosis), removing waste, providing neuroprotection, and contributing to the growth of new neurons. They interact with a number of cell types, including astrocytes, neurons, and endothelial cells. In conditions such as AD, they fail to clear away waste, including beta-amyloid deposits.
Glial Cells. Glial cells maintain homeostasis, form the myelin sheath that protects nerve cells, and provide support and protection for neurons. In addition, they support synaptic contacts and the signaling abilities of neurons. Glia are more numerous than nerve cells in the brain, outnumbering them by a ratio of perhaps 3 to 1.
Glial cells include astrocytes, which are essential in maintaining brain homeostasis and neuronal metabolism. They support brain plasticity and synaptogenesis, provide neurons with mechanical support, control neuronal cell development, release nutritional and energy substrates like glucose and lactate that regulate neurotransmission, vasomodulation, and repair, and protect neurons from oxidative damage, and control the blood brain barrier and blood flow.  Oligodendroglia cells are found in the central nervous system. Their main function, along with Schwann cells (found in the peripheral nervous system), is the formation of myelin, the protective covering of nerve cells. Satellite cells are glial cells that cover the surface of nerve cell bodies in sensory, sympathetic, and parasympathetic ganglia, and help regulate the external chemical environment. Like astrocytes, they are interconnected by gap junctions and respond to ATP (as a neurotransmitter) by elevating intracellular concentration of calcium ions.
Epigenetics. The study of epigenetics has shown that gene expression could change throughout one’s lifetime, determined by many environmental factors, including diet, emotional nurturing, social interactions, exercise, smoking, alcohol consumption, air pollution and other exposure to toxins, working habits (particularly those who have shift work), chronic stress, and even how one sleeps. In diseases such as cancer, congenital diseases, neurodegenerative diseases, and neuropsychiatric disorders,    various genes are switched into an opposite state, away from the normal/healthy state. Numerous historical studies show that patterns of famine, smoking, or breast feeding, affect future generations related to potential impact on development and health, especially during critical developmental periods.
Vascular Risk. Chronic high blood pressure in which blood vessels lose their elasticity cause the muscular layer of the vessels to enlarge, making it more difficult for the body to get the blood effectively to the brain. Hypertension may contribute to cognitive decline by causing cerebral small vessel pathology and increasing neurofibrillary tangles and amyloid plaques. Elevated plasma homocysteine is an independent risk factor for cardiovascular disease, stroke, and dementia, including AD.
Environmental Toxins. Children and young adults who live in areas with significant air pollution are much more likely to have the hallmarks of Alzheimer’s. These include twisted protein fibers, deteriorating neurons, and amyloid beta plaque deposits.  
Exposure to toxins in the environment can have a substantial effect on brain functioning. For example, high levels of blood lead (Pb) are associated with reduced ability to recall and define words, identify line-drawn objects, and difficulty in a perceptual comparison test, as well as fatigue, decreased processing speed, fine and gross motor deficits, and generally decreased cognitive functioning. These declines are greater than changes observed with normal aging alone.
Cumulative lead exposure is associated with an increased risk of amyotrophic lateral sclerosis  and Parkinson’s disease. In regions with high levels of air pollution even children exhibit the hallmarks of Alzheimer’s: twisted protein fibers, deteriorating neurons, and amyloid plaque deposits.   The same is true of industrial-, combustion- and friction-derived nanoparticles.
Cholinergic Circuit Dysfunction. Problems of the cholinergic circuit, such as with the neurotransmitter acetylcholine, are important factors. Cholinergic circuit dysfunction has been associated with neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s as well as psychiatric disorders such as schizophrenia.
Blood Sugar Imbalances. A strong school of thought is that insulin resistance with chronic blood sugar elevations are involved in depression and neurodegenerative disorders such as Alzheimer’s disease.  Insulin regulates glucose (sugar) and directs the body to store energy. In the brain, insulin not only breaks down glucose but also regulates the clearance of b-amyloid protein and tau phosphorylation (essential for avoiding AD). Insulin supports healthy blood flow and the removal of fats from the brain, inhibits apoptosis (cell death), manages the response to inflammation, supports the ability for the formation of new synapsis, and supports new memory formation. It can also facilitate neurotransmitter receptor trafficking. Therefore, any change in insulin balance can have serious consequences. There is a great similarity between AD and type 2 diabetes as both ultimately result in one’s body becoming resistant to insulin, thereby reducing its effectiveness. In both conditions, inflammation with increased levels of oxidative stress occurs. The b-amyloid levels increase in both the brain and pancreas along with hyperphosphorylated tau protein and cognitive decline. Fifty percent of Americans between the ages of forty-five to sixty-four and seventy-six percent of those over sixty-five have an insulin imbalance, which becomes a critical health issue for Americans.
High Cholesterol and Homocysteine Levels. One study concluded that high total cholesterol levels at midlife have been associated with a nearly threefold increase in the likelihood of developing AD, even after controlling for ApoE genotype.
High homocysteine levels double the risk of Alzheimer’s. Elevated plasma homocysteine is an independent risk factor for cardiovascular disease, stroke, and dementia, including AD. 
Mitochondria. Mitochondria are the energy batteries of our cells, producing ATP, which powers metabolic processes. Mitochondrial dysfunction appears to be a critical factor in the pathogenesis of AD.  This results in reduced membrane potential, increases permeability, and produces excess free radicals, which damage proteins, lipids, and nucleic acids.
Nutrients that support mitochondrial function (and against mitochondrial dysfunction) include vitamins B1, B2, B6, C, D, and E, l-carnosine, l-taurine, CoQ10, benfotiamine, alpha-R-lipoic acid, PQQ (pyrroloquinoline quinone), luteolin [from orange extract fruit), l-carnitine, trans-resveratrol, curcumin, magnesium, and schisandra.
Blood Brain Barrier Compromise (BBB). The BBB is critical for preventing particles and pathogens for reaching the brain, allowing only essential nutrients to pass through. Astrocyte destruction is associated with BBB (blood-brain-barrier) disruption. Astrocytes induce and maintain the BBB, and in particular form the glia limitans. 
Immune reactions to gluten (see Celiac Disease below) can break down the blood-brain barrier, increasing autoimmune reaction risk in the brain and nervous system.
Nutrients that support the BBB include resveratrol and baicalein.
Glymphatic System. The glymphatic system is a waste clearance pathway for the central nervous system and may play a significant role in clearing waste build-up in the brain. It is most active during sleep and may have implications in headache and in neurodegenerative diseases associated with pathologic protein aggregation, including Parkinson’s disease and Alzheimer’s. disease. The glymphatic system functions much like the lymphatic system but is managed by the glial cells within the brain. Glial cells are non-neuronal brain cells with several regulatory and protective roles, including destruction of pathogens and removal of dead nerve cells.
The Gut-Brain Axis. Through two-way communication with the brain via the nervous system, endocrine system, and immune system, the gut and central nervous system form a gut-brain axis. They communicate with each other constantly, in both sickness and health. Researchers have concluded mechanisms that degenerate the neurons in the brain also degenerate neurons in the enteric nervous system. The enteric nervous system (ENS) is a large division of the peripheral nervous system (PNS) that can control gastrointestinal behavior independently of central nervous system (CNS) input.
Changes in gut microbiota affect the nervous system, and dysfunction of the delicate interconnections between the two are closely associated with neurodegenerative conditions such as Parkinson’s and Alzheimer’s diseases. In this way intestinal microbiota are directly linked to various forms of dementia because of the action of metabolic disease and chronic low-grade inflammation.
Candidiasis and leaky gut syndrome are two common forms of flora imbalances in the gut. Brain infection was found in half of patients with systemic candidiasis. Leaky gut is often associated with fungal infections. Fungal proteins and diffuse mycoses in the blood of AD patients suggest that chronic fungal infection associates with high risk of AD.
Celiac Disease (CD). CD is an immune-mediated affected by the intake of gluten (a protein present in wheat, rye, or barley) that occurs in about one percent of the population.  Non-celiac gluten sensitivity (NCGS) also remains undertreated and under-recognized as a contributing factor to psychiatric and neurologic manifestations. NCGS is estimated to occur six times greater in the general population than CD.
Data suggests that up to twenty-two percent of patients with CD develop neurologic or psychiatric dysfunction, and as many as fifty-seven percent of people with neurological dysfunction of unknown origin test positive for anti-gliadin antibodies. A 2006 study identified a number of patients who had cognitive impairment due to CD  or dementia.
Non-celiac gluten sensitivity can trigger neuroinflammation, gut-brain axis dysfunction, leaky gut, and vulnerability for dementia.
Essential nutrients for celiac patients include vitamins B6, B12 (cobalamin), and folate, as well as iron, calcium, selenium, and vitamins D and K. 
Drug Contraindications. There are many drugs that may be contraindicated for AD; discuss with your doctor. For example, anticholinergic drugs are those that block the neurotransmitter acetylcholine in the central and the peripheral nervous system. They are typically used to treat a variety of conditions such as urinary incontinence, overactive bladder, chronic obstructive pulmonary disorder (COPD), and certain types of poisoning. Although brain dysfunction systems can often disappear after discontinued use of these drugs, sometimes the damage is more permanent and can look like Alzheimer’s disease and/or they may be associated with increased dementia risk. A well-known risk with anticholinergic medications is acute impairment in specific aspects of cognition (e.g., working memory, attention, psychomotor speed) which has been demonstrated in single dose experimental studies and cohort studies. In addition, anticholinergics may be associated with global cognitive impairment.
Lifestyle considerations play an essential role in brain and overall health. Risks include long-term consumption of high-fat, high-sucrose, refined-grains diet, poor nutrition and/or nutrient absorption, sedentary lifestyle, chronic insomnia, social isolation, chronic stress, cognitive inactivity, and epigenetic (environmental) factors.
More specifically, research points to genetic inheritance, cardiovascular and cerebrovascular problems, excessive alcohol consumption, traumatic brain injury, chronic inflammation, compromised blood-brain barrier, biochemical imbalances, oxidative stress, and having one or two copies of the APOEϵ4 genetic variant.
Exercise. Normal brain aging involves potentially reversible loss of resilience, which, for example, can often be counteracted by regular physical activity, as well as regular forms of meditation, stress management, a healthy diet, and targeted supplementation, particularly related to deficiencies in certain nutrients. Sedentary behavior increases the risk of Alzheimer’s as much as genetic factors because inactivity may negate the protective effects of healthy genes. Moreover, and even more encouraging, they found that people who didn’t get in shape until middle age or later still enjoyed the benefits of markedly lowered risk of dementia.
Do not smoke. Nicotine can kill brain cells, stop new neurons forming in the hippocampus, and significantly impact the ability to promote new neurons. Smoking may affect plasticity and refinement of cortical connections, and may have functional implications for maturation and function of the prefrontal network.
Learning. The process of learning new knowledge, skills, and information also stimulates hippocampal neurogenesis. Learning tasks that are related to the hippocampus are linked to new cell generation there, while learning tasks that do not require the hippocampus do not alter the number of new cells. Learning, spaced over time, induces more enduring memory, which is linked to the number of new cells in the hippocampus.
Healthy Diet. Scientists agree that nutritional factors have a role in protecting and enhancing neurogenesis. Diets that include lots of sugars and high fats reduce neurotrophic factors in the hippocampus, nerve plasticity and learning capacity.
Social Support. Mood may influence social behavior, and social support is one of the most studied psychosocial factors in relation to health and disease. Lack of support can possibly result in mimicking symptoms of dementia.
Sleep. Not getting enough sleep at night and chronic insomnia cause many cognitive and related problems.
Top Brain Nutrients
These top four nutrients or foods are the most important for supporting neurogenesis and/or BDNF. They are discussed in detail in the diet and nutrition chapters.
Other important nutrients and foods to support brain health and neurogenesis include acetyl-l-carnitine, apigenin, ashwagandha, other berries, choline, cruciferous vegetables, garlic, ginkgo, ginseng, grapeseed extract, green tea, glutathione, green, leafy vegetables, gut microbia, hesperidin, huperzine A, iron, lecithin, lotus root extract, lutein, magnesium, magnolol, melatonin, milk thistle extract, mulberry, mushrooms (lion’s mane, shiitake, reishi), olive leaf extract, PQQ (Pyrroloquinoline quinone), quercetin, red sage (salvia), resveratrol, taurine, vinpocetine, zeaxanthin and vitamins A, B6, B12, E, and D.
Most Important Brain Foods/Herbs
Top brain foods include ashwagandha, avocado, blueberries (and other dark berries) dark chocolate, eggs, fish, fruits and vegetables, ginseng, goji berry, green and black teas, nuts, mulberry, mushrooms (reiki, shitake, and lion’s mane for example), olive oil, pomegranate juice, prunes, pumpkin seeds, yogurt (organic plain), and walnuts. These foods along with others contain high amounts of flavonoids that have many potent benefits to the brain, including reducing beta amyloid and fibril formation.    
The body produces some of its own antioxidants that neutralize free radicals before they destroy healthy cells, but it also needs antioxidants from food. If antioxidants are missing in the diet, then higher levels of oxidative stress exist within the brain.
Diets that are rich in omega-3 fatty acids and antioxidants, epidemiological studies indicate that diets with high contents of trans and saturated fats adversely affect cognition.
Eat more raw or slightly steamed vegetables and fruits to supply digestive enzymes. The typical Western diet does not provide enough antioxidants to support proper digestion, enzyme production, or to support normal metabolic activity. The nutrient composition of processed foods in the Western diet can also negatively affect the brain and contribute to the development of degenerative diseases. 
Juicing is an excellent way to get essential antioxidants, enzymes, and other nutrients into one’s body. Whenever possible, juice with organic products.
Exercise daily which can include fast walking, swimming, tennis, or other sports, work-outs at the gym, yoga, etc. Not only does exercise strengthen the physical body but improves neurogenesis (the growth of new nerve cells). Participants of the study did at least 150 minutes per week of walking, running, swimming or other exercise. They experienced lowered levels of key biological markers of Alzheimer’s disease in their cerebrospinal fluid, including tau (a protein that builds up in the brains of people with Alzheimer’s). Another study showed that people with a history of exercise that have the ApoE4 gene (increases the risk of AD onset 10-30 percent) did not develop dementia and had less b-amyloid in their brains.
Foods to Avoid
A diet high in “junk food” and saturated fats elevates the neurological burden that is associated with brain injury, as evidenced by a worse performance in learning tasks and a reduction of BDNF-mediated synaptic plasticity.  This type of diet increases the vulnerability of cells to damage by causing free-radical formation that surpasses cellular buffering capacity. The nutrient composition of processed foods in the Western diet can negatively affect the brain and contribute to the development of degenerative diseases.
In a similar study with over five-thousand people, it was found that a diet high in red meat, processed meat, baked beans and fried food was associated with inflammation and a faster decline in reasoning over ten years.
Diets high in sugar (including refined carbohydrates) can be highly detrimental to brain health. High sugar levels (as in uncontrolled diabetes) cause oxidative stress, which produces high amounts of free radicals (damaging healthy cells). Research strongly supports the fact that people without diabetes but with above normal blood sugar levels have an increased risk of developing dementia.
Avoid artificial sweeteners. Artificially sweeteners such as used in diet soft drinks are associated with an increased risk of ischemic stroke, and all types of dementia including AD. Some of the adverse effects on the central nervous system caused by the intake of aspartame are headaches, mood changes, insomnia, and seizures.
Avoid canned foods as aluminum can leach out and has been implicated as a causative factor of AD.
Nutrients Found to Be Deficient in the Brains of AD Patients
Deficiency or low levels of specific vitamins such as vitamin D3 and B vitamins can result in cognitive difficulty, mood swing, and depression. These deficiencies can mimic symptoms of dementia and AD. Specific nutrient deficiencies such as zinc, vitamins B1, B2, B6, B12, D3, can result in cognitive difficulty, mood swings, and depression; and magnesium deficiencies can contribute to brain dysfunction and reduced learning, memory, and cognitive function. Magnesium helps suppress amyloid beta build-up in the brain. Zinc deficiency may induce learning and memory impairment. B12 deficiency has been linked to mental decline (which can often be mistaken for dementia). Deficiency in melatonin, produced by the pineal gland and essential for a good night’s sleep, may be directly related to age-related cognitive impairment.   Note that exposure to blue light (computers and mobile devices) inhibits the production of melatonin.
DHA (Docosahexaenoic acid) is found in higher concentrations in brain synapses than any other tissue in the body and found in highest concentrations in the hippocampus of the brain. DHA concentrates in the structures involved in forming new memories, such as synaptic membranes and tiny outgrowths called neurites.Those at risk for AD and those with cognitive impairments often have a DHA deficiency., AD patients have significantly lower levels of DHA in the neurons of their hippocampus. Changes in DHA levels in cerebral spinal fluid (CSF) were inversely correlated with CSF levels of total and phosphorylated tau.
Glutathione is especially important as it is the antioxidant in the greatest quantity in the brain and found to be deficient in the brains of AD and Parkinson’s patients. Glutathione is referred to as the “anti-agent” antioxidant due to its effectiveness in neutralizing the full spectrum of free radicals.
Several studies have documented the positive impact of mindfulness-based programs on symptoms of anxiety and depression, and improvements in sleep patterns,, and attention.
Some Top Essential Oils
Use of essential oils has many benefits, including reducing anxiety, depression, improving mood and sleep, stimulating the mind and improving cognitive function, reducing stress, improving digestion and loss of appetite, and much more.
There is some evidence that aromatherapy using various essential oils may have some potential for improving cognitive function, especially in patients with AD.    Used with massage, they may help to calm agitated people with dementia.
The book goes into greater depth into different essential oils and best ways to apply them, but here are a few great ones.
One study looked at the effects of massage with a cream containing lavender, sweet marjoram, vetiver, and patchouli on dementia patients in a residential care facility. They saw a decrease in “dementia-related behaviors.
Lemon balm and lavender are the most used aromatherapeutic treatments for behavioral and psychological symptoms in dementia.  
Bergamot can be used to relieve anxiety, agitation, mild depression, stress, and relieve insomnia (in a study, combined with lavender and ylang ylang).
Frankincense helps relieve chronic stress and anxiety, reducing pain and inflammation, boosting immunity.
Saffron is an antibacterial, blood purifying, antioxidant, decongestant, and memory enhancer.
Other modalities shown to be helpful in managing Alzheimer’s and dementia include Ayurvedic and Chinese medicine, craniosacral treatments, yoga, qigong, tai chi, and meditation practice.
There are many studies regarding Chinese medicine and herbs for brain issues, including post-traumatic stress disorder, dementia and AD discussed in the book, but here are a few. In a randomized, controlled, parallel-group study of over twelve weeks with a twelve-week follow-up, it was found that acupuncture treatment improved cognitive function more effectively than Donepezil.
A 2019 review of acupuncture and acupressure techniques for behavioral and psychological symptoms of dementia found that there were statistically significant improvements in activities of daily living (75% improvement), agitation (100%), anxiety (67%), depression (100%), mood (100%), neuropsychological disturbances (67%), and sleep disturbances (100%).
Regarding Parkinson’s disease, some Chinese herbal medicines are useful as an adjunct to help improve both motor and non-motor symptoms, permit lower doses of dopaminergic drugs, and reduce dyskinesia. 
Michael Edson is a co-founder and president of Natural Eye Care, Inc. He is co-author of Natural Eye Care: A Comprehensive Manual for Practitioners of Oriental Medicine and Natural Eye Care: Your Guide to Healthy Vision and Healing (2019). He’s also written Natural Parkinson’s Support: Your Guide to Preventing & Managing Parkinson’s (2020) and Natural Brain Support: Ways to Help Prevent and Treat Dementia and Alzheimer’s Naturally (2021).
Consult your doctor before using any of the treatments mentioned in this article.