How to Heal Alzheimer’s Disease

by Dr. James A. Howenstine

Alzheimer’s disease (AD) is one of the most feared diseases currently afflicting humankind. Many people rightly regard the loss of mental faculties and personal independence as tragic events.

The first neuromuscular skills acquired by a child become the last to be destroyed by AD as it progresses. As the child acquires skills in eating, language, behavior, coordination, and cognition, so the adult suffering from AD loses cognition, coordination, behavior, language, and ultimately ability to self-feed. The development of these skills is associated with the appearance of a protective myelin sheath forming around neurons starting in the motor cortex and progressing to the hippocampus at age 3. The hippocampus is the site for consolidating immediate thoughts into memories. This explains why children below 3 only rarely can recall permanent memories. The earliest symptom of AD is loss of recent memory. AD destroys the protective myelin sheath surrounding neurons, with the last area of the brain to become myelinated in childhood – the hippocampus – becoming the first to be demyelinated. This progressive loss of neuromuscular skills in AD is termed retrogression.¹

By 2000, there were 4,500,000 people in the US with AD. It is estimated that by 2030 there will be 9,000,000 people with this disease. Fifty percent of people over age 85 are believed to have AD.

Causes of

Alzheimer’s Disease

Electric Lighting

AD appears to be a disease of advanced civilization. In parts of rural Africa lacking electricity, there is nearly complete disappearance of AD. Normal sleep results when darkness permits the release of melatonin from the pineal gland. Where there is no electricity, people will probably have more prolonged daily exposure to melatonin, a powerful antioxidant capable of neutralizing oxidative toxins. This makes AD less likely to occur. Electric lights will result in individuals’ having decreased exposure to melatonin and greater vulnerability to oxidative injury and malignancies.

Aluminum

Aluminum, like other metals, directly increases the production of free radicals that can damage the myelin sheath; AD appears to be an inflammatory reaction to this injury. People taking NSAIDs (Motrin, Clinoril, Relafen, etc.) for more than two years have 40% less risk of developing AD, although the risk of internal bleeding and ulceration from these drugs counteracts this benefit.

There is a 250% increased risk of AD in people drinking municipal water high in aluminum content for more than ten years. Much municipal drinking water in North America is treated with alum (aluminum) to purify it.

In the 1970s, patients with AD were found to have blood levels of aluminum 1.4 times greater than those in unafflicted people. Subsequent studies determined that a characteristic brain AD lesion (nerve “tangles”) contained very high levels of aluminum. Hip-fracture patients with AD had significantly higher levels of aluminum in bone samples than did other people with hip fractures.

A group of 48 patients with AD were treated with desferrioxamine injections twice daily for five days each week for two years. This drug binds aluminum (chelation) so that it is excreted in the urine. There was slower deterioration in these patients when compared with patients who did not receive the injections.

In another study, rabbits were given aluminum injections into brain tissue to create Alzheimer’s-type degeneration. Later, half the rabbits were given desferrioxamine and half received nothing. The animals that did not receive the antialuminum treatment suffered more extensive neuron damage than the treated animals.

The critical unfavorable environmental changes needed to cause AD are:

• long-duration exposure (10 years) to acidic drinking water;

• high levels of an easily assimilated form of aluminum in this water;

• fluoride, often also present as aluminum fluoride, which readily crosses the blood–brain barrier;

• absence or low quantities of silicic acid (silica), magnesium, and calcium in this drinking water. These three substances bind aluminum in the gut (silicic acid) or chemically so that it is not able to form tangles or plaques (magnesium and calcium).

Mercury

Many people with high levels of exposure to aluminum from acidic water, aluminum cookware, aluminum cans, antacids, deodorants, and vaccines have also been heavily exposed to mercury, probably from silver (mercury) amalgams in teeth, consumption of fish, and a history of 35 vaccines per US child.

One could easily reason that exposure to both aluminum and mercury ought to be twice as hazardous as aluminum exposure alone. But the risk is much higher. Animal experiments have shown that exposure to both these highly toxic substances produced a multiplication of the toxic effects greater than that seen with either substance alone. This means that animals exposed to both aluminum and mercury may have 30%, 60%, or 90% more deaths than if their exposure had been limited to only one toxic metal. When you recall that most of us also have toxic lead, cadmium, arsenic, iron, uranium, and other metals in our bodies, the overall picture is frightening.

What is the best solution for exposure to multiple toxic metals? I think the simplest, least expensive option is long-term oral chelation. It can take 15 years of chelation to get lead out of our bones (modern people have 400 times more lead in bones than those living 400 years ago). Maintaining normal hormonal levels will decrease the time needed to replace contaminated bone by increasing the turnover rate of bone tissue. It is only with normal hormonal levels that osteoclasts and osteoblasts, the cells required to rebuild and remodel bones, work at optimum levels. Most US senior citizens are operating with abnormal levels of estrogen, progesterone, and testosterone, so they cannot optimally remove these metals.

Electromagnetic Waves

Researchers from University of Southern California School of Medicine confirmed that there was a direct relationship between exposure to electromagnetic radiation and the development of AD.² People employed as electricians, machinists, machine operators, seamstresses, sewing factory workers, sheet metal workers, typists, key punch operators, welders, and machine shop workers have a four times greater risk of AD than the general populace. Certainly, current heavy use of cell phones, personal computers, electric blankets, clock radios near the head, and hair dryers are potentially even more hazardous to health now than 23 years ago, when the study was published.

The Genetic Connection

The gene primarily incriminated in causation of most AD is APOE4. The normal function of APOE4 is transportation of cholesterol throughout the body. APOE4 is found to be carried in about 40% of cases sporadic-type AD in the elderly. People with one APOE4 gene will develop AD at a lower age than AD victims who have no APOE4 genes. Those people without an APOE4 gene have an average age of onset of AD of 85 years. People who carry this gene have impaired ability to remove the sticky beta-amyloid protein. This inability causes a greater possibility of developing AD than in people without the APOE4 allele, who easily remove beta-amyloid deposits. Presence in an individual of the APOE4 gene does not produce AD; the disease only occurs when there is a favorable environment for it to perpetuate.

The most obvious sign of AD is clusters of protein. These proteins can occur inside and outside cells. Inside cell clusters are called neurofibrillary tangles. These resemble wound-up, helical threads composed of tau protein. Tau plays an important role in cells because it binds to another protein called tubulin to create microtubules. These microtubules act like pillars, giving structure and shape to cells. In addition, they provide pathways for nutrients, molecules, and cell components to pass through the cells. These tangles contain an oxidized form of iron as well as aluminum. The iron probably contributes to cell damage. Excess phosphorylation of tau leads to twisting of microtubules. The cell membrane collapses, and the neuron withers and dies, unable to support cell nutrition and communication.

The beta-amyloid deposits are found in the spaces between cells. A peptide, containing 42 amino acids, forms – and it is toxic. This builds up plaque outside nerve cells. This specific beta-amyloid amino acid interferes with calcium regulation, promotes free-radical injury, and causes immune cells to aggregate. A metal protein containing copper, zinc, and iron is found within the plaques. At low levels, zinc appears to protect against plaque formation; whereas at high levels, it promotes plaque formation.

Homocysteine, Vascular Disease, and Other Health Issues

There is a 200 % increased risk of AD in people with elevated homocysteine levels in their blood. Homocysteine blood increases are associated with many disease processes.

• High homocysteine values are common in arteriosclerotic diseases (heart attack, stroke, gangrene). Thickening of the lining of arteries (plaques) and excessive clotting seen in high homocysteine states probably contribute to artery problems. This type of vascular disease is quickly helped by therapy with organic vitamin B complex.

• Osteoporosis: Elderly males in the highest quartile of homocysteine values have four times the risk of hip fracture as those in the lowest quartile. Women in the highest quartile had a 1.9 times greater risk of hip fractures than women in the lowest quartile. Pernicious anemia (lack of vitamin B 12) damages nerves, which could also contribute to falls by impairing balance. Osteoporosis may be a consequence of homocysteine excess, perhaps related to flawed oxygenation of bone.

• Drugs such as acetaminophen and antibiotics (Tylenol, Septra, Bactrim) can raise homocysteine levels. Acetaminophen causes decreased production of the critical brain antioxidant glutathione. Two years of acetaminophen therapy in the elderly increases the risk of AD by 35%.⁴ Premature aging is seen in patients taking acetaminophen. Acetaminophen is used to create cataracts in research studies performed on animals. Acute fatal liver failure can occur with acetaminophen therapy of febrile infectious illnesses in previously healthy youths. All people should cease using acetaminophen.

• Twenty-five women who had three to five episodes of pregnancy loss between the 8th and 16th weeks of amenorrhea were found to have elevated blood homocysteine levels. Therapy with folic acid 15 mg daily and vitamin B6 (pyridoxine) 750 mg daily resulted in 20 successful pregnancies with no fetal malformations.⁵ This suggests that women with recurring miscarriages should be evaluated for high homocysteine levels, which can be easily corrected with organic vitamin B complex or taking high dosage of folic acid and B6. The mechanism for this problem is not certain but may relate to impaired nutrition to the placenta from vasoconstriction in the presence of hyperhomocysteinemia, poor maternal diet, delivery of less oxygen to body tissues in hyperhomocysteinemic states related to sludgy blood flow, or all of the above.

All people with hyperhomocysteinemia are suffering from a nutritional deficiency of B complex vitamins (B12, B6 [pyridoxine], folic acid, and trimethylglycine). Repletion of these nutrients restores homocysteine values to normal. High doses of trimethylglycine appear to be a very effective therapy for lowering homocysteine values; up to 9 grams daily may be needed to bring them into a safe range (below 10 micromoles per liter). Organic vitamin B complex is a simple, effective approach for hyperhomocysteinemia. Its ability to replace these nutrients quickly is probably one reason that it is so effective in AD.

Why Do Some People Get Alzheimer’s Disease While Others Do Not?

Normal people can excrete only about 20 mg of aluminum daily.³ This quantity can easily be exceeded by intake of alum water, baked goods, and antacid tablets, which often contain up to 200 mg of aluminum apiece.

There is some research evidence that deficiencies of omega-3 fatty acids may cause injury to cell membranes that permits aluminum to enter tissues which are normally safe from aluminum deposits. Such deficiencies are widespread in the US population. When the body is forced to use less-desirable fats because essential fatty acids are lacking from the diet, the resulting myelin sheath cannot function normally.

People with borderline or diminished kidney function are more likely to encounter trouble with brain deposits of aluminum. This is certainly true for uremic patients.

Another factor of considerable importance is that the presence of fluoride in the drinking water of many cities, which greatly enhances the absorption of aluminum, thus making brain damage more likely to develop.

There is clear evidence that individuals who ingest large quantities of aluminum are at an increased risk of AD. In a study, 23 people with AD were compared with 23 similar unafflicted people. The researchers learned that the people with AD had a high lifetime consumption of pancakes, waffles, biscuits, muffins, and other baked goods. This diet doubled their chance of developing AD. All these bakery products contain baking powder, which has considerable aluminum used to leaven the product (Rumford Baking Powder contains no aluminum). Other unwanted sources of aluminum include nondairy creamers, self-rising flours, cake mixes, and processed foods, including individually wrapped cheese slices.

Deposits in the Alzheimer’s “tangles” are particularly heavy in the olfactory lobe region of the brain. This is where stimuli from smell are processed. This is also where the inhaled aluminum from spray-type antiperspirants would eventually appear. Almost certainly, users of spray antiperspirants and deodorants containing aluminum are at increased risk for AD. For many people, the use of antiperspirants may be the greatest source of aluminum.

Cookware is another source of aluminum, including pots, pans, and utensils, as well as cans, which leach aluminum into our food and beverages. Researchers in Australia studied 106 cans containing 52 different beverages and found that non-cola beverages in cans had five times the aluminum content of the same drinks packaged in glass bottles.

What Should Be Done to Prevent and Treat Alzheimer’s Disease?

Stop using products that contain aluminum. This means our aluminum kitchen utensils need to be replaced with cookware from glass or porcelain. Purchase food and beverages in glass containers instead of cans, and use deodorants that contain no aluminum. Avoid the use of aluminum foil; wrap foods in cellophane or cardboard instead. (The cooked food could react chemically with the aluminum in the foil.) Many antacids contain aluminum, so be careful to purchase only aluminum-free antacids. Drink purified water (Prill beads are an inexpensive method). Cease using baking powder that contains aluminum, and do not buy commercial baked products containing aluminum. This means you will have to avoid most commercially baked pies, cakes, doughnuts, and cookies.

It is far more important (and easier) to keep aluminum out of your body than to try to remove it after it has done its damage.

Aluminum directly increases the production of dangerous free radicals, which injure the delicate membranes (myelin sheaths) that surround nerve fibers in the brain. When enough of these membranes are sufficiently injured, normal brain electrical signaling ceases with memory loss, and inability to reason becomes a larger problem. The exact mechanism of how the beta-amyloid deposits typical of AD become established in the brain is not certain. It seems clear that these deposits enhance brain inflammation, which appears to be the primary cause for brain degeneration in AD.

Has Anyone Ever Recovered from Alzheimer’s Disease?

There are two well-documented cases of recovery from AD. In 1993, Louis Blank became very disturbed when a brazen woman followed him into an elevator and then into his apartment. This woman was his daughter, who had come for a visit. His diagnosis of AD was established by CAT scan. At his worst, he was unable to converse, dress, leave his apartment, wash, or eat without assistance. His therapy consisted of removal of all aluminum cooking utensils and cans from use. He was given a high-magnesium diet designed to chelate aluminum. By May 1994, he had regained his ability to converse and leave his apartment. He regained long-term memory but still has a 6-month hiatus of no memory for what occurred during his worst period. In the progression of AD, the patient reaches a point at which he cannot form short-term memories but still retains long-term memory. In 1996, Blank’s book Alzheimer’s Challenged and Conquered was published.

In June 1983, a CAT scan established a diagnosis of Alzheimer’s disease for Tom Warren. Four years later, a repeat CAT scan revealed complete disappearance of the signs of AD. His therapy included correction of an absence of stomach hydrochloric acid; removal of all teeth and mercury amalgam fragments from his gums; EDTA chelation; and high dose of vitamins and minerals, including calcium, magnesium, vitamins B3, B6, B12, and folic acid. His book was titled Beating Alzheimer’s: A Step Towards Unlocking the Mysteries of Brain Diseases.

The keys to his recovery were correction of decreased gastric acid production, elimination of exposure to aluminum and mercury, and chelation of toxic metals (aluminum and mercury). A healthy diet was supplemented with vitamins and extra minerals, especially magnesium. Supreme-B (an organic form of vitamin B complex combined with Biosil, liquid magnesium chloride, and a multivitamin) has healed 12 patients with AD. Supreme B is taken ½ oz. twice daily after meals. The dose of Biosil was 6 drops in water twice daily for a month, after which the dose was reduced to 6 drops daily. Magnesium chloride was taken in a dosage of 30 drops in water twice daily. A good multivitamin like BAM (Beyond Any Multiple) would be fine taken three times daily with meals. Most patients were improved within 30 days.

One of the patients was of considerable interest, as she failed to respond promptly to Supreme-B therapy. The clinician caring for her went to the family house and was warmly greeted with the offer of a cup of coffee. Following the clinician’s acceptance, it was discovered that the coffee percolator was made of aluminum. Changing the percolator was followed by complete recovery.

Diet for Alzheimer’s Patients

Because the cause for AD is clearly tied to inflammation, low-inflammatory foods are important. Foods that produce inflammatory residues (dairy products, meat, eggs) should be minimized. Anti-inflammatory foods and nutrients such as fish, vegetables, flax oil, fish oil, evening primrose oil, and fruit should be increased in the AD diet. Arachidonic acid, a breakdown product of dietary fat, profoundly enhances inflammation.⁶ This is generated in high amounts by eating meat, dairy products, and eggs. The daily need for arachidonic acid (AA) is only 1 mg; the typical Western diet provides between 100 and 200 mg daily. All people with inflammatory illnesses (AD, rheumatoid arthritis, arteriosclerosis, multiple sclerosis, psoriasis, malignancies) would probably be less symptomatic with noninflammatory foods in their diet.

Valuable Therapies

Twelve persons with AD have been healed with therapy that included the supplements Supreme B, BioSil, vitamin C, magnesium chloride (liquid), and a good multivitamin.

Supreme-B:

This formulation contains about 100 mg daily of readily absorbed lithium orotate, as well as thiamin propyl disulfide 150 mg, riboflavin-5-phosphate 15 mg, vitamin B6 (pyridoxal-5′-phosphate) 50 mg, biotin 500 mcg, folic acid 500 mcg, vitamin b12 as hydroxocobalamin 500 mcg, pantothenic acid (as pantethine) 500 mg, calcium(as calcium pangamate) 100 mg, zinc (as zinc citrate) 25 mg, selenium (as L-selenomethionine) 100 mcg, potassium ( as potassium orotate) 200 mg). It also contains a proprietary blend of 233 mg S-adenosylmethionine, N-acetyl-L-cysteine, and alpha-lipoic acid. Each B vitamin found in Supreme-B has specific benefits for brain cells as well as the myelin sheath. Production of this product is so complex that it is unlikely to be duplicated.

Remarkable healings of patients with painful neurological conditions (diabetic neuritis, lumbar stenosis, multiple sclerosis etc.) are being reported after use of Supreme-B. Children with attention deficit/hyperactivity disorder have been able to discontinue Ritalin. My own presbyesophagus subsides for two months after two months of Supreme B therapy, which is probably healing diabetic sympathetic neuropathy.

In addition, advanced cardiac problems, probably related to homocysteine excess, are repaired by the organic B complex. Homocysteine excess is known to cause plaque formation and sludgy blood flow in arteries, promoting clots and ischemia. Divided daily doses of an enzyme could be valuable to dissolve the offending plaque and speed up slow blood flow (Vitalzyme X, Wobenzyme, nattokinase, lumbrokinase, or bromelain).

We think that ½ oz of Supreme-B twice daily is a key therapy for all patients with AD. The physiological dosage of lithium orotate should facilitate growth of new neurons and benefits to cholinergic neurons injured by aluminum and electromagnetic waves. Side effects have not been found with Supreme-B. As mentioned earlier, 12 of 12 AD patients have been healed using Supreme B and BioSil.

Silica:

BioSil was used to decrease the quantity of aluminum that could be absorbed from drinking water. This probably facilitates healing from AD.

Lithium:

Lithium has long been known to be an effective therapy for bipolar disorder (manic depression). Conventional medical opinion has always believed that there is a steady loss of brain cells with aging, culminating in gradual shrinkage of the brain. However, recent research has shown that lithium in low divided dosage (10 to 20 mg of lithium aspartate daily) can preserve and renew brain cells.⁷ Eight of ten people given lithium showed an increase in brain grey matter of 3% in only four weeks. This is safe and appears worthwhile.

Lithium also accomplishes the following benefits for brain cells:

• It enhances DNA replication, the first step to formation of new cells.

• The damaging effects of excitotoxins (aspartame, monosodium glutamate) can be blocked by lithium.⁸

• Animal research shows that lithium can decrease the areas of cell death after induced strokes by 50%.

• Lithium protects rat brain cells from the increased levels of brain cell death caused by anticonvulsant drugs.

• Lithium may protect against adverse effects from alcohol, tobacco, caffeine, stimulants, tranquilizers, marijuana, and other mood-altering drugs, all of which cause brain damage with long-term use.

• Abnormally functioning signaling pathways may become repaired by lithium.

• The aluminum thought to be a possible cause of AD is chelated by lithium so it can be more easily removed.⁹

• Lithium slows the growth of beta-amyloid.¹⁰ Research has suggested that lithium blocks the secretion of beta-amyloid and prevents damage from preexisting beta-amyloid. Over activity of the brain cell protein tau contributes to death of neurons in AD. I like lithium as a basic therapy for AD and all dementias because it causes growth of new neurons, which ought to be desirable. Geographic research in the state of Texas has revealed that counties with high-lithium water clearly have less violent crime (murder, rape, suicide), less alcoholism, fewer robberies, and less schizophrenia.¹¹

Prill Beads:

Drinking pure water is valuable in AD, as it may facilitate recovery. Prill beads are small beads of magnesium oxide treated with bioresonance. After this preparation, the water takes on the characteristics of dew and has a hexagonal shape when viewed after freezing. Prill bead water facilitates absorption of nutrients and elimination of toxins from the body, probably including aluminum.. My limited research suggests that Prill bead water has never been studied to see if it increases urinary excretion of aluminum. Because it alkalinizes water, thus making drinking water less acidic, it decreases absorption of aluminum, which should result in less deposition of aluminum in brain tissue. We feel that Prill bead water will benefit all patients trying to recover from AD and bring health benefits to the whole family. It is inexpensive.

Oral Chelation of Aluminum and Heavy Metals

Essential Daily Defense (EDD)

: Knowing that aluminum excess and probably mercury play an important role in causing AD suggests that chelation of toxic metals could be an effective way to reverse the inflammatory process caused by aluminum and mercury, which steadily injure neurons. EDD contains malic acid, garlic, and EDTA, which acts to remove toxic metals aluminum, cadmium, lead, mercury, arsenic, and iron. There is a possibility that the heavy metal uranium might also get removed. Taking one or two EDD capsules before each meal begins removal of toxic metals from the body.

Beyond Any Multiple (BAM)

: Oral chelation with EDD over time removes sufficient toxic metals that the chelating agents begin to clear some calcium and magnesium from the body. These ingredients in BAM permit satisfactory levels of calcium and magnesium to be maintained in the blood. BAM supplies all important minerals, vitamins, and nutrients in a one-source site when taken one tablet before each meal.

Smart Drugs (Nootropics)

While smart drugs are not needed to heal AD, having knowledge of this interesting therapy can aid elderly individuals who are constantly fighting to preserve their ability to think and remember. Much disability in the elderly is caused by unrecognized side effects of drugs. Tragically, many seniors live out their lives in confusion because of excessive doses or unrecognized side effects of pharmaceutical drugs. A classic example of this problem is the mental confusion, transient global amnesia, and peripheral neuritis commonly caused by the widely prescribed statin drugs, which lower cholesterol values.

Smart drugs are substances that promote optimal brain function. Any drug that increases the amount of acetylcholine in the brain by blocking the action of the enzyme cholinesterase has the potential to improve memory, alertness, verbal fluency, and creative thinking. Therapies that increase activity of cholinesterase will tend to lower the amount of acetylcholine in the brain, which tends to impair cognitive functioning. If these changes occur, the guilty therapy might be considered a “dumb drug” for that particular individual. A variety of drugs and nutrients make up the smart drug portfolio.

Evaluation of these therapies is quite complex, as not everyone reacts to each of these substances in the same way. Preexisting moodiness can cause a depressed result with decreased productivity subsequent to the increased cholinergic effect of a smart drug. Additionally, cholinergic smart drug therapy in patients who are under considerable stress may lead to a changed person who becomes less responsive to reward, unable to maintain sustained effort, and who exhibits suppressed instead of enhanced performance. In the future, AMPA-type glutamate receptors may even be able to increase intellectual performance in healthy young adults.

AD patients, because of adverse effects from aluminum, mercury, and electromagnetic energy exposure, have suffered a progressive disproportionate loss of cholinergic neurons. Increasing the level of acetylcholine in these patients with a smart drug (Pramiracetam, galantamine, Piracetam, and vinpocetine) can increase blood flow to the brain, ATP energy production, and brain uptake of glucose and oxygen, and improve brain performance.

Piracetam

is derived from the neurotransmitter GABA (gamma-aminobutyric acid). Because of a wide variety of favorable effects, Piracetam has become widely used in:

• improving cell membrane fluidity;

• nerve protection, along with anticonvulsant properties;

• moderates neurotransmission of cholinergic and glutaminergic systems;

• improving neuroplasticity

• in vessels, reducing adhesion to the endothelium, blocking vasospasm, and improving the microcirculation;

• benefit for cognitive disorders, dementia, vertigo, cortical myoclonus, dyslexia and sickle-cell anemia.

The dosage is 800 mg three times daily.

Pramiracetam (Neupramir)

is similar chemically to Piracetam but 7 times more potent. This appears to be the most effective of the smart drugs used to treat AD. The dosage is about 1500 mg daily. Therapeutic results with Pramiracetam take about 1 month to become noticeable and may increase over the second month of therapy. Combining other nootropic drugs often improves the therapeutic result. Combination may permit the dose of Pramiracetam, which is expensive, to be reduced. Pramiracetam can produce the following results in patients with AD:

• improvement in intelligence and memory;

• reduction in anxiety and aggressive behavior;

• improvement in learning capability;

• increase in will power;

• improvement in long term memory;

• enhancement of neurotransmitter function;

• increase in the number of receptors for acetylcholine.

Steroid hormones, including aldosterone, corticosterone, dehydroepiandrosterone (DHEA), estrogens, pregnanediol, progesterone, and testosterone, enhance the function of Pramiracetam. In fact, they are essential for it to be effective. Patients with low levels of steroid hormones or their precursors cannot derive therapeutic benefits from Pramiracetam.

There is generally little toxicity and few to no side effects in patients taking Pramiracetam. The usual dosage is 1200 to 1500 mg daily, in divided doses. Uremic patients need to be given reduced amounts. Pramiracetam can improve attention span, learning capacity, memory, time–space orientation, and mental performance. Rare side effects have been seen, including heartburn, mild nervousness, dizziness, nausea, anorexia, insomnia, trembling, dry mouth, and incontinence of urine and stool.

Pramiracetam seems to be available in China, South Africa, Australia, and Europe. Whether it can be brought into the US is not known to me.

Vinpocetine

significantly decreases the decline in the release of dopamine that normally occurs in tandem with the progression of the aging process.¹³ Persistence of dopamine prevents depression from developing, along with aiding in preservation of cholinergic nerve cell membranes.

Vinpocetine improves blood circulation to the brain and thereby prevents and alleviates cerebral insufficiency symptoms caused by strokes and narrowed arteries.

A middle-aged employee at Smart Nutrition had suffered from poor vision (myopia) all her life and had worn contact lenses for many years. She took a 20 mg Vinpocetine capsule one day. Later that day, when standing behind the owner of the company, she remarked that she could read the monitor on his computer. Previously, she had been unable to read anything from that distance. The next day, she mentioned that in driving home on the same familiar route she visualized many things she had never seen before. She was confident that her vision had improved from one capsule of Vinpocetine.

Vinpocetine was given to 100 elderly arteriosclerotic patients to improve circulation to the eyes. Visual acuity improved in 88 people by an average of 73%. Improvement was most striking in patients who had already experienced retinal changes from occlusion of the central retinal artery. The 20 mg dosage of vinpocetine was administered by drop infusion three times daily or was given by intravenous infusion 10 mg three times daily. The improvement in vision paralleled blood pressure increases in the central retinal artery.¹⁴

Treatment Suggestions

One hundred percent successful outcomes for 12 AD patients suggests that organic B complex should become the mainstay of AD therapy. This must be taken along with silica. The correction of high homocysteine values; brain damage from mercury, aluminum, and lead; and cessation of electromagnetic wave exposures needs to be permanent. When the AD patient can function mentally in a normal fashion, organic B complex can be discontinued. It would be prudent to continue taking oral chelation with EDD and supplementation with BAM nutrients, vitamins, and minerals, because toxic metals are undesirable and take years to eliminate.

All measures improving general health (organic food, omega-3 fatty acids, Prill bead water, vitamin D, physical activity, sunlight) should continue. People desiring to improve their mental sharpness might wish to take Piracetam 800 mg three times daily and Vinpocetine 20 mg three times daily on a permanent basis. My impression is that continued production of new neurons is a good idea, so I intend to stay on lithium aspartate 10 mg twice daily permanently. This dosage of 20 mg daily is well below the 100 to 120 mg daily used in manic depressive disorder.

Dr. James A. Howenstine

dr.jimhow@gmail.com.

The author is indebted to Professor Harold D. Foster, for much of the material in this article came from his fine book What Really Causes Alzheimer’s Disease (Trafford Publishing, 6E-2333 Government St., Victoria, BC; 250-383-6864).

Dr. James A. Howenstine is a board-certified specialist in internal medicine who became convinced that natural therapies were more effective, safer, and less expensive than pharmaceutical drugs. He has written a book titled A Physician’s Guide to Natural Health Products That Work. This book, as well as Supreme B, BAM, EDD, and Prill beads, can be obtained from www.mynaturalhealthteam.com. Supreme B can also be obtained from Level Nutraceuticals (RhetIII@aol.com; 866-615-3835, 407-619-4959).

Notes

1. Reisberg B et al. Retrogenesis: clinical, physiologic and pathologic mechanisms of brain aging, Alzheimer’s and other cementing processes. Eur Arch Psychiatr Clin Neurosci. 1999;249(3):28–36.

2. Sobel E et al. Occupations with exposure to electromagnetic fields: a possible risk factor for Alzheimer’s Disease. Am J Epid. 1995;142:515–24; Sobel E et al. Elevated risk of Alzheimer’s Disease among workers with likely electromagnetic field exposure Neurology. 1996;47:1477–1481

3. Birchall JD et al. Aluminum, chemical physiology and Alzheimer’s disease. Lancet. 1988;2(8618)1008–1010.

4. Stewart WE et al. Risk of Alzheimer’s Disease and duration of NSAID use. Neurology. 1997;48:626–632.

5. Quere I, Grial JC, et al. Fertil Steril. April 2001;75(4):823–825.

6. Sano M et al. A controlled trial of selegine, alpha tocopherol, or both as treatment for Alzheimer’s Disease. N Engl J Med. 1997;336:1216–1222.

7. Moore GL et al. Lithium-induced increase in human grey matter. Lancet. 2000;356:1241–1242.

8. Nanaka S. Chronic lithium treatment robustly protects neurons in the central system against neuro excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx. Proc Natl Acad Sci U S A. 1998;95:2642–2647.

9. Radesater A et al. Inhibition of GSK 3 beta by lithium attenuates tau phosphorylation and degeneration. Abstr Soc Neurosci. 2001: 1, 437.

10. Phiel CJ et al. GSK regulates production of Alzheimer’s Disease amyloid-beta peptides. Nature. 2003;435–439.

11. Schrauzer G et al. Lithium in drinking water and the incidence of crimes. Suicides, and arrests related to drug addiction. Biol Trace Elem Res. 1990:105–113.

12. Pyetela M. Personal communication.

13. Schmidt J et al. Effect of neurotropic drugs on age dependent changes in neurotransmitter (dopamine) release. Drug Dev Res. 14:293–295

14. Kahan A. Olah M. Arzneimittelforschung. 26(10a):1969–1972,1976.