Underlying Causes and Natural Treatments for Alzheimer’s and Dementia


By Michael Edson, MS, LAc

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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.1 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 2019.2

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,3 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.4 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.5 Loss of resilience can, for example, be counteracted by regular physical activity.6 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.7

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.8

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.9

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.10 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,11 including atrophy and neurogenesis disorders.12 Chronic stress and, consequently, an increase in plasma cortisol, leads to a reduction in the number of dendritic branches,13 and neurons,14 structural changes in synaptic terminals,15 and decreased neurogenesis in hippocampus tissue.16

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,17 kill brain cells,18 and actually shrink the size of the brain.19

Chronic stress causes an increase in excitatory amino acids, particularly glutamate,20 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.21 Chronic stress results in immune suppression,22, 23 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.  

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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,24 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.25 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.26 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.27

Glucocorticoids can diffuse through the blood-brain barrier and exert long-term effects on processing and cognition.28 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.29

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.30

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 AD31-36 leads to overproduction of amyloid beta protein-associated free radical production and cell death,37,38 causing yet more oxidative stress39–a dangerous cycle.

Inflammation in the brain causes shrinkage, decreased neurogenesis, and neurodegeneration in pathologically vulnerable regions of the brain, as in AD.40-42 Chronic intestinal inflammation is associated with decreased neurogenesis in the subgranular region of the hippocampus, which is responsible for learning, memory, and mood control.43

Many studies have shown a connection between inflammation and Alzheimer’s, dementia, and cognitive decline, including circulating inflammatory markers.44-47 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.48

Chronic inflammation49 and oxidative stress50, 51 are prominent issues related to contributing nerve damage and the onset of AD, and may play a role in other forms of dementia. 52

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.53-56

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.57