Written by Dan Wagner, PharmD, RPh, MBA edited by Gregory H. Hoeper DC

    Unpacking Alzheimer’s Disease and Memory Loss

    Alzheimer’s disease (AD) is a common type of dementia, or decline in intellectual function that is regarded as a loss of mental faculties and personal independence. It is one of the world’s most feared afflictions. Alzheimer’s disease is the fourth leading cause of death for people in the Western world, afflicting 10% of Americans over sixty-five and as many as 50% of those over eighty-five. The number of those stricken with the disease is expected to triple from 4.5 million to 12 million by 2020.

    Alzheimer’s is characterized by progressive mental deterioration to such a degree that it interferes with a person’s ability to function at work or in social situations. Memory and thought processes are impaired. It appears that Alzheimer’s is irreversible, although the progression of the disease can be extremely slow. Frequently long-term memory remains, but short-term memory is particularly impaired.  There is an increasing consensus among researchers that Alzheimer’s and other dementia have multiple etiologies. In addition to normal aging, which actually features very little cell death, the extent of nerve cell deterioration in Alzheimer’s is widespread and sometimes catastrophic. As a child learns skills in language, coordination, cognition and behavior, so the adult suffering from AD loses these skills one by one can lead to a point where her/she cannot self-feed.

    There is direct evidence that Alzheimer patients suffer from mitochondrial abnormalities.  The mitochondria are the powerhouses of energy in the cells. Since the brain’s ongoing vitality is dramatically dependent on energy from glucose (sugar), bio-energetic impairment can appear early and progress rapidly with time.  Alterations in mitochondrial enzymes are consistently linked to dementia so much of the research done in this area centers on this dysfunction.


    Increasingly, there is evidence that diet plays an important role in causing Alzheimer’s disease. Although there is no specific diet associated with improving AD, it is believed that a diet high in antioxidants with plenty of fresh fruits, green and yellow vegetables, and fish is strongly recommended. Low body weight and weight loss is a concern, so maintaining adequate food intake and an appetite is important. Feeding the brain not only requires whole and raw foods that are preferably organic, but also more pure water and oxygen.

    A 2002 study published in the British Medical Journal concluded that the consumption of fish (rich in polyunsaturated fats) lowered the risk of Alzheimer’s dementia. Supplementation with antioxidants is one of nature’s strongest free-radical scavengers. They are found in many foods such as carrots, oranges and almonds.  It has been said that “a carrot a day keeps dementia away.”

    Causes And Risks

    The role of inflammation may go a long way in actually representing the progression and mechanism of AD. Evidence suggests that AD involves low-level inflammation of the brain’s gray matter. Over time this buildup may directly damage brain nerve cells. Use of non-steroidal anti-inflammatory drugs (NSAIDS) and aspirin may decrease the risk (possibly 40% over 2 years); however, ingestion of acetaminophen (Tylenol) has been shown to decrease glutathione–a primary brain antioxidant. Internal inflammation caused by arachidonic acid formation can be limited by avoiding acidic foods like soft drinks, alcohol, coffee, sugar and processed foods.

    Alzheimer’s affects nearly 15% of the elderly. In almost all cases free radical damage is elevated. Thus, antioxidant activity and supplementation should improve energy, intracellular membranes, and neurotransmission. Other factors that may contribute to the cause or proliferation of Alzheimer’s disease include:  

    • Heavy metal toxicity. Toxic poisoning by heavy metals must be investigated as a potential cause of AD.  Especially worthy of investigation are mercury and aluminum. Mercury (found mainly in dental amalgams, ocean fish, vaccines, other injections, and industrial emissions) is uniquely toxic to nerve cells.  Elevated mercury levels in childhood correlate with lifelong cognitive impairment. Early onset Alzheimer’s patients demonstrate a three-fold higher mercury elevation. Aluminum appears to be another heavy metal that may be linked to early onset of the disease.  Victims have 10-15% more than the average person. One study reported a 250% increased risk of AD in people drinking municipal water high in aluminum content over ten years. Hip-fracture patients with AD have significantly higher levels of aluminum in their bone samples. Aluminum is found in cans, cookware, toothpaste, baking powder, vaccines, underarm deodorants and antacids.  Another potential danger is consumption of fluoride (often present as aluminum fluoride). Detoxification and chelation may be effective ways to rid the body of these toxins.
    • Oxidative stress. Oxidative stress is clearly evident in AD patients. There are numerous oxidative stress biomarkers that are elevated in the brain and blood. Oxidative stress refers to an increase in the ratio of free radicals (short-lived, unstable electrons in the environment that are slowly tearing down our immune system) to antioxidant capacity. Brain tissue is especially vulnerable to oxidative attack due to high oxygen consumption, low antioxidant capacity, high content of poly-unsaturated fats and environmental metals and toxins. 
    • Artificial sweeteners. Aspartame is a common food additive that is highly risky and potentially toxic. This artificial sweetener contains methanol (in paint thinners) and formaldehyde. Over consumption of aspartame over a period of time likely destroys the nervous system and stimulates the neurons of the brain, causing brain damage of varying degrees. (Aspartame is found in Nutrasweet, Equal and Spoonful). The commercial product “Splenda” also is risky to consume. Try using stevia and honey.
    • GMOs. There is increasing suspicion that genetically modified organisms (GMOs) may cause Alzheimer-like symptoms after years of ingesting foods that are genetically modified.  GMOs most likely are found in processed and junk foods and are becoming a world-wide health risk. When possible, try and eat more organically grown foods, however fruits and vegetables that are chemically sprayed still have a health advantage over consumption of GMO foods. No one knows at this time how GMO foods will play out in the future.  It is risky business.
    • Nutrient deficiency. It is well known that Vitamin B-12 may be one of the few effective treatments for dementia. Improvement has been shown after elderly patients were given vitamin B12 supplementation. The fact is that many AD patients (as well as 30% of American seniors) suffer from atrophic gastritis which hinders the absorption of B-12 and other nutrients. There is a 200% increase in the likelihood of vascular dementia in individuals with elevated homocysteine levels (which are directly related to the intake of B-complex vitamins). German studies reveal that women with high levels of homocysteine are twice as likely to develop AD.  AD patients also have low quantities of magnesium, calcium and silica in their bodies. 
    • Bacteria and microorganisms. There is evidence that people with a gastritis problem called Helicobacter pylori may indirectly contribute to the development of AD.  Since H. pylori is the most common cause on gastritis, chronic conditions can cause atrophy of the stomach lining leading to mal-absorption of vitamin B12 and folic acid, leading to elevated homocysteine levels, which can lead to atherosclerosis and vascular dementia.
    • Electromagnetic waves. The latest phenomenon that may have a direct affect on AD is the relationship between people and electromagnetic radiation. It is more obvious that over exposure to cell phones, personal computers, I-pads, microwaves, cordless phones, electric blankets, TVs, and Wi-fi’s are all potential hazards. More research needs to be done in this area since it directly affects most of the people on the planet in the decades to come.


    Beneficial Supplements

    Omega–3,6 Fatty Acids (DHA-EPA)

    Alzheimer’s patients have low concentrations of omega 3,6 fats in the gray matter of the brain. Omega fats are important for those with AD because they reduce inflammation in the brain, protect the vascular system, and play a specific role in brain development and the regeneration of nerve cells. Adequate DHA-EPA (from fish oil) is necessary for proper neurotransmission, and deficiencies have been linked to memory loss. Omega-6 fatty acids such as Evening primrose oil and gamma-linolenic acid appears to lessen depression and improve test scores. 

    Gingko Biloba Extracts

    Ginkgo Biloba standardized leaf extracts has been exhaustively tested and has been well documented to improve cerebral blood flow and to supply antioxidants to the nerves. Gingko boosts mental performance (focus and memory), enhances circulation throughout the body, and works to improve or prevent memory problems. (A combination of Ginkgo and Ginseng may increase mental function). Ginkgo has been compared to the cholinesterase drugs and has shown equal efficacy and fewer side effects.

    Acetyl-L-Carnitine (ALC)

    Acetyl-L-Carnitine, the acetyl-ester of the amino acid carnitine, is critical for mitochondrial function and aids in transforming fatty acids into energy for the brain. ALC also plays an important role in muscular activity and nerve transmission. It’s concentrated in the brain and helps improve memory and cognitive function, while decreasing depression and fatigue among the elderly. ALC has proven beneficial for all AD patients and can further help to normalize elevated cortisol levels caused by added stressors on the body. Those who use it as a supplement (even younger patients) definitely show improvement as well as less deterioration on tests measuring mental functions.

    B-Complex Vitamins

    B-complex vitamins should always be a mainstay of AD therapy. The B vitamins are needed for brain function, energy and the digestion of food. Extra Vitamin B12 is also important for brain function. Vitamin B12 deficiency is common in Alzheimer patients and may be one of the few treatable causes of dementia. Mice experiments suggest that folic acid plays an essential role in protecting the brain against Alzheimer’s disease. In humans, there is a strong association between low blood folic acid levels and severity of atrophy in the neocortex of the brain. Folic acid supplementation may prevent the buildup of plaque in their brains that kill neurons. Folic acid also aids in controlling homocysteine levels. Folic acid is best taken in combination with Vitamin B12.

    Coenzyme Q-10

    Coenzyme Q-10 helps strengthen the heart to pump more blood to the brain. Deficiencies of CoQ-10 have a profound effect on cellular activity and viability. CoQ-10 enhances mitochondrial energy production which utilizes glucose to improve brain function. Recent research published in various medical journals reports that some patients taking mega-doses of CoQ-10 (400-2,400 mg a day) retarded the progression of Alzheimer’s.

    Phosphatidylserine (PS)

    It is well known that phospholipids are molecular building blocks for cell membranes. PS is present in large amounts in brain tissue and is thought to be necessary for cognitive function. PS is safe, effective, and supports many cellular functions important to the brain, including mitochondrial integrity for energy production and activation of the protein kinase, which is an important enzyme needed for neuron signal transmission. PS may be more effective when given with ginkgo and acetyl-L-carnitine. In one study a woman taking 500 mg per day for 3 weeks had a significant increase in energy production to the brain. Doses daily consistently benefits memory, learning, concentration, word choice, and mood. 

    Huperzine And Vinpocetine

    Both of these herbs are potent inhibitors of cholinesterase. They improve cognition in patients with senile dementia, protect the brain’s memory messenger, and increase oxygen supply. Huperzine (an alkaloid of the Chinese Club Moss) may significantly improve short-term memory, behavioral functions and other cognition compared to placebo. Like Ginkgo biloba, Vinpocetine increases blood supply to the brain, stimulates the brain’s uptake of glucose, and decreases the decline of dopamine (which can lead to depression).

    Turmeric (Curcumin)

    The yellow pigment in the Indian spice curry may be a frontline herb in the battle against Alzheimer’s disease according to a UCLA researcher.  They found that curcumin was more effective at preventing the buildup of plaque in the brain than many leading drugs (like Aricept) currently being used. It may boost brain power and help prevent the onset of Alzheimer’s. Curcumin is a potent anti-inflammatory agent.

    Ashwagandha (Withania Somniferum

    This Ayurvedic herb has been used for thousands of years as an adaptogen.  It relieves stress, boosts the adrenal glands, prolongs longevity, and arouses sexual energy.  It also has been shown to protect the brain from stroke-related and age-related memory decline.  Combining ashwagandha with essential fatty acids and plenty of fruits and vegetables, it is believed that it can help to reverse the ravages of age-related dementia.

    Alpha Lipoic Acid

    Alpha lipoic acid is an important discovery in the treatment of neuro-degenerative disease. It has the ability to recycle vitamins C and E, and it regenerates glutathione–the brain’s most important antioxidant that protects the body from oxidative damage.

    Bacopa Monnieri

    Like Ginkgo biloba, Bacopa works on the memory and focus problems that many people experience. Bacopa grows in India, and recent findings show much promise.


    Chinese researchers report that melatonin protects the brain against several biochemical processes linked to the development of Alzheimer’s.  Melatonin levels decline with age, but it appears that Alzheimer’s patients experience an even more dramatic reduction. Dosage: 2-10 mg nightly.


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