Author Sidebar: When I first came out of the diabetic coma, I was surprised to find out from my doctors that my blood glucose was over 1200 points above normal (1337) and that I would have to take insulin for the rest of my life.

During my research and my recovery, I was surprised to discover that lifestyle-driven diseases such as heart disease, cancer, Type 2 diabetes, Alzheimer's, and other similar systemic diseases were on the rise.

I was even more surprised to discover from my doctors that there was nothing that I could do because (as they said): "DeWayne, Type 2 diabetes is a progressive disease -- your health is not going to get better, but, we can control it with the insulin."

My doctors also told me that there was a strong possibility that my brain and my mind would be affected because of my diabetes. In fact, one of my doctors suggested that I consider taking an anti-depressant drug to prevent the onset of depression! 

I thought to myself: With all of the thousands of  intelligent people in medicine and research, you're telling me that no one has found a way to cure Type 2 diabetes or, at least, slow down the progression of the disease? Really?

As an engineer, that just didn't make any sense to me! So, I started looking at cell biology, diabetes pathology, etiology, epidemiology, pathogenesis, and other areas of medical science.

During my research, I discovered a major disconnect between medical science, pharmacology, cell biology and cell repair.  It turns out that our cells have the built-in ability to repair themselves -- as long as the cells have the necessary raw materials (e.g. vitamins, minerals, macro-nutrients, phytonutrients, etc. from food). There is nothing within a drug that our cells require to repair themselves! 

My doctors told me that my research was anecdotal, theoretical and not provable. But, after I changed my diet and weaned myself off the insulin and other drugs, my doctors were surprised. My endocrinologist told me that it was temporary and that I would have to go back on insulin within 3 months ... then, it was 6 months ... 9 months ... well, it's been more than 15 years now and I still don't require any insulin or any other drug.

During my research, because one of my doctors told me that my mind would be affected causing me to become severely depressed, I started looking at how diabetes and high blood glucose levels affected the brain's anatomy, nerve cells and the mind (our emotional state).

I discovered a diabetes-Alzheimer's connection during my research about cellular biology and pathogenesis relative to systemic disease pathology, and how biological processes such as cellular inflammation and oxidation cause damage to neurons and various regions (lobes) of the brain! 

Back when I was still diabetic, I discovered that there was a lot of shame and secrecy associated with Type 2 diabetes within families and communities. Some people felt ashamed and embarrassed to be diabetic. And, other people within various families didn't really talk about it.

As a result, people didn't seek knowledge and suffered unnecessarily as the disease remained in the darkness, allowing it to grow and spread throughout families and beyond.

It appears that a similar kind of shame and secrecy may exist for Alzheimer's Disease. As a result, people are suffering unnecessarily, because they are unaware of what to do to prevent the disease or what to do before the disease gets worse.

Because of our work and research in diabetes, we provide support and services to senior clients, who are dealing with Type 2 diabetes, obesity, high blood pressure, and heart disease.

These diseases are fueled by some of the same biological processes that may trigger Alzheimer's Disease in some of our diabetic clients. Some of these biological processes include cellular inflammation, oxidative stress, excess cell toxicity, insulin resistance, and protein glycation.

And, since our diabetes nutritional program has been very effective with fighting these biological processes in our Type 2 diabetic clients, we decided (after some research) to expand our nutritional program to help people with Alzheimer's.

Unfortunately, most caregivers are unaware of these types of nutritional programs and how they can be beneficial to people with early onset Alzheimer's, primarily Stages 1 to 3.

So, let's bring this disease out of the darkness and take a look at how Alzheimer's develops and how a sound nutritional program with brain-stimulating lifestyle changes can help to prevent and treat Alzheimer's  Disease naturally without the need for medications -- before the disease gets worse and becomes too difficult to treat.

FYI: During our research, we came across a Dr. Bredesen of UCLA, who has written two books and conducted research and clinical trials indicating that memory loss can be reversed and sustained.  

Alzheimer's Disease (AD), also known as Type 3 diabetes, is a progressive neurodegenerative disease that causes damage to the brain and is the most common form of mental decline, or dementia, in older adults. The damage to the brain eventually causes problems with memory, intelligence, judgment, language, and behavior.

Alzheimer's Disease does not affect all memory capacities equally: short-term memory (the ability of hold information in mind in an active, readily-available state for a short period of time) is the first to go.

Next comes episodic memory (memory of autobiographical events); then, semantic memory (memory of the meanings of words and facts about the world); and finally procedural memory (how to perform tasks and skills).

As the disease advances, parts of memory which were previously intact also become impaired, and eventually all reasoning, attention, and language abilities are disrupted.

The earliest recognized symptoms of Alzheimer's Disease are often mild memory loss -- for example, a sufferer may begin to forget recent conversations or what year it is. There may be some disorientation (e.g. getting lost in familiar surroundings), problems with routine tasks (like using the stove), and changes in personality and judgment.

As the disease progresses, patients begin to have difficulty with the activities of daily living, and may require help feeding and bathing. There may be anxiety (suspiciousness and agitation), sleep disturbance, wandering and pacing, difficulty recognizing family and friends.

In the most advanced stages of the disease, patients suffer loss of the ability to speak, weight loss, lack of appetite, and loss of bowel and bladder control. By this point, patients require round-the-clock caregiving.

While AD itself is not directly fatal, it may leave patients vulnerable to infections and other diseases such as pneumonia, which may become the ultimate cause of death. Often, patients with the disease suffer increasing debilitation over a period of about 4-8 years, but an otherwise healthy individual can survive for decades.

Unfortunately, people with diabetes and heart disease are very susceptible to this disease because diabetes is an inflammatory and vascular disease that affects all organs of the body, including the brain.

As depicted in the following diagram, the gradual loss of brain function that characterizes Alzheimer's Disease seems to be due to two main forms of nerve damage:

  • Protein deposits known as amyloid plaques build up in the brain
  • Nerve cells (neurons) develop neurofibrillary tangles

As both the plaques and the tangles increase and spread throughout the brain, theymay cause cellular inflammation and oxidative stress -- biological processes that may fuel the progression of Alzheimer's Disease. 

Alzheimer's Brain with Amyloid Plaques and Fibrullary Tangles

In addition, these other pathologies and biological processes (e.g. inflammation, oxidation) may actually fuel the spread of Alzheimer's just as they fuel the spread of Type 2 diabetes and other vascular-related diseases!

Other biological processes that may fuel Alzheimer's include chronic inflammation, oxidative stress, insulin resistance, increased toxicity, protein glycation, immune system dysfunction, etc.

For example, in response to the plaques and tangles, the immune cells in the brain try to reduce this buildup.

The resident macrophages (immune cells) in the brain (called microglia) play multiple physiological roles, including maintenance of the brain’s micro-environment.

In an injured brain, activated microglia migrate to the inflamed site, where they remove neurotoxic elements such as amyloid plaques by phagocytosis (ingesting and devouring).

However, aged resident microglia are less efficient than their circulating sister immune cells in eliminating Aβ deposits from the brain, causing the Alzheimer's to continue to spread andget worse.

Another example, for people with Type 2 diabetes, the high glucose levels trigger insulin resistance, chronic inflammation, oxidation, and glycation. And, any or all of these processes may cause damage to the brain, its cells and its blood vessels.

Alzheimer's Disease Statistics

Here is a summary of the key statistics associated with Alzheimer's Disease:

  • Alzheimer's disease is the 6th leading cause of death in the United States.
  • There are approximately 700,000 people dying each year because they have Alzheimer's.
  • 1 in 3 seniors dies with Alzheimer's or another dementia.
  • More than 5 million Americans are living with Alzheimer's.
  • Every 66 seconds, someone in the United States develops Alzheimer's Disease.
  • Nearly half of care contributors -- those who are caregivers of someone with Alzheimer's and/or contribute financially to their care -- cut back on their own expenses (including food, transportation and medical care) to pay for dementia-related care of a family member or friend.
  • In 2015, 15.9 million caregivers provided an estimated 18.1 billion hours of unpaid care valued at more than $221 billion.
  • At least 25% of people who are at risk for Alzheimer's could avoid the disease if they were warned about their risk factors and the early signs of the disease.

Alzheimer's Disease has 7 stages of progression as these plaques and tangles increase and kill more nerve cells, eventually debilitating the patient as the brain ends up shrinking significantly in size.

1. No Cognitive Impairment: There are no obvious signs at this stage and people are able to function independently.

Major Tip!: During this stage and the next, be proactive and check the Risk Factors! If you have 3 or more of the risk factors, take preventive actions now and use some of our Natural Remedies!

2. Very Mild Cognitive Impairment: Symptoms at this stage are slight and seem to appear as forgetfulness associated with aging.

3. Mild Cognitive Impairment: Patients are still able to do daily routine and tasks. Symptoms include the following:

  • Forgetfulness, e.g. misplaced car keys, person's name
  • Memory loss, losing items
  • Trouble managing finances
  • Confusion while driving
  • Impaired work performance
  • Verbal repetition
  • Trouble managing medications
  • Loss of concentration, impaired organization
  • Trouble with problem-solving and complex tasks

4. Moderate Cognitive Impairment: Patients typically have trouble performing daily routine and tasks. Symptoms include the following:

  • Worsening of symptoms in previous stage
  • Trouble with routine tasks
  • Increased social withdrawal
  • Emotional moodiness
  • Lack of responsiveness
  • Reduced intellectual acuity
  • Increased memory loss and forgetfulness
  • Inability to use or find the correct words
  • Difficulty doing challenging mental math
  • Denial of symptoms
  • Trouble holding urine

5. Moderately Severe Cognitive Impairment: Beginning with this stage and continuing into the later stages of dementia, the patient may no longer be able to carry out normal day-to-day activities such as dressing or bathing without some caregiver assistance. 
Symptoms include the flowing:

  • Worsening of symptoms in previous stages
  • Pronounced memory loss, including memory of personal details and current events
  • Confusion about location or previous events
  • Further reduced mental acuity and problem solving ability, e.g. trouble with less challenging mental math
  • Needing help with selecting appropriate wardrobe

6. Severe Cognitive Impairment: This dementia stage is characterized by a need for caregiver help to perform even basic daily activities, such as dressing, eating, using the toilet and other self-care. 
Symptoms include the following:

  • Needing assistance when getting dressed
  • Needing assistance when using the restroom
  • Wondering and getting lost
  • Unable to recognize or recall names of loved-ones or caregivers
  • Sleep disturbances
  • Incontinence
  • Dramatic personality changes including paranoia or delusions
  • Changes in personality (paranoia or hallucinations)

7. Very Severe  Cognitive Impairment: In this stage patients will need constant care as he or she is essentially unable to care for themselves, and suffers from both communication and motor impairment. They may lose the ability to speak, smile or walk without help.
Symptoms include the following:

  • Loss of language skills
  • Loss of awareness of surroundings
  • Assistance when eating
  • Unable to control urination
  • Loss of muscle control to smile, swallow, walk, or sit without support

To summarize: As more and more neurons shrink and die, Alzheimer's Disease spreads and advances through several stages of cognitive dysfunction, from Very Mild Cognitive Impairment to Mild, Moderate, Moderately Severe, Severe, and Very Severe Cognitive Impairment.

Alzheimer’s-Disease-Pathology-Pathogenesis-Stages-Death-to-Diabetes

Key Point: If you are over the age of 50, have diabetes or heart disease, and begin to experience any of the symptoms in the early stages, you should take a proactive preventive approach and follow the nutritional and lifestyle strategies identified in our Alzheimer's Natural Remedies section below.

Similar to Type 2 diabetes development, Alzheimer's Disease (AD) is a progressive disease.

Unfortunately, Alzheimer's Disease is not recognized and diagnosed as early as Type 2 diabetes because there are no regular blood tests like there are for diabetes, e.g. fast blood glucose test, hemoglobin A1C test. There are symptoms (e.g. memory loss), but, nothing that clearly identifies that you're developing Alzheimer's.

Alzheimer's Disease is defined by the presence of specific abnormalities in the brain, called amyloid plaques and neurofibrillary tangles.

Amyloid plaques are sticky clumps of protein fragments which accumulate between the nerve cells in the brain. Amyloid is a protein fragment that the body produces normally. In a healthy brain, these protein fragments would break down and be eliminated by the microglia (immune cells). But, in Alzheimer's Disease, these fragments accumulate to form hard, insoluble plaques.

In Alzheimer's this protein begins to divide improperly, creating a substance called beta amyloid (Aβ) which is toxic to brain cells. As the beta amyloid builds up, it clumps to form plaques and the brain cells begin to die.

Neurofibrillary tangles (NFTs) are insoluble twisted fibers which consist of a protein called tau, which normally binds to and stabilizes part of a structure in the brain cell called a microtubule. The microtubule helps to hold the brain cell in its proper shape and also helps to transport nutrients and other important substances from the cell body of the nerve cell to its axon and dendrites.

In Alzheimer's Disease, the tau protein undergoes abnormal chemical changes that cause it to detach from the microtubules and stick to other tau molecules, forming threads that eventually clump together to form tangles.

The tangles disrupt the microtubule network, which collapses, causing brain cells to die and the brain to shrink over time.  In addition, these tangles create blocks in the neuron’s transport system; and, may also cause blocks in synaptic signaling.

As a result, synaptic loss increases as the synaptic connections between certain groups of neurons stop functioning and begin to degenerate. When neurons lose their connections, they cannot function properly and eventually die.

As more plaques and tangles accumulate in the brain and neuronal injury and death spread throughout the brain, connections between networks of neurons break down, and affected regions begin to shrink in a process called brain atrophy.

In other words, the physical size of the brain shrinks due to the shrinkage of neurons and due to the death of neurons.

By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly. 

Amyloid plaques, neurofibrillary tangles, synaptic loss, and cell death are the most striking features of the Alzheimer’s brain when it is viewed under the microscope after death.

However, scientists are now realizing that many other cellular changes occur in the brain during the Alzheimer’s Disease pathogenesis. For example, glial cells show abnormalities, as certain populations of glial cells begin to swell up and divide to produce more glial cells.

The Alzheimer’s brain also shows signs of cellular inflammation, a tissue response to cellular injury.  The inflammation, along with the amyloid plaques and fibrillary tangles, increase the production of free radicals. This, in turn, leads to oxidative stress and damage to the cell's mitochondria and DNA, which can trigger gene mutations.

In addition, if a person has had a vascular-related disease such as heart disease or Type 2 diabetes for many years, this triggers many harmful biological processes including insulin resistance, cellular inflammation, oxidation, toxicity, glycation, and immune system dysfunction.

This, in turn, increases the probability that this person may develop Alzheimer's, especially if they are apathetic, depressed and living a sedentary lifestyle -- both physically and mentally.

Some studies have shown that some patients with significant amyloid plaque and tangles did not develop Alzheimer's. However, many of the patients who had developed Alzheimer's did have other health issues, e.g. heart disease, obesity, high blood pressure, or Type 2 diabetes.

So, amyloid plaque and tangles alone do not guarantee that a person will develop Alzheimer's. But, if that person has other health issues, there is a high probability that that person can develop Alzheiemr's.

Alzheimer’s Disease Pathogenesis and Natural Remedies -- Death to Diabetes

In addition, brain blood vessel cells as well as brain neurons show signs of degeneration. Some of these other cellular changes likely occur in response to neuronal malfunction, and many of them could contribute to neuronal malfunction.

Brain Anatomy & Function 

The brain is comprised of over 100 billion interconnected neurons (nerve cells) and glial cells.  

Each neuron consists of a cell body, dendrites, and an axon. The cell body contains the nucleus and cytoplasm. The axon extends from the cell body and often gives rise to many smaller branches before ending at nerve terminals.

Dendrites extend from the neuron cell body and receive messages from other neurons. Synapses are the contact points where one neuron communicates with another. The dendrites are covered with synapses formed by the ends of axons from other neurons.

When neurons receive or send messages, they transmit electrical impulses along their axons, which can range in length from a tiny fraction of an inch (or centimeter) to three feet (about one meter) or more.

Many axons are covered with a layered myelin sheath, which accelerates the transmission of electrical signals along the axon. This sheath is made by specialized cells called glia. In the brain, the glia that make the sheath are called oligodendrocytes, and in the peripheral nervous system, they are known as Schwann cells.

The brain contains at least ten times more glial cells than neurons. Glial cells perform many jobs. Researchers have known for a while that glial transport nutrients to neurons, clean up brain debris, digest parts of dead neurons, and help hold neurons in place. Current research is uncovering important new roles for glia in the brain.

FYI: Glial cells are the most abundant cell types in the central nervous system. Types of glial cells include oligodendrocytes, astrocytes, ependymal cells, Schwann cells, microglia, and satellite cells.

The Brain and Its Lobes

In addition to the neurons and glial cells, the brain contains many other components as well as specific regions that perform specific types of work -- these regions are called lobes

The brain is able to function because of the structural and functional properties of interconnected neurons within these lobes.

There are four lobes on each side of the brain:

  1. The frontal lobe is important for cognitive functions and control of voluntary movement or activity.
  2. The parietal lobe processes information about temperature, taste, touch and movement
  3. The occipital lobe is primarily responsible for vision.
  4. The temporal lobe processes memories, integrating them with sensations of taste, sound, sight and touch.

Regions of Brain Affected by Alzheimer's Disease 

When Alzheimer's Disease attacks the brain, it kills millions of neurons, which eventually destroys the ability of the lobes to function.

Neurons cannot be regenerated except in the hippocampus. However, the brain can be retrained to use existing neurons to create new neural pathways.

In the early stages of Alzheimer's Disease, short-term memory begins to decline when the cells in the hippocampus and entorhinal cortex degenerate and die. Those with the disease lose the ability to perform routine tasks, retain short-term memory and create new memories.

As more neurons die, this affects areas in the cerebral cortex (the outer layer of the brain) responsible for language, reasoning, and social behavior. Judgment worsens, emotional outbursts and agitation may occur, language is impaired, and wandering may occur.

Specifically, Alzheimer's Disease spreads and causes damage to the temporal lobes, amygdala, frontal lobes, parietal lobes, occipital lobes, cerebellum, and, finally, the brain stem.

As depicted in the following diagram, each region of the brain affects specific functions, causing a person with Alzheimer's to eventually become, over a period of years, helpless and unresponsive to the outside world.

Alzheimer's Disease (AD) Impact on the Major Regions of the Brain

The specific regions of the brain that are damaged by Alzheimer's Disease include the following:

Hippocampus: The hippocampus (in each temporal lobe) is the part of the brain primarily responsible for short-term memory. Alzheimer’s disease starts in the hippocampus, deep within and part of the temporal lobe of the brain.

The hippocampus is the structure responsible for creating new memories from our experiences. This organ receives input from the various sensory centers of the cortex in the form of perceptions.

These sensory inputs are combined by the hippocampus into a complete experience. For example, the perception of an ocean sunset combines a multitude of visual impressions; a vast color palette with numerous shapes (a round red sun, the line of the horizon, purple clouds of all shapes and sizes, etc.).

But the experience is more than just visual. The sound of the waves and the gulls flying overhead. The smell and the taste of the salt water and the way the warm breeze feels against your face. You may be enjoying the moment with friends, and this also becomes a part of the overall experience, and of the memory.

It is the hippocampus that sorts and compares these impressions (like the sunset) and creates a memory. Memories at this stage are short-term memories. The hippocampus then decides if a particular memory will be committed to long-term memory.

As a result, the hippocampus plays a crucial role in learning and in processing various forms of information as long-term memory. Damage to the hippocampus produces global amnesia.

So it is not surprising that forgetting a recent event (short-term memory) is one of the very first symptoms of this disease. In addition to creating memories, the hippocampus also helps with spatial memory which allows us to navigate our world. Getting lost, even in familiar places, is another early sign of the disease.

As Alzheimer's continues to degenerate the hippocampus, short-term memory becomes severely impaired. 

Locus Coeruleus: The locus coeruleus is a small, bluish part of the brainstem that releases the neurotransmitter norepinephrine and is involved with physiological responses to stress and panic. 

Norepinephrine is responsible for regulating heart rate, attention, memory, and cognitive functions in the hippocampus, cortex, cerebellum, and other regions of the brain.

The neurons in the locus coeruleus send branch-like axons throughout much of the brain and help regulate blood vessel activity. Its high interconnectedness may make it more susceptible to the effects of toxins and infections compared to other brain regions.

FYI: It appears from a recent study that the locus coeruleus may be impacted by Alzheimer's before the hippocampus. According to Mara Mather, Professor of Gerontology and Psychology at the University of Southern California, stated that the locus coeruleus is the first brain region to show tau pathology. Though not everyone will get Alzheimer’s, autopsy results indicate that most people have some initial indications of tau pathology in the locus coeruleus by early adulthood.

The norepinephrine released from the locus coeruleus may contribute to preventing Alzheimer’s symptoms. Studies conducted with mice have shown that norepinephrine helps protect neurons from factors that kill the cells and accelerate Alzheimer’s disease, such as inflammation and excessive stimulation from other neurotransmitters.

Key Point: Norepinephrine is released when someone is mentally engaged or challenged by an intellectual activity — anything from reading a book, doing a word puzzle, or tackling a difficult problem-solving or musical task. Keeping your mind and body active throughout life — especially during older years — may help slow the progression of Alzheimer’s disease.

According to Professor Mara Mathers: “Education and engaging careers produce late-life ‘cognitive reserve’ or effective brain performance, despite encroaching pathology. Activation of the locus coeruleus-norepinephrine system by novelty and mental challenge throughout one’s life may contribute to cognitive reserve.”

FYI: The locus coeruleus is also damaged from the lack of sleep, recent studies have shown. Not sleeping enough harms neurons in the locus coeruleus. As a result, researchers have linked a lack of deep sleep to a brain more vulnerable to Alzheimer’s disease.

Temporal Lobe: From the hippocampus, the disease spreads outward into the cerebral cortex, the outer layer of the brain, beginning in the temporal lobes.

The temporal lobes, along with the prefrontal cortex, play an important role in processing sounds and language comprehension.

The temporal lobes, located behind each ear, are also involved in understanding sounds and spoken words, as well as emotion and memory.

Communication becomes difficult once this part of the brain in affected, where the patient struggles to find a word, or to string words together into a sentence. This difficulty with language gets more pronounced as the disease spreads toward the front of the brain.

The temporal lobe is the part of the brain also involved in sensory processing, long-term memory, and linguistic skills.

The damage to the temporal lobe caused by Alzheimer's can result in an increasing inability to articulate ideas, and retain complex ideas, as well as impaired linguistic skills.

It is also quite common for vivid visual and auditory hallucinations to occur. Moreover, the damage that Alzheimer's inflicts on the temporal lobe impairs the ability to recognize familiar places, objects, and people. 

Amygdala: The amygdala is the section of the brain responsible for managing basic emotions such as fear and anger.

When Alzheimer's has severely damaged the amygdala, the result is emotional instability. It is quite common for episodes of paranoia, temper outbursts, and bouts of anxiety to occur due to the damage Alzheimer's has inflicted upon the amygdala.

Frontal Lobe: The frontal lobe is responsible for logic, decision-making, regulating behavior, complex planning, learning, and has a major role in personality.

It is involved with controlling responses to input from the rest of the central nervous system (brain and spinal cord). It is responsible for voluntary movement, emotion, and execution of behavior, intellect, memory, speech, and writing.

As Alzheimer's gradually damages the frontal lobe, complex tasks such as driving, cooking, or multi-step planning may become severely impaired by Alzheimer's.

Moreover, the damage Alzheimer's inflicts upon the frontal lobe also results in the loss of motivation, resulting in sluggishness and apathy.

The damage that Alzheimer's disease inflicts upon the frontal lobe also results in the gradual loss of inhibition and impulsive behavior.

The frontal lobes and the prefrontal cortex are the parts of the brain most associated with making us who we are. The frontal lobes lie directly behind the forehead and in large part control voluntary movement like walking and finger tapping.

It plays an important role in preserving memories, especially emotion based memories arriving from the brain’s limbic system. The frontal lobe contains the dopamine system which is associated with reward, attention, short-term memory tasks, planning, and motivation. It moderates responses so that our behavior is appropriate and acceptable in social situations.

The prefrontal cortex covers the forward part of the frontal lobes. It is responsible for our executive functioning. Many researchers believe it to be the center of our personality. Executive functions include our ability to differentiate between conflicting thoughts, between good and bad, for example. It is the prefrontal cortex that gives us the ability to choose between alternatives and to make decisions.

This is the part of the brain that allows us to project possible future outcomes from current actions. To a large extent, the prefrontal cortex is the part of the brain that makes us who we are. Most of our conscious thinking is done here. Once Alzheimer’s disease progresses to this point a person will begin to lose the ability to care for himself or herself.

When the disease gets to the front of the brain, it continues to do damage to the hippocampus and the temporal lobes. And it not only damages brain cells, it damages connections. Much of our ability to think and process information is a result of the interconnectedness of all of the different areas of the brain.

Parietal Lobe: From the prefrontal cortex, Alzheimer’s Disease spreads toward the back of the brain, into the parietal, then the occipital lobes.

The parietal lobe (located above the ear) is primarily responsible for integrating and processing sensory information as it receives and interprets sensations of pain pressure, temperature, touch, size, shape, and body part awareness. Tasks such as reading, writing, mathematics, and spatial navigation are typically processed by the parietal lobe.

Alzheimer's systematically destroys the parietal lobe throughout the various (7) stages of the disease's progression. Symptoms, such as a deterioration of reading and writing skills, as well as an increasing inability to properly locate objects within a three-dimensional space, or correctly gauge distance, occur with increasing frequency and severity. 

Our sense of touch, the somatic sense, is located in the parietal lobe. This structure is responsible for processing information coming in from various receptors under our skin, in our bones and in our organs that collectively make up our sensates.

These "sensates" include awareness of sensations like hunger, heat and cold, and the spatial awareness of our bodies (proprioception). Like so many other parts of the brain, the parietal lobes play a role in language processing.

It seems that people in the later stages of dementia can often be engaged through these somatic senses when other sensory stimulation fails. This has given rise to a category of Alzheimer therapy called Comfort Care. Comfort Care includes dolls and stuffed animals, soft gloves and socks containing skin conditioners, and items containing attachment to be “fiddled” with.

Occipital Lobe: From the parietal lobes, Alzheimer’s Disease spreads to the occipital lobes, which are located at the back of the head.

The occipital lobes contain the visual cortex, responsible for understanding the meaning of the written word and for understanding visual images and processing information coming from the eyes.

Damage to the occipital lobe compromises visual perception, and often causes visual hallucinations. Hallucinations of any of the senses can occur with dementia.

Compromised visual perception doesn’t just result in poor vision or blindness, or in hallucinations, though those are all possible outcomes.

Perceptual problems can cause an alternating pattern in carpeting or tile to be interpreted as holes in the floor. A beautiful bathroom can become an obstacle course. Lines in the carpet becomes steps, and walking becomes very tenuous. These changes in perception need to be considered when designing and decorating for a person with dementia. 

These lobes process much of the information coming in from our sense organs, and when these areas are damaged it becomes harder to make sense of the world.

Alzheimer’s is now progressing into its later stages. Language processing, movement, perception, and memory are being radically affected due to the areas of the brain damaged by the disease. At this point safety becomes a primary concern, and the individual needs almost constant care.

Cerebellum: Located under the occipital lobes the cerebellum is responsible in large part for our kinesthetic (muscle) sense, and controls balance and how we move. It is also believed to add something to cognitive functioning and language.

Movement is initiated in the frontal lobes, primarily in the motor cortex, but the cerebellum “fine tunes” that movement. It adds coordination and precision to motion.

“Cerebellum” is latin for “little brain”, and indeed it looks like something separate from the rest of the brain. It does not have the familiar cortical convolutions we associate with the brain, but looks a bit more like muscle.

Like the rest of the brain it is a highly complex structure and not completely understood, but it is clear that movement is its primary function. “A standard test of cerebellar function is to reach with the tip of the finger for a target at arm’s length: A healthy person will move the fingertip in a rapid straight trajectory, whereas a person with cerebellar damage will reach slowly and erratically, with many mid-course corrections.”

This type of motion is noticed in the later stages of Alzheimer’s; and, once the disease reaches the base of the brain it is nearing the end of its progression.

Brain Stem: Finally the path of destruction reaches the brainstem. The brainstem includes the midbrain, the pons, and the medulla oblongata. The brainstem connects the brain with the spinal cord and is the conduit through which signals are passed back and forth between the brain and the body, including the organs.

The brain stem controls the flow of messages between the brain and the rest of the body, and it also controls basic body functions such as breathing, swallowing, heart rate, blood pressure, consciousness, and whether one is awake or sleepy.

More specifically, the midbrain serves as a relay center for visual, auditory, and motor system information. It regulates autonomic functions, those that the body carries out without conscious thought, such as digestion, heart rate, and breathing rate.

The pons, a major structure in the upper part of the brain stem, regulates breathing and deep sleep; and, is involved in the transmission of signals to and from other structures in the brain, such as the cerebrum or the cerebellum. The pons is also involved in sensations such as hearing, taste, and balance. 

The medulla oblongata, located in the lower portion of the brainstem, is very important in things like heart rate and blood pressure; and, is responsible for many reflexes in the body, or involuntarily controls, such as vomiting, sneezing, and coughing.

The brainstem is the last area to be affected, and when damage here becomes severe enough autonomic functions including breathing and heart rate will cease.

During the early stages of Alzheimer's Disease, progressive damage to the brain stem can result in erratic sleep patterns. As Alzheimer's develops, sensory problems involving vision and hearing will occur.

As Alzheimer's continues to damage the brain stem, other complications, such as difficulties swallowing, breathing and erratic blood pressure and arrhythmia, develop.

Final Stages of Alzheimer's Disease

In the final stages of Alzheimer's, the brain has completely atrophied and is unable to perform most tasks required for day-to-day living.

Patients may lose the ability to feed themselves, speak, recognize people and control bodily functions. Memory worsens and may become almost non-existent.

By this time, constant care is typically necessary. On average, those with Alzheimer's live for 8 to 10 years after diagnosis, but this terminal disease can last for as long as 20 years.

Unfortunately, these plaques and tangles can only be detected by direct examination of brain tissue, which means that Alzheimer's Disease is only diagnosed after death, via autopsy.

In a living patient, doctors diagnose "probable AD" if a patient shows all the behavioral symptoms of AD, and if all other possible causes of dementia are ruled out.

Here is a list of the key risk factors associated with Alzheimer's Disease (AD):

Age. Increasing age is the greatest known risk factor for developing Alzheimer's. After you reach age 65, your risk of developing the disease doubles about every five years. Nearly half of those over the age of 85 have Alzheimer's. 

Family history and genetics. Your risk of developing Alzheimer's appears to be somewhat higher if a first-degree relative (e.g. parent, sibling or child) has the disease. Scientists have identified rare changes (mutations) in three genes that guarantee a person who inherits them will develop Alzheimer's. But these mutations account for less than 5 percent of Alzheimer's disease. 

Sex. Women may be more likely than are men to develop Alzheimer's disease, in part because they live longer.

Depression. People who are depressed all the time and full of apathy are at a higher risk of developing Alzheimer's.

Sedentary thinking. People who stop learning and are not social have a higher risk of Alzheimer's due to the lack of brain stimulation. Mental exercise of some kind is just as important to the brain as physical exercise is to the body.

Insomnia, sleep apnea. Lack of quality sleep (7-8 hours, no interruptions) and deep sleep (with REM) may prevent the brain from storing and retaining memories. Also, studies indicate that it is during REM sleep when the body releases growth hormone and initiates cell repair.

This can be very important when fighting a progressive disease like Type 2 diabetes. Since, as the disease progresses, it causes increased cell and tissue damage, it is imperative to eat healthy, exercise and sleep well to help promote cell repair at night.

Mild cognitive impairment. People with mild cognitive impairment (MCI) have memory problems and have an increased risk of later developing dementia.

Being diabetic. If you have had diabetes for many years with uncontrolled blood sugar and the use of diabetic medications, this may increase your risk for developing Alzheimer's Disease.

Having heart disease. If you have had heart disease for many years with the use of various heart medications, this may increase your risk for developing Alzheimer's Disease. Heart disease affects the blood vessels of the cardiovascular system, which includes the blood vessels that feed the brain.

Lifestyle and heart health. Some evidence suggests that the same factors that put you at risk for heart disease and diabetes may also increase the chance that you'll develop Alzheimer's. These factors include:

  • Poor diet
  • Excess exposure to heavy metals, neurotoxins 
  • Lack of exercise
  • Smoking
  • High blood pressure
  • High cholesterol
  • High blood sugar
  • Inflammation markers, i.e. homocysteine, CRP, lp(a)
  • Insomnia, sleep apnea
  • Excess prescription/OTC drug usage

In addition, these risk factors are also linked to vascular dementia, a type of cognitive decline caused by damaged blood vessels in the brain.

Key Point: This cannot be emphasized enough: If you are over the age of 50, have diabetes or heart disease, and begin to experience any of the symptoms in the early stages of dementia, you should take a proactive preventive approach and follow the nutritional and lifestyle strategies identified in our our Alzheimer's Natural Remedies section below.

Studies have found that people with Type 2 diabetes have nearly twice the risk of developing Alzheimer's or other forms of dementia as people without diabetes.

That could partly be due to their higher rates of stroke and narrowing in the arteries supplying blood to the brain, according to Srikanth's team.

But it could also be related to degeneration in brain tissue. In an earlier study, the researchers found that older adults with diabetes tended to show more brain "shrinkage" than those without the disease.

Diabetes can cause several major complications because of the damage to your blood vessels, e.g. retinopathy, neuropathy, nephropathy, cardiovascular disease.

Because of this, diabetes is considered a risk factor for vascular dementia. This type of dementia occurs due to brain damage that is often caused by reduced or blocked blood flow to your brain as well as damage to the neurons in the brain.

Diabetes may also increase the risk of developing mild cognitive impairment, a condition in which people experience more thinking (cognitive) and memory problems than are usually present in normal aging. Mild cognitive impairment may precede or accompany Alzheimer's disease and other types of dementia.

Many people with diabetes have brain changes that are hallmarks of both Alzheimer's disease and vascular dementia. Some researchers think that each condition fuels the damage caused by the other.

Several research studies following large groups over many years suggest that adults with Type 2 diabetes have a higher risk of later developing Alzheimer’s Disease.

Medical researchers don’t know yet what causes Alzheimer’s disease or exactly how Alzheimer’s and diabetes are connected. But they do know that high blood sugar and insulin can harm the brain in several ways:

  • Diabetes raises the risk of heart disease and stroke, which damages the heart and blood vessels.
  • Damaged blood vessels in the brain may contribute to Alzheimer’s disease.
  • The brain depends on many different chemicals, which may be unbalanced by too much insulin. Some of these changes may help trigger Alzheimer’s disease.
  • High blood sugar causes inflammation. This may damage brain cells and help Alzheimer’s to develop.

Note: In addition to the connection to diabetes, Alzheimer's also has a connection to heart disease.

Scientists are discovering that cardiovascular disease and Alzheimer’s disease are closely linked, sharing common triggers and physiological characteristics such as cellular inflammation and increased oxidative stress.

A key factor linking cardiovascular disease and Alzheimer’s disease is hypoxia, or insufficient tissue levels of oxygen, caused by impaired blood flow. The brain is especially vulnerable to hypoxia’s damaging effects.

Cellular Inflammation -- a Common Link? 

Heart disease, specifically atherosclerosis, is due to inflammation in the arteries; arthritis is due to inflammation in the joints; Alzheimer's is due to inflammation within the brain; Type 2 diabetes is fueled by hyperglycemia and chronic inflammation.

See the common link here? Cellular inflammation!

Cellular inflammation in Alzheimer's is called neuroinflammation. Other than Aβ and tau, neuroinflammation is the most important factor involved in the pathogenesis of AD.

The effects of neuroinflammation are mediated by activated microglial cells which are a source of cytokines and a potent generator of free radicals.

As a result, the increase in free radicals causes oxidative stress, which causes mitochondrial DNA mutations, mitochondrial dysfunction and more oxidative stress. This process is accelerated in AD by the action of the amyloid plaques (Aβ) and activated microglia, also a source of free radicals.

And, if the Alzheimer's patient has Type 2 diabetes, the increase in insulin and blood glucose levels increase the production of protein glycation and advanced end products (AGEs), which, in turn, increase inflammation and oxidation.

Consequently, it becomes imperative for people with Type 2 diabetes to get their diabetes and blood glucose under control during the early years of the disease in order to stop the progression of cellular inflammation, oxidation, and glycation; and, hopefully, prevent the onset of Alzheimer's down the road.

Here is a flow chart that shows you how chronic inflammation and oxidationcan lead to Alzheimer's and other similar diseases.

Inflammation: Prevents Reversing Diabetes

Alzheimer's Disease is a very complex disease with multiple causes, some of which are similar to the causes associated with other systemic, lifestyle-driven diseases such as heart disease, cancer, Type 2 diabetes, and obesity.

Because these diseases are associated with some of the same biological causes and processes (e.g. cellular inflammation, oxidation (free radicals), insulin resistance, toxicity, protein glycation), then, these diseases can be treated effectively with natural treatment strategies such as a plant-based anti-inflammation and antioxidant-rich diet that specifically targets these diseases.

However, it is unfortunate that people with Alzheimer's Disease are unaware that there are proactive and natural treatment strategies for fighting this horrific disease.

To make matters worse, the caregivers and loved ones who care for people with Alzheimer's are also unaware of these proactive and natural treatment strategies.

As a result, caregivers, loved ones and Alzheimer patients primarily focus on helping the patient with prescription drugs and with ways to cope with their disease while it steadily progresses. But, they do nothing to, at least, stop the progression of the disease!

Years ago, the same problem existed with Type 2 diabetes -- most diabetics were taught how to cope with the disease as it progressed and caused more tissue and organ damage.

Although many diabetics still focus on coping with their diabetes by taking medications, more and more diabetics are learning how to, at least, slow down the progression of their disease with diet and exercise and without the need for medications. 

Unfortunately, very little progress has been made in these areas with Alzheimer's because there are no medical tests that a patient can perform to track and measure their Alzheimer's. 

However, given some of the similarities between Alzheimer's and diabetes, there are some safe and reasonable actions that people with Alzheimer's can take.

At a minimum, most diabetics (and non-diabetics) can prevent the onset of Alzheimer's by using one or more of the following natural remedies:

  1. Nutrition
  2. Supplementation
  3. Cleanse and Detox
  4. Regular Exercise Regimen
  5. Anti-Stress and Emotional Support
  6. Social Engagement

These strategies include eating a plant-based, anti-inflammatory diet (that supports brain function) and by exercising the body and brain on a consistent basis. Detoxing on a periodic basis to help remove heavy metals and toxins is also important.

Based on some recent research from a Dr. Dale Bredesen at UCLA, caregivers, love ones, and people with Alzheimer's should still make changes to their diet and exercise regimen, especially before the disease progresses to a point where the patient can no longer take care of himself or herself.

Dr. Bredesen of the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging has conducted research and a small clinical study indicating that memory loss can be reversed and sustained.  

The study is the first to suggest that memory loss in patients may be reversed — and improvement sustained — using a complex, 36-point therapeutic program that involves comprehensive diet changes, brain stimulation, exercise, sleep optimization, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

Key components of his program include:

  • Eating a Mediterranean diet high in vegetables and good fats
  • Regular cardio exercise
  • Fasting at least 12 hours after dinner
  • Brain training exercises
  • Getting at least 8 hours of sleep
  • Taking nutritional supplements to address patient's deficiencies

The findings of his study are published in one of the online editions of the journal Aging (http://www.aging-us.com/article/100981).

Dr. Bredesen, UCLA’s Augustus Rose Professor of Neurology, said the findings are “very encouraging,” but he added that the results are anecdotal, and a more extensive, controlled clinical trial is needed.

Nutritional Strategy for Alzheimer's Disease

Diet. A Mediterranean-type diet (e.g. Death to Diabetes Diet) based on vegetables, some whole fruits, fish, nuts, seeds, herbs, plant oils and some (organic) whole grains has been proven to benefit both heart and brain function.

Foods that have been scientifically shown to fight Alzheimer's are green tea, pomegranates, apples, wild blueberries, flaxseed, garlic, extra virgin coconut oil, and green leafy vegetables such as broccoli and spinach. 

These foods have high antioxidant content, and others, like blueberries, have have high anthocyanin and antioxidant content, which are known to guard against Alzheimer's and other neurological diseases. 

Make sure that you eat fiber-rich foods (e.g. beans, flaxseed, broccoli) because fiber helps to remove PCBs and other contaminants from the body.

Foods that should be avoided include: refined flour, sugar, gluten, grains, trans fats, vegetable oils, processed foods, excess animal meat (especially beef), etc. Also, OTC and prescription medications should be kept to a minimum.

In addition, reduce exposure to heavy metals and other neurotoxins, e.g. avoid using aluminum pans to cook with; avoid drinking soda and diet soda; avoid fast foods and junk foods; etc.

Omega-3 EFAs. Found primarily in cold-water fish, this powerful nutrient has been shown to slow down cognitive degeneration. University of California researchers experimented with mice bred to develop Alzheimer’s symptoms. They found that a DHA diet decreased the presence of specific proteins responsible for neural damage in the brains of these test subjects.

The study indicates that DHA fat may be helpful in suspending the progression of Alzheimer’s symptoms. DHA is a an omega-3 fatty acid found in eggs, fish, organ meats and algae.

Extra Virgin Coconut Oil. This fat has anti-bacterial, anti-viral and anti-inflammatory properties, all of which are beneficial to anyone dealing with a disease such as Alzheimer's. refer to the Olive Oil and Coconut Oil web page for details.

Nutritional Supplementation for Alzheimer's

Antioxidants. The consumption of foods that provide specific anti-oxidants has been shown in studies to help offset some of the toxic effects of amyloid beta compounds in the brain cells, as well as improve brain function. Some of these anti-oxidants include grapeseed OPC, ginkgo biloba, turmeric, lipoic acid, and CoQ10.

Acetyl-L-Carnitine (ALC). ALC is a natural amino acid-derived molecule that contributes to movement of fatty acids and other vital fuels from the cell into mitochondria. As such, it contributes to brain mitochondrial health and efficiency.

Animal studies show that acetyl-l-carnitine supplementation decreases buildup of amyloid beta and tau proteins, and speeds degradation of amyloid beta, contributing to its rapid clearance from brain cells.

At the same time, acetyl-l-carnitine boosts natural cellular antioxidant levels. These changes are accompanied by improved memory, cognition, and behavior, including slowing the rate of deterioration.

Alpha lipoic acid (ALA). ALA is a universal antioxidant that can stabilize cognitive functions among Alzheimer's patients and may slow the progression of the disease.

Ashwaganda. This adaptogenic herb has been a part of India's Ayurvedic medical system for thousands of years and is regarded as a wonder herb.

This herb is primarily used for stress reduction and improved energy and vitality, but, recent research has revealed this herb may also fight off the devastating effects of Alzheimer's disease.

Researchers at the National Brain Research Centre (NBRC) have conducted studies on mice that suggest ashwaganda extract may reverse memory loss and improve cognitive abilities in those with the disease.

After 30 days, the behavior of the mice returned to normal. Researchers reported: A reduction in amyloid plaques along with tangles of nerve fibers, and improved cognitive abilities. Rather than impacting the brain directly, researchers found that the herb worked by boosting a protein in the liver, which enters the bloodstream and helps clear amyloid from the brain. Researchers concluded:

"The remarkable therapeutic effect of ashwaganda reverses the behavioral deficits and pathology seen in Alzheimer's disease models."

Chlorella, Wheatgrass. These nutrients contain chlorophyll, which helps with detoxing the body. Chlorella is well-known for its ability to remove heavy metals. 

Coenzyme Q10. CoQ10 is an essential nutrient that helps keep mitochondria healthy by improving their efficiency at burning foods to produce energy.

Laboratory studies show that CoQ10 supplementation reduces the amount of amyloid beta plaque formation in brain cells, resulting in improved behavior.

Ginkgo biloba. This herb contains several compounds that may have positive effects on cells within the brain and the body. Ginkgo biloba has both antioxidant and anti-inflammatory properties, to protect cell membranes and to regulate neurotransmitter function.

Ginkgo has been used for centuries in traditional Chinese medicine and currently is being used in Europe to alleviate cognitive symptoms associated with a number of neurological conditions.

Ginseng. Panax ginseng and its extracts are used in traditional Chinese medicine to enhance memory and cognition. This natural plant product has multiple mechanisms of action, including reducing amyloid beta plaque formation, enhancing amyloid beta clearance, and reducing brain cell death.

Animal studies show that ginseng treatment reverses many of the memory and behavioral abnormalities found in models of Alzheimer’s.

Human clinical trials show good efficacy of ginseng extracts in terms of improving scores on the standard Alzheimer’s rating scales. One study of ginseng showed improvements that continued until treatment was stopped, after which scores declined to those of the control group.

Green Tea. Green tea is rich in a variety of polyphenols, especially one called EGCG, that has multiple beneficial attributes. EGCG interferes with the Alzheimer’s disease process in several important ways.

EGCG physically blocks the assembly of amyloid beta proteins, preventing them from clumping together to form plaques. The compound also generates a unique set of stable proteins from the amyloid beta precursor molecule; these proteins can’t bind together at all, further reducing the burden of plaque.

EGCG, given before exposure, prevents mitochondrial dysfunction induced by amyloid beta in brain cells, while also normalizing cells’ responses to the excitatory neurotransmitter NMDA.

Huperzine. Huperzine A is a biochemical component of the Chinese club moss Huperzia serrata. It binds reversibly to the enzyme that destroys the neurotransmitter acetylcholine, helping to maintain the signaling molecule’s presence in the synapses, where nerve cells communicate.

This mechanism is similar to that of most common Alzheimer’s drugs available today, but Huperzine also blocks the excitatory NMDA channels that overstimulate brain cells, offering a path not only to symptom relief but also to slowing the disease itself.

Finally, huperzine protects mitochondria from the destructive effects of amyloid beta, and triggers enzymes that degrade the toxic protein.

Magnesium. Some preliminary research strongly suggests a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Unfortunately, most magnesium supplements do not pass the blood- brain barrier, but a new one, magnesium threonate, appears to and holds some promise for the future for treating this condition and may be superior to other forms.

N-acetylcysteine (NAC). NAC is an amino acid precursor of the cellular antioxidant glutathione. As such, it can boost intracellular protection against the ravages of oxidant stress. NAC has been used in the laboratory successfully to clean up reactive oxygen species and ameliorate the behavioral changes seen in older animals and those with features of Alzheimer’s.

A recent study in mice showed that NAC supplementation could mitigate isolation-induced oxidant stress and amyloid beta formation.

Phosphatidylserine (PS). PS is a kind of lipid, or fat, that is the primary component of the membranes that surround nerve cells. The theory behind treatment with phosphatidylserine is its use may shore up the cell membrane and possibly protect cells from degenerating.

Turmeric. This herb contains curucumin, a power antioxidant and anti-inflammatory that may work synergistically with Vitamin D3 to trigger specific immune cells (macrophages) to target and eliminate amyloid fibrils and other waste products that accumulate in the brain before they manifest into detectable disease conditions.

Vitamin B-Complex. A study in Sweden, published in Proceedings of the National Academy of Sciences, found that vitamins B6, B12, and folic acid may help slow the progression of the disease, confirming and supporting previous studies. As reported in the featured article:

"The fact that B-family vitamins may play a significant role in dementia, or more specifically in warding it off has been consistently illustrated. What is news from the current study, however, is that high-dose B-vitamin treatment in people at risk for the disease 'slowed shrinkage of whole brain volume,' and especially reduced shrinkage in areas known to be affected in Alzheimer's disease."

Vitamin C. This vitamin is well-known for its antioxidant capabilities to help fight oxidative stress. However, eats lots of vegetables and fruits to get your Vitamin C. If you take a Vitamin C supplement, avoid ascorbic acid -- it is synthetic and is not true Vitamin C!

Vitamin E. Foods with Vitamin E provide antioxidant protection against the development of Alzheimer's. Foods include nuts, seeds, wheat germ, olives, avocado, broccoli, spinach and other greens as well as fruits like blueberries and dark grapes.

If you take a Vitamin E supplement, avoid alpha-tocopherol and especially dl-alpha tocopherol. Instead, look for a Vitamin E supplement with mixed tocopherols and tocotrienols.

Note 1: Make sure that the supplements are not synthetic since synthetic supplements are known to contain heavy metals and other chemical additives.

Note 2: Since some supplements may interact negatively with your medications, always consult with your physician first.

Note 3: For more information about inflammation and oxidation and how to fight it, refer to the Inflammation/Oxidation and Anti-inflammatory Foods web pages.

Other Strategies for Alzheimer's Disease

Detox. Perform a periodic detox (at least once every 6 months) to help remove heavy metals and toxins from the liver and colon.

Avoid exposure to heavy metals such as aluminum (cookware, antiperspirants), mercury (dental fillings), and neurotoxins (e.g. aluminum and mercury in vaccines). 

Stress. The reduction in the stress in your life has been proven to decrease the production of stress hormones (such as cortisol). These hormones damage the brain, eroding your mind and body. Meditation, yoga, art, deep breathing, music, a hobby, dreaming, and gardening are several ways that you can manage your stress. 

Exercise your body. In conjunction with a good diet, regular physical activity has been shown to reduce cognitive decline and to prevent its early onset.

In one study, it was found that just 45 minutes of exercise three days a week actually increased the volume of the brain. Even for people who have been very sedentary, exercise improves cognition and helps people perform better on things like planning, scheduling, multitasking and working memory.

For people with diabetes, since high insulin levels prevent brain cells from accepting glucose (the brain's primary fuel), it is imperative that all diabetics exercise regularly and follow a plant-based diet to reduce insulin levels as well as other levels such as blood pressure, blood cholesterol, and blood glucose.

Exercise your mind. Stimulate your mind, by learning something new, such as learning to play an instrument or a new language. Researchers suspect that mental challenges help to build up your brain, making it less susceptible to the lesions associated with Alzheimer's Disease.

Drugs. Avoid prescription drugs and OTC drugs, especially flu vaccines, antacids, antihistamines and statins.

  • Mercury and aluminum are neurotoxins from the vaccines, which can build up in the brain and kill brain cells.
  • Antacids block stomach acid, which is needed to digest food and nutrients, especially protein and B vitamins, which are fuel for your brain.
  • Antihistamines, OTC sleep aids like Benadryl, allergy medications like chlorpheniramine and antidepressants like doxepin and amitriptyline are now known to be major culprits in memory loss.
  • Statin drugs have a bad track record when it comes to causing memory loss.While most cases are slow and insidious, some people have experiences sudden and catastrophic memory loss. For some people, their memory is never the same, even after they stop taking the statin drugs.

Mental stimulation. Learning a new skill such as playing the piano or writing a book stimulates your brain and its cells such that new memories, new motor skills and new neural pathways are created! 

Learning these types of new skills help to ward off dementia by strengthening the connections between parts of your brain. While brain games improve a limited aspect of short-term memory, challenging activities such as playing a piano strengthen entire networks in the brain.

In addition, learning a new skill is enjoyable and rewarding on so many levels.  

Lifelong learning and social engagement. It appears that using your brain develops more cell-to-cell connections, which protects your brain against the impact of Alzheimer-related changes. 

Social/learning factors that may reduce your risk of developing Alzheimer's include:

  • Dancing, socializing with others
  • Higher levels of formal education
  • A stimulating job
  • Teaching others
  • Mentally challenging leisure activities, such as reading, playing games or playing a musical instrument
  • Travel, hobbies, volunteer work
  • Frequent social interactions
  • Music, Dancing (sensory therapy)

Turmeric and its active ingredient curcumin have multiple properties that provide health benefits to prevent Alzheimer's Disease and help people with Alzheimer’s Disease.

1. Curcumin prevents accumulation beta amyloid plaques

Curcumin inhibits formation of beta amyloid plaques by various mechanisms. It inhibits the action of presenilin-1, one of the core proteins that contribute to formation of these plaques.

Curcumin disrupts beta amyloid plaques fibrils and prevents neurotoxicity. Curcumin and demethoxycurcumin (a natural curcuminoid) is found to prevent accumulation of both beta amyloid and tau proteins in Alzheimer’s.

References: Bukhari et. al have identified various curcumin derivatives that clear beta amyloid toxicity and can benefit in Alzheimer’s. Curcumin derivatives are also found to inhibit tau protein aggregates.

Animal as well as experimental studies reveal that curcumin reduces aggregation of amyloid beta plaques even at a low dose.

2. Curcumin reduces cellular inflammation

Neuroinflammation or inflammation of the brain is observed in Alzheimer’s disease which occurs as a result of trauma, exposure to oxidative agents, infection and formation of beta amyloid plaques.

Curcumin inhibits inflammation in Alzheimer’s by preventing amyloid beta plaques and acting on nuclear factor kappa B, a major protein that regulates inflammation.

References: Lim et. al have proven that curcumin can be a natural alternative to help reduce neuroinflammation.

A study published in Neurochemistry International, 2016 identifies curcumin as one of the candidates that reduce inflammation in Alzheimer’s.

3. Curcumin provides antioxidant defense to reduce oxidation

Exposure to heavy metal contaminants risks the accumulation of such metals in the brain which trigger inflammation and accumulation of amyloid beta plaques in the brain.

Curcumin derivatives are found to inhibit accumulation of such heavy metals in Alzheimer’s diseases.

Among the various antioxidants tested, curcumin was found to benefit in various aspects of treatment and prevention of Alzheimer’s disease including metal chelation or removal of heavy metal.

Curcumin’s antioxidant action counteracts reactive oxygen species that contribute to progression of Alzheimer’s disease and protects from neurotoxicity.

Mitochondria are power houses of the cells and dysfunction of these units are observed in Alzheimer’s disease. Curcumin as an antioxidant can protect from such mitochondrial dysfunction in Alzheimer’s disease.

References: A study published in Food Chemistry, 2016 investigated the role of various dietary antioxidants in Alzheimer’s disease. They served as metal chelators, prevented formation of reactive oxygen species and amyloid beta plaque.

Huang et. al have demonstrated that curcumin reduces oxidative stress in animal model of Alzheimer’s and thereby decreasing brain cell loss.

4. Curcumin is neuroprotective

Curcumin nanoparticles are being investigated in relation to treatment of Alzheimer’s and experimental study suggests that curcumin can support neurogenesis- a brain self repair mechanism.

Curcumin may offer neuroprotection in Alzheimer’s disease by inducing autophagy- a form of cell death which in normal conditions can help degrade amyloid beta.

References: Chin et. al comment that curcumin can serve as a neuroprotective (protecting the brain) agent in Alzheimer’s disease by virtue of its anti-amyloidogenic, anti-inflammatory, anti-oxidative, and metal chelating properties.

An animal study shows that curcumin reverses amyloid beta formation and ameliorates structural changes in neurons.

Though most studies are focussed on curcumin’s therapeutic efficacy in Alzheimer’s disease, a study published in Phytotherapy Research, 2014 reveals that curcuminoids mixture present naturally in turmeric may have a better medicinal value in Alzheimer’s disease.

Another experimental study by Ahmed et. al also suggests that curcuminoids mixture is more beneficial than curcumin in balancing brain related chemicals and protecting memory in Alzheimer’s.

5. Curcumin protects memory and cognition

Research proves that curcuminoids enhance memory in Alzheimer’s.

Glial fibrillary acidic protein is commonly expressed in nerve cells but in Alzheimer’s it is identified as a marker of neurodegeneration or degeneration of nerve cells.

Experimental study shows that curcumin regulates the expression of this protein in order to protect memory and prevent Alzheimer’s disease progression.

References: Curcumin protects nerve cells and improves learning and memory abilities in Alzheimer’s disease. A study published in Plos One 2015, suggests that curcumin improves cognitive function in Alzheimer’s disease by elevating the levels of BDNF- a protein that supports nerve growth.

A study published in British Journal of Nutrition, 2016 examined the effect of curcumin supplementation in older individuals and their cognitive function. The study lasted for 12 months.

Cognitive decline was observed in placebo group but not in curcumin group.

Brondino et. al comment that curcumin is safe for short term use in dementia but till date there is insufficient evidence to comment upon the clinical use of curcumin in dementia.

Various animal studies suggest that curcumin enhances memory and protects from dementia in Alzheimer’s. Clinical study demonstrates that curcumin protects cognitive function in elderly but more studies are required to confirm this.

6. Curcumin can strengthen immune responses

Neuroimmunomodulation describes the nerve cell damage caused by uncontrolled inflammatory processes.

Alzheimer’s disease is characterised by certain immune defects; under normal conditions the immune system clears amyloid beta plaques but this is not the case in Alzheimer’s.

References: Cashman et. al have proven that bisdemethoxycurcumin, a natural curcuminoid restores immune function in Alzheimer’s and stimulates immune cells to clear amyloid beta plaques by phagocytosis (process by which immune cells engulf damaged cells and debris).

Bisdemethoxycurcumin does this by regulating the expression of genes that have caused defective immune function.

Zhang et. al isolated immune cells from Alzheimer’s disease patients and treated them with curcuminoids. Treatment with curcuminoids enhanced the ability of immune cells to clear amyloid beta under experimental conditions.

This suggests that curcuminoids can serve as an immunotherapy in Alzheimer’s disease.

7. Curcumin can prevent Alzheimer’s

Dietary curcumin protects accelerated aging of the brain which suggests why India has a lower incidence of neurodegenerative disorders than the United States.

Reference: A review article published in British Journal of Nutrition, 2016 suggests that curcumin can prevent Alzheimer’s owing to its ability to prevent deposition of beta amyloid plaques, affect its metabolism and prevent cognitive dysfunction.

The expression of certain genes predispose one to develop Alzheimer’s. Dietary intake of curcumin and grape seed polyphenols can prevent such genomic instability in Alzheimer’s.

Histone deacetylase is an enzyme that regulates DNA formation and genetic expression. Inhibitors of this enzyme find their use in various disorders such as psychiatric conditions, cancer and neurodegenerative diseases.

Curcumin also acts as an inhibitor of this enzyme and prevents development of Alzheimer’s disease.

References: Reddy et. al suggest that curcumin works better in prevention rather than treatment of Alzheimer’s disease.

A study published in Nutrition Journal, 2010 reveals that low dose supplementation of curcumin with lipids (fat) in healthy individuals results in lowering of plasma beta amyloid levels.

Caregiving for an Alzheimer's patient requires a lot of love, patience, and empathy.

There are a lot of dementia-related websites that provide caregiver guidelines and lists of do's and don'ts associated with providing care to someone suffering with Alzheimer's or dementia.

Here are just a few examples to give you some idea how to help and care for an Alzheimer's  patient:

  • Make sure that you educate yourself about Alzheimer's and how it affects patients. Take a local class and/or join a support group.
  • Explain this disease to your children and other loved ones so that they understand what is happening.
  • However, be prepared, because most people, especially children and relatives or friends who were close to the patient may find it difficult.
  • Don't take the patient's loss of memory or verbal attack personally -- remember, it's the disease that's destroying the person's memory, personality, behaviors, thinking, etc.
  • Help the patient if it appears they need your help.
  • Don't overwhelm the patient with multiple activities -- focus on one activity at a time.
  • Speak clearly, but, don't "talk down" to the patient.
  • Be respectful at all times and smile, even if you are having a bad day.
  • If they lash out verbally, don't engage in an argument! Look for what may be bothering the person since even little things can agitate them.
  • Play the patient's favorite song or other calm music that they make like.
  • Use prayer and meditation to try to connect to the person's inner spirit.
  • Don't imnpose your own faith or belief system on the patient, especially if you know that they're an agnostic.

Key Point: Although these do's and don'ts are very helpful, it focuses on taking a reactionary approach to the behaviors of the Alzheimer's patient instead of a proactive approach to try to address the disease pathology and prevent or slow down the progression of the disease.

For example, Alzheimer's is due to the increase of amyloid plaque and tangles, which are caused by cellular inflammation, oxidation, toxicity, insulin resistance, and glycation (AGEs).

Consequently, in addition to providing personal care to the patient, the caregiver should educate him/herself about effective alternative (non-drug) therapies such as superior nutrition, raw juicing, raw food diet, supplementation, detox, spirituality, and exercise.

Many of these alternative therapies can, at least, help to slow down the progression of the Alzheimer's, especially, when multiple therapies are used together.

Note: If you need help with providing care to a loved one, contact our office or get the author's Caregiver's Guide for Diabetes.

Unfortunately, there is no medical cure for Alzheimer’s Disease, however, strategies such as a plant-based diet, daily exercise, mental stimulation, and social interaction can prevent and slow down the progression of this disease.

So, be proactive and prevent the onset of Alzheimer's Disease by getting one or more of the following author's books, which address inflammation, oxidation, toxic load, etc..

In general, if you've been diabetic for more than 5 years or if you've been taking toxic medications and eating poorly for more than 5 years, then, we recommend that you get one or more of the following books to help you with your diabetes:

References:

  1. de la Monte SM, Tong M, Lester-Coll N; et al. (2006). "Therapeutic rescue of neurodegeneration in experimental type 3 diabetes: relevance to Alzheimer's disease". Journal of Alzheimer's Disease. 10 (1): 89–109.
  2. ^ Suzanne M. de la Monte & Jack R. Wands (2008). "Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed". Journal of Diabetes Science and Technology. 2 (31): 1101–13. PMC 2769828Freely accessible. PMID 19885299.
  3. "Alzheimer's 'is brain diabetes'". BBC News. 2009-02-03.[unreliable medical source?]
  4. ^ Freiherr J, Hallschmid M, Frey WH, et al. (Jul 2013). "Intranasal insulin as a treatment for Alzheimer's disease: a review of basic research and clinical evidence". CNS Drugs. 27 (7): 505–14. doi:10.1007/s40263-013-0076-8. PMC 3709085Freely accessible. PMID 23719722.
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  6. Sánchez-Chávez, G.; Salceda, R. (2000-04-01). "Effect of streptozotocin-induced diabetes on activities of cholinesterases in the rat retina". IUBMB Life. 49 (4): 283–287. doi:10.1080/15216540050033140. ISSN 1521-6543. PMID 10995030.
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  8. Arvanitakis, Zoe. "Dementia And Vascular Disease".
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  10. ^ Tang W, Chan S, Chiu H, Ungvari G, Wong K, Kwok T, Mok V, Wong K, Richards P, Ahuja A (2004). "Impact of Applying NINDS-AIREN Criteria of Probable Vascular Dementia to Clinical and Radiological Characteristics of a Stroke Cohort with Dementia". Cerebrovascular Disease. 18 (2): 98–103. doi:10.1159/000079256. PMID 15218273.
  11. ^ Pantoni L, Inzitari D (1993). "Hachinski's Ischemic Score and the Diagnosis of Vascular Dementia: A Review". Italian Journal of Neurological Sciences. 14 (7): 539–546. doi:10.1007/BF02339212. PMID 8282525.
  12. ^ Bonte FJ, Harris TS, Hynan LS, Bigio EH, White CL. Tc-99m HMPAO SPECT in the Differential Diagnosis of the Dementias with Histopathologic Confirmation. Clinical Nuclear Medicine. July 2006;31(7):376–378. doi:10.1097/01.rlu.0000222736.81365.63. PMID 16785801.
  13. Arvanitakis, Zoe. "Dementia And Vascular Disease".
  14. ^ Wetterling T, Kanitz RD, Borgis KJ (January 1996). "Comparison of Different Diagnostic Criteria for Vascular Dementia (ADDTC, DSM-IV, ICD-10, NINDS-AIREN)". Stroke. 27 (1): 30–36. doi:10.1161/01.str.27.1.30. PMID 8553399.
  15. ^ Tang W, Chan S, Chiu H, Ungvari G, Wong K, Kwok T, Mok V, Wong K, Richards P, Ahuja A (2004). "Impact of Applying NINDS-AIREN Criteria of Probable Vascular Dementia to Clinical and Radiological Characteristics of a Stroke Cohort with Dementia". Cerebrovascular Disease. 18 (2): 98–103. doi:10.1159/000079256. PMID 15218273.
  16. ^ Pantoni L, Inzitari D (1993). "Hachinski's Ischemic Score and the Diagnosis of Vascular Dementia: A Review". Italian Journal of Neurological Sciences. 14 (7): 539–546. doi:10.1007/BF02339212. PMID 8282525.
  17. Baskys, A; Cheng, JX (November 2012). "Pharmacological Prevention and Treatment of Vascular Dementia: Approaches and Perspectives". Experimental Gerontology. 47 (11): 887–891. doi:10.1016/j.exger.2012.07.002. PMID 22796225.
  18. Bruandet, A; Richard, F; Bombois, S; Maurage, C A; Deramecourt, V; Lebert, F; Amouyel, P; Pasquier, F (1 February 2009). "Alzheimer disease with cerebrovascular disease and vascular dementia: clinical features and course compared with Alzheimer disease". Journal of Neurology, Neurosurgery & Psychiatry. 80 (2): 133–139. doi:10.1136/jnnp.2007.137851.
  19. Battistin L, Cagnin A (December 2010). "Vascular Cognitive Disorder A Biological and Clinical Overview". Neurochemical Research. 35 (12): 1933–1938. doi:10.1007/s11064-010-0346-5. PMID 21127967.
  20. Dale E. Bredesen, Edwin C. Amos, Jonathan Canick, Mary Ackerley, Cyrus Raji, Milan Fiala, Jamila Ahdidan. UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging.  "Reversal of cognitive decline in Alzheimer's disease."  http://www.aging-us.com/article/100981  

    2014 study published in the journal "Aging," Bredesen found his program boosted cognitive functioning in nine out of 10 Alzheimer's patients within six months. Some could even return to work.

    The study is the first to suggest that memory loss in patients may be reversed — and improvement sustained — using a complex, 36-point therapeutic program that involves comprehensive diet changes, brain stimulation, exercise, sleep optimization, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

    Dr. Bredesen books:

    • The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline, 2017
    • Stop Alzheimer's Now!: How to Prevent & Reverse Dementia, Parkinson's, ALS, Multiple Sclerosis & Other Neurodegenerative Disorders, 2011

Additional References and Sources

https://www.alz.org/
http://www.alzfdn.org/
https://alzheimers.acl.gov/
http://www.j-alz.com/
http://www.aging-us.com/

https://www.ncbi.nlm.nih.gov/
http://emedicine.medscape.com/
http://neuropathology-web.org/
http://www.medscape.com/
https://www.britannica.com/
http://www.mayoclinic.org/
http://www.webmd.com/alzheimers/

http://www.caregiving.org/
https://www.caregiver.org/
http://www.familycaregiving101.org/
http://www.brightfocus.org/alzheimers/
http://www.aplaceformom.com/

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