The Alzheimer’s Disease Chapter from Smart Drugs II
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From the book Smart Drugs II. Copyright (c) 1993, 1997.
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The Alzheimer’s Disease Chapter from Smart Drugs II
Suggested Treatment Protocol for Alzheimer’s DiseaseThe primary focus for Smart Drugs & Nutrients and this book is the use of cognition-enhancing substances for normal people wanting to improve their brain power and prevent or treat age-associated memory impairment. However, we know that many patients suffering from Alzheimer’s disease also benefit from many of the substances we discuss. We have received many gratifying reports from the families of Alzheimer’s patients, and from the sufferers themselves, about the relief obtained through the use of various combinations of smart drugs and nutrients.
Alzheimer’s disease is considered to be the number one health problem by the National Institute on Aging [Goldsmith, 1984]. Alzheimer’s disease attacks between 2% and 6% of people over the age of 65. It is more common in women than in men, and there appears to be a genetic predisposition to being afflicted. The likelihood of a close relative of an Alzheimer’s patient developing the disease is about four times greater than the general population. If the onset is after age 65, the average course of the disease from onset to death is about five years, with a general range of one to ten years. The duration is somewhat longer if the onset is before age 65. Three characteristics of Alzheimer’s disease are: 1) severe cognitive impairment, 2) its onset and course are insidious and progressive, and 3) the diagnosis is one of exclusion (i.e., no other discernible causes of dementia can be determined) [Cohen, 1981].
The problem with finding a cure for Alzheimer’s disease is that the cause has not been determined. Scientists have made a number of educated guesses as to the cause(s), and have identified a number of contributing factors. First, as noted above, there appears to be a genetic component to Alzheimer’s disease. Other suspected causes include free radical damage, slow viruses, reduced blood flow to the brain, immune system malfunction, abnormal calcium regulation within nerve cells, hormonal factors which adversely effect brain cell functioning (both too much and too little of specific hormones), malnutrition, and toxic levels of aluminum, lead and iron. All of the above factors have been implicated at one time or another as potential contributory causes of Alzheimer’s disease. In fact, there may not be a single cause of this disease. If this is the case, there is probably not going to be a single treatment that will work for everyone. Thus, treatment modalities should be developed which approach Alzheimer’s disease by attacking as many of the most likely causes that can be identified.
Another approach to treatment is to correct the biochemical and physiological changes which characterize the disease. The most widely held theory of the cause of Alzheimer’s disease is the cholinergic theory [Drachman and Glosser, 1981]. This theory attributes the cognitive deficits of Alzheimer’s disease to a breakdown in the cholinergic neurotransmitter system. Contributions by other neurotransmitter systems have also been implicated by other researchers. Thus, a useful therapeutic approach would be to 1) identify the neurotransmitter systems involved, 2) prevent their breakdown, 3) enhance sensitivity of the nerve endings to the neurotransmitters, and 4) restore normal (or supernormal, if necessary) levels of the neurotransmitters.
The most cost-effective, least invasive way to treat any illness is to prevent it in the first place. Aluminum has been frequently implicated as a primary cause of Alzheimer’s disease. We therefore recommend that all sources of aluminum ingestion be eliminated. This includes disposing of all aluminum cookware, avoiding beverages and foods which come in aluminum cans, not using aluminum-containing deodorants and anti-perspirants, and not taking aluminum-containing antacids and aluminum-buffered aspirin. Some cities treat drinking water with aluminum compounds that have been implicated in the incidence of Alzheimer’s disease. Many water filter manufacturers advertise that their products remove aluminum.
We highly recommend the book, Reducing the Risk of Alzheimer’s Disease, by Dr. Michael A. Weiner. This book not only provides comprehensive brand-name sources of aluminum-containing products, but also provides comprehensive preventive nutritional recommendations. It is available from Dr. Weiner at 415-388-1006.
Dr. Robert Sapolsky, of Stanford University, believes that brain cell loss in aging and Alzheimer’s disease may be due to high levels of cortisol, a hormone which increases when we are under stress. He therefore recommends that efforts be made to minimize stressors in the lives of Alzheimer’s disease patients. He also believes that corticosteroids should not be used in Alzheimer’s disease patients for other medical problems like asthma or arthritis [Sapolsky and McEwen, 1986].
Since loss of brain cells is a characteristic of Alzheimer’s disease, it is clear that any therapeutic approach must be initiated early in the disease. Although the regrowth and regeneration of brain cells is under investigation by many different research teams around the world, no clinical therapy is yet available. Loss of brain cells must be considered permanent, and prevented whenever possible. Early intervention is essential.
Our suggested combined approach attacks Alzheimer’s disease from many different directions, with very little overlap of mechanism for each component. Thus, nearly all bases are covered, with very little risk of adverse effects, and no known adverse cross-reaction between any of the substances listed. This combined approach is, however, experimental, and should not be undertaken without a physician’s supervision. With the insidious, progressive downward course of Alzheimer’s disease, the risk (compared to doing nothing) is certainly minimal, and the potential for dramatic improvement is substantial.
Therapeutic modalities should be tailored to the needs of the individual and the stage of the disease. The use of alcohol, tobacco and caffeine-containing beverages should be minimized. Care should be taken not to withdraw these items too rapidly, to minimize the stress of this process [Roberts, 1981].
A number of nutrients have been tested alone and in conjunction with other nutrients and drugs for Alzheimer’s disease, with varying degrees of success (see references in Table 1). Our combined recommended protocol incorporates all nutrients that have either 1) demonstrated efficacy in clinical tests, or 2) a strong theoretical basis for potential benefit in Alzheimer’s disease, even though they may not have been effective when tested as isolated nutrients. These substances are inexpensive, extremely safe, and may be of benefit by themselves — or they may augment other, more effective therapies. Inclusion of these nutrients appears to be in accord with Drachman and Glosser’s recommendation [1981] to provide general metabolic support of neural function when developing treatment strategies.
Although this may at first appear to be quite a “drug and nutrient cocktail,” it is no more complicated than the nutritional regimens that many people follow each day. An Alzheimer’s patient should not, of course, be expected to carry out this regimen without supervision. However, family members or care providers can certainly set up a routine that can be easily carried out. Because of the non-toxic and non-habit-forming nature of all of the above substances, missed doses or even moderate overdoses are not particularly harmful.
We also believe that every Alzheimer’s patient should have a complete thyroid work-up, to rule out overt or sub-clinical hypothyroidism. Many of the symptoms of hypothyroidism mimic those of Alzheimer’s disease, and traditional blood tests are now recognized to be inadequate for accurate diagnosis. Appropriate doses of thyroid hormone may produce dramatic alterations in energy levels, depression, and cognitive function. I [WD] prefer Armour Desiccated Thyroid.
Another medication which has unfortunately fallen into undeserved disrepute is Cylert (pemoline), a controlled drug which is a derivative of amphetamine. Cylert may dramatically improve the somnolence (daytime sleepiness) of many Alzheimer’s patients, and may also improve cognitive performance.
Although tacrine (THA) has been recently recommended for FDA approval for use in treating Alzheimer’s disease, we do not believe that it is more effective by itself than many other substances discussed in this book and in our previous book, Smart Drugs & Nutrients. In addition, in contrast to most of the substances that we have reviewed, tacrine (trade name Cognex) is fairly toxic, and its adverse effects may outweigh the modest benefits which may be obtained. This toxicity may prohibit many patients from taking it. This is definitely a subject which should be addressed by a physician.
Chelation therapy is a treatment administered by physician members of the American College of Advancement in Medicine (for the name of an ACAM physician in your area, call 714-583-7666). It consists of multiple intravenous infusions of EDTA (ethylenediaminetetraacetic acid), a synthetic amino acid, in combination with selected vitamins and minerals.
Chelation therapy is used to treat a number of chronic degenerative conditions, including angina pectoris, intermittent claudication (reduced circulation in the muscles), coronary artery disease, diabetes, hypertension, and Alzheimer’s disease. These treatments are usually administered once or twice a week, requiring about three hours per treatment. They are relatively painless and non-invasive (requiring only insertion of an IV needle), and usually administered in a pleasant social environment with other patients.
Chelation therapy is the most effective way to remove aluminum, a component of the neurofibrillary tangles found in the brains of Alzheimer’s patients. I [WD] recommend a minimum course of twenty to thirty treatments be administered as early as possible in every Alzheimer’s patient. For more information about chelation therapy, see Dr. Elmer Cranton’s book, Bypassing Bypass, available from Medex Publishers, Inc. at 800-426-3551.
Although some Alzheimer’s patients show almost immediate improvement, many do not begin to improve for a minimum of six months. As an example, in a double-blind, placebo-controlled study of Hydergine on Alzheimer’s disease patients, Kugler and colleagues [1978] found no benefit from 6 months of Hydergine therapy. However, at a second follow-up 9 months later (15 months after the beginning of therapy), they found that the Hydergine group had improved 5-7% on the Wechsler Intelligence Test. Hoffer [1993] reports that one of his patients was worse after six months on a combined nutritional/aspirin therapy, but improved after ten months. Hoffer’s patient continued to improve during two years of follow-up. These examples confirm that it is necessary to use prolonged therapy on Alzheimer’s disease patients.
Since Alzheimer’s disease is a chronic condition of many years duration, it will probably require an extended period of time for any truly significant therapeutic agent to alter its course. Physicians and researchers (and patients and family) must adopt a therapeutic attitude much like that which currently exists for cancer (i.e., five-year outcome).
For example, oncologists (cancer doctors) accept heroic measures including major surgery, whole-body irradiation, and chemotherapy in return for increases in five-year survival rates of 10% or less. However, just the opposite attitude prevails with respect to Alzheimer’s disease. Everyone wants a short-term cure. If an agent does not exert a dramatic clinical effect in a short-term study, it is regarded as virtually useless by the research community. This attitude must change [Reisberg, 1981].Altman H, Mehta D, Evenson RC, and Sletten IW. Behavioral effects of drug therapy on psychogeriatric inpatients. II. Multivitamin supplementation. Journal of the American Geriatrics Society 21: 249-52, 1973.
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