Alzheimer’s: Herbal and Nutritiona...

The Ohlone Center of Herbal Studies - Berkeley, California > Research Papers > Alzheimer’s: Herbal and Nutritional Support

Alzheimer’s: Herbal and Nutritional Support

Alzheimer’s: Herbal and Nutritional Support

Kelsey Barrett

October 2013


According to the Alzheimer’s Association is a growing epidemic.   More than 5 million Americans now have Alzheimer’s disease. By 2050, nearly 14 million (13.8 million) Americans could be living with the disease, unless scientists develop new approaches to prevent or cure it according to the Alzheimer’s Foundation of America.  Alzheimer’s is the only leading cause of death that is still on the rise.

It is estimated that more than 200,000 people have early onset, early onset is considered to be people 65 years and younger.


Alzheimer’s is projected to cripple America’s healthcare system.  Total payments for health care, long-term care, and hospice for people with Alzheimer’s disease and other dementias are projected to increase from $200 billion in 2012 to $1.1 trillion in 2050 (in 2012 dollars). This dramatic rise includes a six-fold increase in government spending under Medicare and Medicaid and a five-fold increase in out-of-pocket spending.



Alzheimer’s has a distinct progression of disease generally starting in the hippocampus.

BRAIN                                                                                                                                        75% of our brain weight is myelin, fatty matter that creates each nerve fiber.


The hippocampus is part of the limbic system, and located in the inner temporal lobe.  Limbic is a Latin term which means border.  Like the word “limbo”, it means an intermediate or transitional state, which is a border.  The limbic system is particularly important in producing emotion, converting short-term memory to more permanent memory, and for recalling spatial relationships in the world around us.  Here long term memory is stored, and is a compilation of data in our conscious memory and all of our gathered knowledge and experiences.  The hippocampus is influenced by stress. Small changes in the blood flow or oxygenation levels of this region of the brain can serve as quantifiable markers for the emotional recognition of and response to stress.  In addition, some neurons in the hippocampus are continually being formed. Therefore the hippocampus is one of only a few regions of the brain that serves as a source for neural stem cells.


Plaques form when protein pieces called beta-amyloid (BAY-tuh AM-uh-loyd) clump together. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells.  Beta amyloid is a peptide of short chain amino acids.  Beta-amyloid is chemically “sticky” and gradually builds up into plaques. Evidence has been found that Aβ is a highly multifunctional peptide with significant non-pathological activity.

The most damaging form of beta-amyloid may be a group of a few pieces rather than the plaques themselves. The small clumps may block cell-to-cell signaling at synapses. They may also activate immune system cells that trigger inflammation and devour disabled cells.


The transport system is organized in orderly parallel strands somewhat like railroad tracks. Food molecules, cell parts and other key materials travel along the “tracks”.  A protein called tau helps the tracks stay straight.  In areas where tangles are forming: tau collapses into twisted strands called tangles.  The tracks can no longer stay straight.  They fall apart and disintegrate.  Nutrients and other essential supplies can no longer move through the cells, which eventually die.


Two types of abnormal lesions clog the brains of individuals with Alzheimer’s disease: Beta-amyloid plaques—sticky clumps of protein fragments and cellular material that form outside and around neurons; and neurofibrillary tangles—insoluble twisted fibers composed largely of the protein tau that build up inside nerve cells. Although these structures are hallmarks of the disease, scientists are unclear whether they cause it or a byproduct of it.


Alzheimer disease is not a single disorder in spite of a common clinical phenotype. At its origin, two different types or even more exist.  As Alzheimer’s progresses, brain cells die and connections among cells are lost, causing cognitive symptoms to worsen.

  1. FAMILIAL ALZHEIMER’S DISEASE, GENETIC: In a minority of about 5% or less of all cases, Alzheimer disease is due to mutations of three genes, resulting in the permanent generation of βA4.
    1. Familial Alzheimer’s Disease (FAD) is caused by any one of a number of different single-gene mutations on chromosomes 21, 14, and 1. Each of these mutations causes abnormal proteins to be formed. Mutations on chromosome 21 cause the formation of abnormal amyloid precursor protein (APP). Scientists know that each of these mutations plays a role in the breakdown of APP, a protein whose precise function is not yet known.
    2. SPORADIC ALZHEIMERS DISEASE, INSULIN: The great majority (95% or more) of cases of Alzheimer disease are sporadic in origin, with old age as main risk factor. However, disturbances in the neuronal insulin signal transduction pathway may be of central pathophysiological significance.  Disturbances in the neuronal insulin receptor-signaling pathway are associated with reduced neuronal glucose/energy metabolism and work in a detrimental concerted action in sporadic Alzheimer disease. Neuronal insulin receptor dysfunction may result in the intracellular accumulation of Aβ and in subsequent cellular damage (and/or disruption of the metabolism of proteins).  One of the important pathogenesis in Alzheimer’s disease is the chronic inflammation of nerve cells. Several studies have demonstrated the associated inflammatory changes such as microgliosis, astrocytosis and the presence of pro-inflammatory substances that accompany the deposition of amyloid-β (Aβ) peptide. (Patients with the prolonged use of certain nonsteroidal anti-inflammatory (NSAID) drugs such as ibuprofen have been shown to have a reduced risk of developing the symptoms of AD; however, the chronic use of NSAID can cause a toxic effect on the kidneys, liver and GI track.)
      1. What is amyloid beta (Aβ)?  A peptide of 36–43 amino acids that is processed from the amyloid precursor protein (APP).
      2. It was found, over twenty years ago, that patients with Alzheimer’s disease had elevated levels of cortisol in their blood streams, compared to healthy patients.  This elevation correlated with the degree of memory impairments that the patients had and appeared early on in the disease progression.
      3. “diabetes of the brain’ “brain starvation”: In Alzheimer’s brain insulin receptor sites have a problem uptaking insulin, and they’re dying off.  Given this description the consequences of the inhibition of neuronal insulin signal transduction may be largely identical to those of disturbances of oxidative energy metabolism.  In late-onset sporadic Alzheimer disease changes in the brain are similar to those caused by non-insulin-dependent diabetes mellitus (disorder of carbohydrate metabolism).
      4. 75% of our brain weight is myelin, fatty matter that creates each nerve fiber.   Our body can only make 10% of our daily need of cholesterol, and then 90% comes from food.  If people cut out cholesterol after 6-10 years people cannot keep up with the repair needs of the myelin sheath.  Dr. Joel Wallach calls this physicians caused disease as related to common dietary suggestions of reducing fat from diet.
      5. SPORADIC ALZHEIMERS DISEASE, CNS: It is believed that too much stimulation of nerve cells by glutamate (an amino acid: key elements of an amino acid are carbon, hydrogen, oxygen, and nitrogen) may be responsible for the degeneration of nerves that occurs in some neurological diseases such as Alzheimer’s disease.  Amino acids re the basis of proteins, and proteins comprise the tangles and plaque found in Alzheimer’s.  Nerve degeneration is dangerous as the nervous system sends synapses, structures that permit a neuron (or nerve cell) to pass an electrical or chemical signal to another cell (neural or otherwise).  Like other neurotransmitters, glutamate is produced and released by nerve cells in the brain. The released glutamate then travels to nearby nerve cells where it attaches to a receptor on the surface of the cells called the N-methyl-D-aspartate (NMDA) receptor.



The U.S. Food and Drug Administration (FDA) has approved two types of medications — cholinesterase inhibitors (Aricept, Exelon, Razadyne, Cognex) and memantine (Namenda) — to treat the cognitive symptoms (memory loss, confusion, and problems with thinking and reasoning) of Alzheimer’s disease.  While current medications cannot stop the damage Alzheimer’s causes to brain cells, they may help lessen or stabilize symptoms for a limited time by affecting certain chemicals involved in carrying messages among the brain’s nerve cells. Doctors sometimes prescribe both types of medications together.   The body has a natural system of creation and decay.  From my research it appears that pharmaceuticals reduce the rate of decay of specific chemicals, leaving old chemical compounds in the body/brain to function

  1. Medications for early to moderate stages

Cholinesterase Inhibitors: Cholinesterase inhibitors prevent the breakdown of acetylcholine (a-SEA-til-KOH-lean), a chemical compound that works as a neurotransmitter in the Central Nervous System.  People with dementia usually have lower levels of this chemical, which is important for the processes of memory, thinking, and reasoning.  Cholinesterase inhibitors slow the breakdown of acetylcholine.  It does this by preventing the action of acetylcholinesterase, the compound that normally breaks it down.  Delays worsening of symptoms for 6 to 12 months, on average, for about half the people who take them.  Are generally well tolerated. If side effects occur, they commonly include nausea, vomiting, loss of appetite and increased frequency of bowel movements.

  1. Donepezil (Aricept) SIDE EFFECTS

Donepezil (Aricept) is the only cholinesterase inhibitor approved to treat all stages of Alzheimer’s disease.

Mild side effects: Nausea, vomiting, diarrhea, loss of appetite/weight loss, dizziness, drowsiness, weakness, trouble sleeping, shakiness (tremor), or muscle cramps may occur as your body adjusts to the drug. These effects usually last 1-3 weeks and then lessen. Serious side effects: slow/irregular heartbeat, fainting, trouble urinating, severe stomach/abdominal pain, black stools, vomit that looks like coffee grounds, seizures. A very serious allergic reaction to this drug is rare: rash, itching/swelling (especially of the face/tongue/throat), severe dizziness, trouble breathing.

  1. Rivastigmine (Exelon) SIDE EFFECTS

Side effects are more common with oral forms of rivastigmine than with the patches.

Common side effects: nausea, vomiting, loss of appetite/weight loss, diarrhea, indigestion, weakness, dizziness, drowsiness, and shakiness (tremors), sleepiness, headache, increased sweating, fever, skin reactions such as irritation, worsening of Parkinson’s symptoms, anxiety or agitation, depression, difficulty sleeping (insomnia), hallucinations, delirium, fainting, ulceration in the stomach or intestines, seizures, chest pain (angina), abnormal heartbeats, increased blood pressure (hypertension), pancreatitis, hepatitis.

Patches side effects: itching or redness at the site of application of patch, rash, shaking, usually of the hands (tremor),

  1. Galantamine (Razadyne) SIDE EFFECTS. Mild side: feeling tired, dizzy, or light-headed; nausea, vomiting, gas, loss of appetite; weight loss; or headache.

Serious side effects: chest pain, slow heart rate, black, bloody, or tarry stools; coughing up blood or vomit that looks like coffee grounds; weakness, confusion, decreased sweating, extreme thirst, hot dry skin; or urinating less than usual or not at all.


  1. Medication for moderate to severe stages

Regulates the activity of glutamate, a different messenger chemical involved in learning and memory.  Delays worsening of symptoms for some people temporarily.

  1. Memantine SIDE EFFECTS
  2. Common side effects: fatigue, pain, increases in blood pressure, dizziness, headache, constipation, vomiting, back pain, confusion, somnolence, hallucination, coughing, and difficulty in breathing. Memantine may cause a serious skin reaction called Stevens-Johnson syndrome.
  3. VIT. E                                                                                                

Some doctors prescribe high doses of vitamin E for cognitive changes of Alzheimer’s disease.


Galantamine: 75% is metabolized in the liver

Rivastigmine: Metabolized by enzymes in the liver

Donepezil: Metabolized by enzymes in the liver

Memantine: Metabolized in the liver

Herbal hepatic, alterative, cholagogue, and bitters can aid in harm reduction and the metabolism of Alzheimer’s medication.  All nutrition suggestions apply.

Alterative: burdock, wild indigo, black cohosh, Echinacea, cleavers, goldenseal, chaparral, Oregon grape, bog bean, poke, pasqueflower, yellow dock, figwort, sarsaparilla, red clover, nettle

Cholagogue: wild indigo, barberry, celandine, artichoke, wild yam, boneset, gentian, rosemary, yellow dock, sage dandelion, lemon balm

Bitters: mugwort, yarrow, boneset, centaury, gentian, goldenseal, horehound, chamomile, rue, tansy, dandelion

Hepatics: Dandelion, verbena, milk thistle, artichoke, yarrow, aloe, celery seed, wormwood, horseradish, turmeric, cleavers, gentian, goldenseal, motherwort, oregon grape, yellow dock, prickly ash, dandelion, wild yam

Antihepatotoxic: licorice, milk thistle, schisandra


VIT. E/ANTIOXIDANTS                                                                                                              Vitamin E refers to a group of fat-soluble compounds with strong antioxidant properties. An antioxidant is a substance that reduces oxidative damage, damage caused by oxygen, which can harm human tissue, cells and organs.

FOODS HIGH IN VIT. E                                                                                                    Almonds, asparagus, avocados, blue crab, brazil nuts, broccoli, cod liver oil, egg yolks, green leafy vegetables, like lettuce, spinach, turnip, beet, collard, and dandelion greens, hazelnuts, mangoes, mayonnaise, olives, papayas, pine nuts, pumpkin, grape seed oil, rockfish, sweet potato, tomato, walnut, wheat germ oil.

HERBAL ANTIOXIDANTS                                                                                          Hawthorne, green tea, ginkgo, elderberry, cinnamon, ginger, burdock, turmeric

TURMERIC                                                                                                                                      A study conducted at UCLA found that curcumin may help the macrophages to clear the amyloid plaques found in Alzheimer’s disease.  Macrophages are white blood cells within tissues, suggesting weakened immune system.  Due to the lipophilic (tending to combine with or dissolve in lipids or fats) nature of curcumin, it crosses the blood brain barrier and binds to plaques. Indian Acad Neurol. 2008 Jan-Mar; 11(1): 13–19. doi: 10.4103/0972-2327.4022

Coconut Oil

The vast majority of the fats and oils eaten, whether they are saturated or unsaturated or come from an animal or a plant, are composed of long-chain triglycerides. Probably 98 to 100% of all the fats we eat consist of LCT. Coconut oil is unique because it is composed predominately of MCT. The size of the fatty acid is extremely important because physiological effects of medium-chain fatty acids in coconut oil are distinctly different from the long-chain fatty acids more commonly found in our diet.  Almost all of the medium-chain triglycerides used in research, medicine, and food products come from coconut oil.  Unlike other fats, they put little strain on the digestive system and provide a quick source of energy necessary to promote healing.

  1. Medium chain triglycerides (MCT) are not processed by your body in the same manner as long chain triglycerides.  Normal fat metabolism depends on bile salts that have been released from your gallbladder before it can be broken down in your digestive system.  MCTs bypass bile metabolism and go directly to your liver where they are converted into ketones, MCTs do not require bile salts for digestion.  The liver then immediately releases the ketones into the bloodstream where they are transported to the brain to be used as fuel. Research has shown that the ketone bodies produced by MCTs provide a stable source of energy for the brain during periods of low blood sugar without the neurological risks associated with high blood sugar.
  2. “Keytosis” creates circulation to the brain.
  3. In feast the brain feeds off of sugar.  In famine the liver converts body fat into ketone bodies, which are fuel for the brain cells.
  4.  Ketones in mice allow new neurons to grow and new nerves to grow, reversal.


Magnesium protects and restores synaptic densityIn a series of laboratory experiments, a highly absorbable form of magnesium was shown to not only increase magnesium blood levels, but it also substantially increases magnesium brain concentrations.  In response to this elevation in cerebral magnesium, there were significant increases in synaptic density and corresponding improvements in synaptic functioning and neuronal signaling.  These improvements in synaptic structure and function translated into improvements in measurements of cognitive function.

Leave a Reply

You must be logged in to post a comment.