Alzheimer's Disease Treatments

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By Michael S. Evers

This special report has been produced by the Alzheimer's Disease Fund as a public service.

About Alzheimer's Disease...

Alzheimer’s disease can occur at any age, but most commonly appears after the age of 50. Symptoms occurring before 65 are designated presenile dementia of the Alzheimer’s type (PDAT); after 65 it is senile dementia of the Alzheimer’s type (SDAT). Diagnosis of Alzheimer’s disease has been extremely difficult as the most definitive diagnosis has been a post mortem biopsy of the brain. However, Japanese researchers have recently developed a brain-scan technique that enables doctors to diagnose Alzheimer’s disease while the patients are still alive, the British medical journal Lancet reported last June.

Dementia refers to a general mental deterioration. In the elderly this is referred to as senile dementia. It can be marked by progressive mental deterioration, loss of recent memory, moodiness and irritability, self-centerdness and childish behavior. This is often due to Alzheimer’s disease, although there are many other causes of senile dementia.

Although much remains to be learned about aging, it is safe to say that Alzheimer’s disease and other senile dementias are not necessarily a normal process. Much can be done, even though the incidence of senile dementia is likely to increase alarmingly for a time as the median age of the population grows.

Currently 1.3 million elderly in the US suffer severe dementia and approximately 2 million endure mild to moderate dementia -- roughly 15 percent of all the US elderly have some degree of dementia, while two-thirds of 1.5 million nursing home patients have dementia. As staggering as these figures may seem, they are expected to increase.

Alzheimer’s disease is the best known of all the dementias. Postmortem studies have found that about 50 percent of all cases of dementia, both presenile and senile periods, are the result of Alzheimer’s disease. Alzheimer’s is characterized by the general destruction of nerve cells in several key areas of the brain devoted to mental functions. This results in tangles of nerve fibers and plaque formation. The disease’s clinical features are believed to be related to a decrease in a transmitting agent in the brain known as acetylocholine, although there is a general reduction in the concentration of all neurotransmitting substances. Under a microscope, the brains of those with Alzheimer’s look as if they have the measles, according to Dr. Marcelle Morrison-Bogorad, a molecular neurobiologist at the National Institute on Aging. The brains are littered with spots, tangles, and "rubbish dumps" of an abnormal, insoluble protein called amyloid.

"Unfortunately, the amyloid deposits are only in the spots of the brain that help us think and make us human," said Morrison-Bogorad. "That’s why Alzheimer’s victims don’t have a light in their eye anymore, but they’re still walking around. Their motor functions aren’t affected."

The Alzheimer’s Association has developed a checklist of symptoms to help promote early detection of the disease. Examples are given to indicate the symptoms that may become manifest.

Recent memory loss that affects job skills: anything from not remembering the boss’ name to forgetting to show up for work on Monday. Difficulty in performing familiar tasks: leaving the door to the house wide open; forgetting to put toothpaste on a toothbrush. Problems with language: forgetting the proper structure of sentences; substituting inappropriate words for the correct ones. Disorientation of time and place: getting lost in one’s own house; losing track of the day, month, year. Poor or decreased judgment: leaving the house wearing pajamas; crossing the street in front of oncoming traffic. problems with abstract thinking: forgetting how to use numbers; not recognizing common symbols such as stop signs. Misplacing things: putting shoes in the oven, keys in the pickle jar. Changes in mood or behavior: shifting moods rapidly and drastically, from laughter to rage without apparent reason. Changes in personality: a person who was once open and friendly may become suspicious and reclusive. Loss of initiative: becoming passive in the processes and activities of everyday living; unable to act on ideas or needs. While none of these things on its own may seem like cause for concern, recurrences or increases in severity of one or more of these behaviors may be an indication of Alzheimer’s or other dementias. Anyone experiencing such symptoms should undergo an examination by a physician.



Fat Consumption In the Alzheimer’s Disease Review 2, an article by William Grant, Ph.D., published June 19, 1997 on the Internet reported on the link between Alzheimer’s Disease (AD) and dietary fat intake. Grant stated recent findings that elderly African-Americans and Japanese living in the United States have much higher prevalence of Alzheimer’s Disease than those still living in their ethnic homelands. Countries in which people ate the most fat and the most calories had the highest incidence of Alzheimer’s disease, according to the study, which took data from 18 community-wide studies examining the prevalence of Alzheimer’s disease in the 65+ age population in 11 countries and compared the rates to national-level information on a person’s estimated diet.

Among Western countries, however, those with diets higher in fish, such as cod, had lower Alzheimer’s rates than predicted by their fat consumption.

The study measured food intake by looking at data from the United Nation’s Food and Agriculture Organization. He found that for each additional 10 grams of fat in the average daily diet of a country, the percentage of seniors over 65 who had Alzheimer’s disease increased by about 0.3 percent.

There was a similar relationship between higher-calorie intake and a higher rate of Alzheimer’s with rates of the dementia increasing by 0.3 percent with every 100-calorie increase in the average daily diet, Grant said.

He suggested that fat intake leads to increased production of free radicals, molecules produced by the body’s natural metabolism that can cause damage to proteins and genetic material.

Of the foods studied, fish seemed to be the only one to provide strong anti-Alzheimer’s effects in regions with relatively high-fat diets, such as Europe and the United States. Grant calculated that each calorie of fish eaten countered the effects of 18 calories of fat, or about 2 grams.

Grant hypothesized that Alzheimer’s Disease might be caused primarily by environmental rather than genetic factors. The primary findings were that fat and total caloric supply had the highest correlations with AD. Furthermore, fish consumption was found to reduce the prevalence of AD in the European and North American countries.

"People have some control over their diet when it comes to preventing Alzheimer’s disease. You can clearly reduce your risk by eating a low-fat diet," said lead researcher Dr. Grant. "There is strong evidence that the incidence and prevalence of AD is affected by diet, with high risk factors found to include alcohol, fat, refined carbohydrates, salt, and total caloric consumption, and preventative factors found to include antioxidants, essential trace minerals, estrogen for post-menopausal women, fish and fish oil, and anti-inflammatory therapeutic agents. The finding that the highest correlation between diet and AD incidence and prevalence is found 3-5 years before the study period suggests that diet modifications late in life can still affect the risk of developing AD...In addition to the analysis on how to combat oxidative stress caused by diet by Harman (1996) there are other popular books on recommended diets to prevent chronic degenerative disease...(including) Ornish et al., 1990," according to the study.



Vitamin E At the annual meeting of the American Academy of Neurology on April 17, 1997, Dr. Jeffrey Cummings presented a research study that has proven that high daily doses of Vitamin E can help moderately affected Alzheimer’s patients maintain "daily living" skills longer. Some members of the test group were able to delay entry into a nursing home by as much as seven months.

Dr. Cummings, director of the UCLA Alzheimer’s Disease Center and professor of neurology and psychiatry, reported on how vitamin E can delay the decay of daily living skills such as bathing and dressing themselves, handling money, and the ability to do other routine chores associated with the disease. It appears to help by protecting brain cells from the damaging effects of oxygen. "We are finding ways to make our patients’ lives better," he said.

A team of researchers from several research institutions and funded by the National lnstitutes of Health, conducted a double-blind, placebo-controlled, randomized, multicenter trial where 341 men and women with an average age of 73 were assigned to different groups for comparative study. This study is the largest ever involving Alzheimer’s. All patients included had moderate memory loss, most could not precisely name the date. Many had poor judgment and needed some help in caring for themselves. Patients received daily doses of drug called Eldepryl (selegiline) (10mg/daily), vitamin E (2,000 IU/daily), both Eldepryl and vitamin E, or a placebo. At the beginning of the trial, all subjects had moderate memory loss, and some had poor judgment or needed help with daily self-care.

At the end of the two-year study, those who had taken Eldepryl, vitamin E., or a combination of both substances were compared to the placebo group. Only one-quarter of patients who had taken vitamin E were institutionalized compared to 39 percent of patients who were taking the placebo. More patients in the placebo group (69 percent) had reached what researchers call Alzheimer’s "end points": institutionalization, loss of daily living skills, increased dementia, or death as compared to the group taking vitamin E (53 percent.) Overall, those who took vitamin E had a 71-day delay in reaching such an end-point. Eldepryl also slowed down the rate of the illness, according to the researchers, but the effects were not judged to be statistically significant. Taking both vitamin E and Eldepryl did not increase the effects of either substance. The estimated median survival days was 440 in the control group compared to 670 in the Vitamin E and 585 in Vitamin E and Eldepryl group.

Dr. John Growdon of Massachusetts General Hospital, one of the researchers, said he had begun routinely giving his Alzheimer’s patients vitamin E, the less expensive of the two treatments. "This is not an overwhelming effect," Dr. Growdon said, "but it is the first time we have seen long-term benefit. I find that very encouraging."

"The obvious question is,’ Should I take vitamin E?’" said Edward Truschke, president of the Alzheimer’s Disease and Related Disorders Association. "Because of the other health benefits it has, it probably can’t hurt. But at the same time, there are some mild side effects. Anyone taking a new medication should consult with their physician."

The study also showed that the use of vitamin E and Eldepryl together appeared to pose a greater risk of fainting or falling, an issue of concern to the elderly. However, the researcher hailed the study as a landmark in the treatment of Alzheimer’s disease. The delay in the deterioration of the health of patients who took vitamin E was significant, and the use of vitamin E is cost-effective when compared to Eldepryl.

The dose of vitamin E given in this study, 2,000 international units, is more than 60 times the recommended dietary allowance of 30 international units a day.

Dr. Cumming’s research also was published in the April 24, 1997, issue of the New England Journal of Medicine.



Ginko Biloba Dementia in the elderly often results from an insufficient blood and oxygen flow to the brain. This lessened flow may also cause short-term memory loss, vertigo, headache, ringing in the ears, lack of vigilance, and depression. An extract from the leaves of the Ginkgo biloba offers hope to keep the proper amount of blood and oxygen flowing.

In a trial involving 112 geriatric patients with chronic cerebral insufficiency, the administration of 120 mg per day of Ginkgo biloba extract (GBE) resulted in a statistically significant regression of this insufficient blood and oxygen flow. The regression of these symptoms induced by Ginkgo biloba suggests that a reduced blood and oxygen supply to the brain may be the major causative factor of age-related disorders, including Alzheimer’s, rather than a degenerative process of nerve tissues. It appears that Ginkgo biloba extract offers relief of the side effects of aging by increasing blood flow to the brain. It may also offer significant protection against the development of these symptoms and strokes.

Ginkgo biloba extract also increases the rate at which information is transmitted at the nerve cell level, according to clinical studies. In one double-blind study one group received GBE, the other a placebo. The time of reaction in healthy young women performing a memory test was improved significantly after the administration of GBE. In another double-blind study, the extract induced near-normal vigilance and improved mental performance in elderly patients.

These findings at the behavioral level correlated with improvements in brain wave patterns as demonstrated by electroencephalograph (EEG) tracings. Patients with a more unfavorable initial situation, as measured in resting EEG activity, displayed the greatest improvement. ‘The results show,’ the study concluded, ‘that chronic GBE medication has a positive effect in geriatric subjects with deterioration of mental performance and vigilance, and this effect is reflected at the behavioral level.

Ginkgo biloba extract may be of great benefit in many cases of senility, including Alzheimer’s disease. It has been shown to normalize the acetylcholine receptors in the brain of aged animals and to increase transmission of nerve impulses, both of which are decreased in Alzheimer’s disease.

In another research study presented at an AMA conference in Washington, D.C., scientists from the New York Institute for Medical Research showed that for one in three patients, an extract from the leaves of the ginkgo biloba tree delayed the progression of dementia by six months to one year.

None of the ginkgo patients’ cognition or social skills improved markedly, researchers said. But those taking the extract did not decline, unlike the group taking placebo pills.

"The study shows a modest result," said Dr. Pierre Le Bars, one of the study’s authors. "But sometimes we forget that even to stabilize a patient with this terrible disease is a fantastic result.

Ginkgo trees are hardy, resistant to pollution, and the only trees around that grew at the time of the dinosaurs. For thousands of years, the Chinese have used ginkgo to improve mental clarity. More than 200 studies in Europe show that ginkgo boosts memory, and it is widely prescribed there.

In the United States, ginkgo has been available in health-food stores as a vitamin supplement for the last 10 years. It is now the fifth-biggest-selling herbal supplement.



NADH Reaction NADH was first discovered in 1934 by Dr. Nathan Kaplan. It plays the central role in the energy production of the cells--the more NADH a cell has available, the more energy it can produce.

For the last 20 years, Dr. Jorg Birkmayer, M.D., Ph.D, Professor of Medicine and Clinical Chemistry, has been conducting research on treating patients with Parkinson’s Disease with coenzyme Nicotinamide Adenine Dinucleotide (NADH) . The similarities between Parkinson’s and Alzheimer’s disease, along with the success of treating cognitive dysfunction with NADH, led him to test the effects of treating Alzheimer’s patients with NADH.

Researchers had measured that NADH activity decreases tangentially with the human aging process. The decrease is magnified in Alzheimer’s patients’ cell activity related to NADH is 25% to 50% lower in Alzheimer’s patients than in similar aged individuals without Alzheimer’s. Dr. Birkmayer hypothesized that the administration of NADH would alleviate the symptoms and halt the progression of the disease by raising the body’s levels of neurotransmitters. The deficit in the neurotransmitters has been identified as a key cause that produces many symptoms associated with Alzheimer’s. By increasing cell energy, Dr. Birkmayer hypothesized that NADH would prevent premature death of brain cells, resulting in reduction of the effects and progression of Alzheimer’s.

After years of research, Dr. Birkmayer was able to produce a completely natural, patented tablet form of NADH with which to conduct a trial. The trial, conducted in Austria, consisted of 17 Alzheimer’s who were given 10 mg of NADH in tablet form each morning, 30 minutes before their morning meal. Following two weeks of treatment, a 240% increase in NADH activity was observed. Improvement was also noted in the patients’ cognitive function and memory. All of the patients evaluated, including those most severe cases of dementia, experienced an improvement in cognitive function. The alertness and mental activity of the patients was also increased. In addition, two effective tests for measuring cognitive function before and after treatment confirmed the patients’ remarkable improvement.

Other tests of NADH have suggested that the coenzyme is effective in boosting athletic performance in national class endurance athletes, in providing elderly individuals with greater levels of energy, and in acting as an effective antidepressant.



Vitamin B12 Forty Alzheimer’s patients in a Canadian study led to finding a direct relationship between vitamin B12 levels and the patients’ degree of impairment. The patients with the highest degree of impairment had the lowest B12 levels.

All ages of Alzheimer’s patients have been found to have lower serum B12 levels, compared to normals and patients with other forms of dementia in several other studies.

Supplementation of B12 and/or folic acid may result in complete reversal in some patients, but there is generally little improvement in patients who have had Alzheimer’s symptoms for longer than six months. Some scientists hypothesize that prolonged low levels of vitamin B12 may lead to irreversible changes.

Modern eating habits may contribute to the lack of sufficient levels of vitamin B12. Red meat is a major source of the vitamin. However, red meat consumption is down due to concern about fat consumption. Further, several other factors can lead to B12 deficiencies. Stress can impair absorption of B12 and drain the approximately 5 milligrams of B12 stored in the average person’s body. High fiber diets can inhibit the absorption of B12. Laxatives, diminished thyroid function, deficiencies in iron, calcium, and B6 can all lead to deficiencies in B12. Drugs used to treat gastric problems can interfere with B12 absorption. Patients who are involved in chronic antacid therapy are advised to continuously monitor their B12 status since antacids reduces or eliminates entirely the body’s absorption of B12.

Generally B12 is prescribed only when laboratory tests determine that anemia is present. However, as many as 1/3 of the patients who experience B12 deficiency don’t have anemia. The effects of a B12 deficiency can show up before anemia develops.

These early effects can include memory loss, fatigue, soreness and/or weakness in the arms and legs, decreased taste sensation, premature graying of the hair, slow reflexes, stammering speech, difficulty with walking, nervousness, inability to match colors of slightly different hues, a brown discoloration of the skin around the small joints, and radiating nerve pain. Apathy, paranoia, and confusion may also be present.

The only certain way to correct a B12 deficiency is through injections. However, the vitamin may also be purchased in tablet form. These tablets may be adequate for maintenance doses of B12 after the body’s reservoirs have been built up.



Co-enzyme Q10 Several studies have been completed, and more are ongoing, regarding the efficacy of Coenzyme Q10 in maintaining the health and well-being of the body. Coenzyme Q10 (Q10) is a nutrient found naturally in both plants and animals. It functions as a vital catalyst in creating the energy that cells need for life. Without Q10, the chain of cellular energy is broken and life ends. It also functions as a potent antioxidant, helping to keep the membranes of nerve cells fee of brain power-damaging substances.

One study, reported in the September 12 issue of the prestigious British medical journal Lancet, detailed two case studies in which Q10 therapy was considered to prevent the progression of dementia for 1.5 - 2 years in two sisters afflicted with Alzheimer’s. The therapy consisted of daily doses of 60 mg. daily of CoQ10, 150mg of sodium ferrous citrate, and 180 mg of vitamin B6.

In fact, the younger of the patients, a 49-year-old female who had a history of one year of progressive memory impairment, improved to almost normal mental state after 6 months of the therapy.

Coenzyme Q10 is available in health stores as an oral dietary supplement, and is recommended in varying doses for the generation of energy in all cells, as well as improving blood circulation in the brain and to improve cardiovascular fitness.



Others Acetyl-L-Carnitine is an amino acid which enhances brain energy, helping to improve mood and to reduce the effects of age-associated memory impairment. A double-blind trial of 7 patients with probable Alzheimer’s disease resulted with clinical and laboratory evidence that acetyl-L-carnitine is beneficial in the treatment of Alzheimer’s disease. The patients treated with acetyl-L-Carnitine showed significantly less deterioration on mental status tests than did patients receiving the placebo during the study. 1,500 mg. daily is recommended by some sources.

Vitamin C concentrations are 15 times higher in the brain than in any other body tissue, making it necessary for brain power fitness. It also extends the life of vitamin E and is needed for the production of several key brain chemicals. Since it can be fully absorbed only at the rate of 500 milligrams at a time, it is necessary to be taken in staggered doses throughout the day. The recommended amount is 3,000-5,000 mg. daily.

Cerebral blood circulation is enhanced by folic acid. Combined with vitamins B12 and B6, folate helps to control levels of a toxic amino acid, homocysteine. When homocysteine is present in present in elevated amounts, it is a risk factor for cardiovascular disease and mental deterioration. Alzheimer’s patients show elevated levels of homocysteine. The daily dose of 40 is recommended.

One of the components of Shen Jin Cao, a traditional Chinese herbal medicine used in that country for centuries to treat fever and inflammation is huperzine A (HupA.) This compound appears to be a powerful inhibitor of acetylcholinesterase (AChE). AChE breaks down excess acetylcholine in the brain. Studies of patients with AD have shown that there is a significant loss of presynaptic cholinergic neurons in their brains. The acetylcholine that is produced in the brains of patients is quickly broken down by AChE and the shortage of the neurotransmitter appears to contribute to patients’ memory loss.A purified version of this compound has been used as a prescription drug for treating dementia in China for the past few years. Clinical trials are now being planned in the United States. Researchers are hopeful that HupA will prove to be an effective alternative to taking already-approved drugs tacrine or donepezil, which have adverse effects on some patients, causing them to discontinue therapy.

Tokyo University researchers performed experiments that have led them to believe a substance called catechin may fight the protein that causes Alzheimer’s disease. Catechin is found naturally in chocolate, green tea, and the guarana tree of Brazil. Researchers feel catechin prevents brain cells from being destroyed by a protein. Beta amyloid peptide is the protein which is believed to cause Alzheimer’s disease by accumulating in the brain, then linking with active oxygen, killing the brain cells and leading to senility. If catechin can block the harmful protein’s action, perhaps it can eliminate the onset or reduce the effect of Alzheimer’s .

Proper cholesterol levels in the blood are important to proper working of brain and nervous system tissue. Foods like butter and eggs are considered brain foods because they encourage correct cholesterol levels in the blood. These foods are also rich in arachidonic acid (AA). AA is necessary for the production of prostaglandins, which play a major role in how well the entire body functions. The trans fatty acids found in margarine, shortening, and hydrogenated fats block proper prostaglandin production and should be avoided, according to some sources.

Medical ozone research has been carried out since 1985 in Cuba. In one double-blind study, 60 patients with senile dementia were divided into two group, one group receiving ozone/oxygen therapy via rectal insufflations for 21 days. The second group received insufflations of oxygen alone. Among the first group, 85% of the patients showed improvement in their degenerative dementia. In contrast, there was no improvement in the second group.

By 1994, over 500 patients had been treated with ozone at a Havana hospital. The therapy is not considered a cure of AD, but is undertaken because of the marked improvement in the overall quality of life of the patients, including greater physical energy and an improved ability to manage their own daily lives.

Zinc, along with vitamins C and E, carotenes, flavonoids, and selenium are natural compounds which are antioxidants, preventing free radical damage. Free radicals are highly reactive compounds that bind to then destroy other molecules. Many people think that free radical related processes are involved in the development of Alzheimer’s disease.

Zinc absorption in the elderly is marginal at best. Even an adequate dietary intake doesn’t mean proper levels of zinc absorption, which seems to be dependent on adequate picolinic acid secretion by the pancreas. Since older individuals usually have some pancreatic insufficiency, zinc picolinate is probably the best form of zinc supplementation for a majority of the older population.

Flaxseed oil can be effective for several diseases, including Alzheimer’s. It is unique because it contains both essential fatty acids and linoleic acids in appreciable amounts. As it increases the body’s level of essential fatty acids, it decreases the susceptibility of the body to diseases caused by a lack of these acids.



Recommendations for avoiding Alzheimer's Disease These recommendations were included in the Encyclopedia of Nutritional Supplements, written by Michael Murray.

Ginkgo biloba extract (24 percent ginkgo flavonglycosides) at a dosage of 80 milligrams three times daily in the early stages of Alzheimer’s





Dietary and Lifestyle Recommendations Avoid aluminum Adopt a healthful lifestyle and diet.

Supplement Protocol

High-potency multiple

Vitamin C, 500 to 1,000 milligrams three times daily

Vitamin E 400 to 800 International Units daily

Flaxseed oil, 1 tablespoon daily

Evening Primrose Oil, 1000mg daily

Thiamin, 3 to 8 grams daily

Phosphatidylserine, 100 milligrams three times daily

Methylcobalamin (active vitamin B12), 1,000 micrograms twice daily

Additional Recommendations

Get a hair mineral analysis to rule out high lead, aluminum, or other heavy metals

Resources

1. The Philadelphia Inquirer October 22, 1997, "AMA Backs Ancient Chinese Herb to Help Stall Progress of Dementia", by Brigid Schulte

2. Townsend Letter for Doctors & Patients, "The NADH Reaction," by Jorg Birkmayer, M.D., Ph.D.

3. Source Unknown Book

4. The Washington Post April 24, 1997, "Alzheimer’s Patients in Study Benefit Slightly From High-Dosage, Daily Vitamin E"

5. Boston, April 23, 1997, "Alzheimer’s Progression May be Eased by Vitamin E"

6. "High-Dosage, Daily Vitamin E Benefits Alzheimer’s Patients," by Kate White, June 2, 1997

7. Natural Healthline, "Interview with Pioneering NASA Scientist on the Diet-Disease Link, by Peter Barry Chowka, Aug. 12, 1997.

8. The New England Journal of Medicine; April 24, 1997. Selegiline and Vitamin E for Treatment of Alzheimer’s Disease in http://www.aceology.com/med/mppsy/allze.htm

9. Alzheimer’s Disease Review 2, pp 42-55, 1997, University of Kentucky, "Dietary Links to Alzheimer’s Disease," William B. Grant

10. "High-Fat Diets Linked to Alzheimer’s," by Damaris Christensen, Medical Tribune News Service, 1997

11. Dubuque, Iowa Telegraph-Herald, Study: "High-fat diet might lead to Alzheimer’s," June 22, 1997



This special report has been produced and distributed by The Alzheimer’s Disease Fund as a public service. The Alzheimer’s Disease Fund is a program of Project Cure, Washington D.C. 20069

Copyright 1996-1998 Project Cure Send any questions or problems regarding this site to webmaster@naturalhealthvillage.com.


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