Overview of Alzheimer’s Dementia
What is Dementia?
Dementia is a medical term referring to a deterioration of mental functioning due to progressive organic disease of the brain. Persons suffering from dementia typically experience loss of intellectual abilities, such as memory, language use, and the ability to learn, solve problems, and make judgments. In its more severe forms, dementia may also produce disorientation, hallucinations, and paranoia. Social functioning is impaired and emotional responses may be atypical or inappropriate. For example, irritability and agitation may be present, with occasional verbal and physical aggression toward family or caregivers.
Family members often describe the deterioration of a demented relative as a gradual death – as a loss of the higher qualities of the mind which distinguish us as human beings. This is an ironic observation since dementia often strikes while the individual still has good physical health. Eventually, even the body succumbs.
A Brief History of Alzheimer’s Dementia
In the past, dementia was viewed as a normal consequence of the aging process. Just as the body tended to lose its strength and suppleness with the passage of time, aging was also thought to naturally result in brain degeneration and decline in mental abilities. This view was (and still is to some extent) reflected in the term “senility.” Although in our daily lives we commonly associate senility with aging, technically it is not a useful medical term. With the increased understanding of the role of the dementias in the aging process, senility has fallen from favor. It is simply too vague in its implications to be useful to health care professionals.
Only a few years ago, senility was employed for diagnostic purposes. To understand how the change in medical terminology took place, we must look back almost a century. In 1907, Dr. Alois Alzheimer published research findings based on a case study which indicated that biological deterioration was linked to the psychological symptoms of certain forms of dementia. This important demonstration of biological causation was a crucial step in recognizing that mental illness can have a physical origin. His description of the tangled and degenerated nerve fibers clearly established the biological dimension of a process then labeled senility.
The curious feature of Alzheimer’s case study was that the patient was only fifty-one years old. The woman’s age was far too young to be considered normal for such extensive degeneration. Alzheimer believed that he had discovered a separate illness occurring before old age. Therefore, he called the disease “presenile dementia” – dementia before old age.
Although his findings were controversial, his diagnostic category was eventually accepted. An arbitrary age limit (sixty-five) was chosen. Sixty-five years of age was thought to reflect the age at which “normal” senility began. Thus, cases of dementia of unknown causation before the age of sixty-five were diagnosed as presenile dementia, while those sixty-five or older were considered senile dementia.
This bit of historical information is very important to our consideration of Edgar Cayce’s perspective. Alzheimer’s disease was not a formal diagnostic category during Cayce’s lifetime. As one would expect, when he did use diagnostic labels, Cayce tended to use terms commonly in use among the health care professionals of his era.
Therefore, many of the readings which appear to be describing Alzheimer-type pathology, simply mention senility as the problem. Apparently, he did recognize the generally accepted medical distinction between presenile and senile dementia. For example, he used the term “premature senility” to distinguish dementia with an earlier onset. However, in terms of treatment, he adopted a position more in line with modern medical thinking. He tended to ignore the distinction by treating them as one disorder.
Until the late 1960s, arteriosclerosis (hardening of the arteries) was viewed as the major cause of senile dementia. This view changed when researchers established that large amounts of fatty deposits could be found in the brain’s arterial walls of both demented and normal elderly individuals. Furthermore, approximately half of the brains of persons suffering from dementia showed no signs of significant arteriosclerosis. So, while some cases of dementia could be attributed to vascular disease, it was not viewed as a major factor.
Research also clarified the nature of the brain lesions in both presenile and senile dementia. The brain pathology was identical. Apparently, the age distinction of sixty-five years was not relevant in making a diagnosis. Medical terminology was modified to reflect this recognition. The two groups were combined and called dementia of the Alzheimer type (DAT).
With further research, this nomenclature could change again. While medical science tends to focus on diseases as specific conditions (with specific causes and specific cures), there is a growing recognition of the complexity of major illnesses such as Alzheimer’s dementia. In other words, this dementia may consist of a group of related diseases with different causes and course of illness which result in the characteristic destruction of brain tissue associated with Alzheimer’s dementia.
The possibility that a variety of factors may be involved in Alzheimer’s dementia is apparent from the list of suspected causes. We will briefly consider the most prominent of these suspects.
Some Possible Causes of Alzheimer’s Dementia
While the cause of Alzheimer’s dementia is unknown, there are several theories which have attracted considerable attention. Researchers have proposed that it may result from viral infections which attack brain cells and cause slow deterioration of nerve tissue. Parallels have been drawn to two similar diseases of the brain (kuru and Creutzfeldt-Jakob disease) which are known to result from viral infection. Scientists at the National Institute of Health have explored the possibility of a viral link in Alzheimer’s dementia by taking brain cells from deceased victims and placing the diseased cells in laboratory dishes containing normal cells. In certain cases, the diseased tissues appeared to cause the normal cells to die.
In related experiments, diseased cells were injected into the brains of chimpanzees. Two of the six experimental animals developed a progressive neurological disease.
Unfortunately, further research failed to support the results of either of these types of experiment. As we shall see, this pattern of apparent initial breakthrough followed by failure of experimental confirmation is common in research of this disorder.
For example, it is widely accepted that aluminum toxicity can produce brain degeneration similar to the lesions of Alzheimer’s dementia. Findings on experimental animals have shown that injections of aluminum compounds produce neurological tangles in the brain similar to those found in Alzheimer’s dementia. Early in the 1970s, researchers at the University of Toronto explored a possible connection between aluminum and Alzheimer’s dementia. Their findings were dramatic. Autopsies of brains from patients who had been diagnosed as Alzheimer’s dementia contained as much as 30 times more aluminum than normal brains.
However, subsequent research has clouded these findings. Investigators at the University of Kentucky failed to find significant amounts of aluminum in the brains of Alzheimer’s patients even though these individuals had spent a life time drinking local water containing high levels of aluminum.
So we are left with the question of whether aluminum toxicity might be a cause of Alzheimer’s dementia. This is a particularly fascinating aspect of the Alzheimer’s puzzle since the Edgar Cayce readings were cautioning against the use of aluminum cooking utensils decades before researchers became aware of its potential link with a major brain disease.
Currently, scientists are focusing a great deal of attention on the genetic aspects of Alzheimer’s dementia. Research indicates that children of parents with the disease have a 50% chance of developing the illness. Furthermore, these individuals are more likely to exhibit the symptoms much earlier with a more rapid progression in the degenerative process.
The genetic link is further emphasized by studies connecting Alzheimer’s dementia with Down’s syndrome. Down’s syndrome is a developmental disorder in which a child is born mentally retarded. It is caused by a flaw in the genetic material of the afflicted person. These individuals have an extra copy of chromosome 21.
Persons with Down’s syndrome who survive beyond the age of forty typically suffer brain degeneration similar to Alzheimer’s dementia. Furthermore, the frequency of Down’s syndrome is 10 times higher among families of persons who experience early onset Alzheimer’s dementia.
As persuasive as the genetic studies are, we should be cautious in interpreting their meaning. Genetics is not likely to hold all the answers to the Alzheimer’s puzzle. For example, even with identical twins, one twin may develop the disease while the other does not. Obviously, there are additional factors at work here. Perhaps certain genetic factors can make an individual vulnerable to developing Alzheimer’s dementia while other factors (such as environment or lifestyle) can increase a person’s vulnerability. We will address this possibility in a later chapter which focuses on preventing dementia.
Direct brain insult is another possible cause of Alzheimer’s dementia. It is known that persons whose brains have been seriously jarred or who have experienced repeated blows to the head may develop the symptoms of Alzheimer’s. For example, prize fighters who have received numerous punches to the head over a period of years may develop “boxer’s dementia,” an irreversible dementia with symptoms and brain degeneration very similar to Alzheimer’s.
Glandular abnormalities have been linked to Alzheimer’s dementia. Researchers at Duke University have found a significantly higher frequency of prior thyroid disease in women patients suffering from Alzheimer’s than in control subjects. Furthermore, studies at the University of Minnesota suggest that the immune system may play a part in Alzheimer’s dementia.
These findings result from statistical analysis of biographical data collected from patients and control subjects. Correlating life history patterns with specific biological pathology has been more difficult. One of the most promising models links certain forms of Alzheimer’s dementia with disorders comprising the “thyroid-gastric-adrenal-thymic autoimmune syndrome.” It is likely that future research will uncover more extensive connections between glandular dysfunction and Alzheimer’s dementia.
We have looked at only a few of the most prominent theories explaining the causes of Alzheimer’s dementia. New hypotheses and variations on the older theories are being proposed continually. The bottom line at this point in time is that we really do not know what causes Alzheimer’s dementia.
Symptoms of Alzheimer’s Dementia
Like many of the other dementias, Alzheimer’s disease results in the progressive loss of “higher” functions, such as thinking, reasoning and memory. It destroys the distinctive qualities of mentality which make us human.
The deterioration is usually gradual, beginning with mild symptoms (such as forgetfulness of minor things like phone numbers or dental appointments). This decline is often accompanied by difficulty in learning new information. As the nervous system becomes more incapacitated, patients may have difficulty controlling their bodies or moving smoothly. Emotional problems commonly develop. The degeneration in functioning may produce deep depression, crying spells or temper tantrums.
The Course of the Disease
While the course of Alzheimer’s dementia may vary in individual cases, the ultimate prognosis is the same – incurable, with progressive decline in functioning at all levels. Premature death can be expected, either directly, as the result of the organic deterioration, or by related syndromes which are caused or exacerbated by the dementia.
Treatment of Alzheimer’s Dementia
Whereas some of the other dementias are treatable (and even curable if the cause is detected and amenable to therapy), the therapeutic options available for Alzheimer’s dementia are mainly limited to adaptive measures. That is, when faced with an incurable progressive illness, the usual strategy is to minimize the effects on patient and family. Rather than directly treating the illness, therapy involves adapting to it.
These adaptive measures range from behavioral interventions (which organize and simplify daily activities) to general physical interventions (such as basic health maintenance). For example, basic health maintenance might involve bowel regulation. Constipation is often a problem for persons suffering from Alzheimer’s dementia. Dietary changes, drinking adequate water and the use of laxatives can help to address this problem.
Individual counseling and support groups for caregivers are two additional forms of therapy which can facilitate the process of adaptation. For many families, institutional care (such as nursing homes) represents the final stage of adaptation.
Research has yielded some promising medicinal therapies over the years. Unfortunately, these drugs have not produced consistent results under the rigors of scientific standards of confirmation. Consequently, the therapeutic effectiveness of drug therapy for Alzheimer’s dementia is controversial.
Antidepressant medications are commonly prescribed for persons with Alzheimer’s dementia since depression is one of the most frequent and debilitating symptoms associated with the disease. Again, however, these drugs do not directly treat the dementia, they are only adaptive measures intended to provide limited symptomatic relief.
Edgar Cayce’s Perspective of Dementia
Edgar Cayce gave many readings for persons suffering from dementia. The readings are in close agreement with modern medicine on the physical pathology of the dementias.
Repeatedly, Edgar Cayce provided graphic descriptions of the nervous system deterioration indicative of these disorders. One almost gets the sense that Cayce used his consciousness as a modern researcher might use a high-tech probe or brain scan. Often, Cayce’s perspective was from the inside of the body, moving freely among the organs and tissue. His portrayal of the delicate interactions within and between the nervous systems is particularly fascinating. Without going into the technical aspects of anatomy and physiology, the important point is that Edgar Cayce anticipated the results of modern brain research which regards dementia as a progressive degeneration of nerve tissue in the brain.
However, Edgar Cayce’s perspective goes beyond brain pathology. The Cayce readings discuss how the brain is dependent upon the rest of the body for its moment to moment existence. Without the continual removal of metabolic waste and the supplying of nutrients, nerve cells in the brain will die in only a few minutes. Cayce explained that the various organs of assimilation and elimination are important in the cause and treatment of dementias such as Alzheimer’s dementia. Cayce also emphasized the importance of “drainages” and nervous system coordination.
Edgar Cayce also recommended the use of electrotherapy to stimulate nerve regeneration. The use of psychological techniques such as hypnotherapy was suggested. Finally, the spiritual aspects of treatment were also strongly emphasized.
To summarize, Edgar Cayce provided numerous readings describing the pathological process and giving recommendations for the treatment of dementia. In general, his approach was to assist the body in cleansing and nurturing the nerve tissue in the brain by a variety of physical, mental and spiritual therapies. In fact, Edgar Cayce even provided a “formula” for rebuilding the brain in cases of dementia.
Cayce’s Formula for Rebuilding the Brain
In reading 1800-16, Edgar Cayce laid out the basics of a treatment approach for dementia.
The key elements are:
- Electrotherapy with gold and silver “vibratory” solutions.
- Spinal manipulations to improve nervous system coordination and eliminations.
- Suggestive therapeutics (a form of natural hypnosis).
- Patience (a key spiritual attribute).
- Other activities in the system, including improved assimilations, circulation and eliminations.
Edgar Cayce’s approach to Alzheimer’s disease and dementia is described in a book titled Alzheimer’s Disease and the Dementias: An Alternative Approach Based on the Readings of Edgar Cayce written by David McMillin. Cayce’s approach to nervous system regeneration is discussed in detail in Principles and Techniques of Nerve Regeneration. Both books are available from A.R.E. Press.
- Check, William, A. Alzheimer’s Disease. New York: Chelsea House Publishers, 1989.
- Selkoe, Dennis J. Amyloid Protein and Alzheimer’s Disease, Scientific American (November, 1991).
Note: As this information is not intended for self-diagnosis or self-treatment, your use of this database of information indicates that you are aware of our recommendation that you consult with a professional healthcare provider before taking any action.