PREVENT ALZHEIMER’S DISEASE

Just in the last century Alzheimer’s disease has become an epidemic. The multiple causes, stemming from the industrial revolution, are to be found in the vast changes in what we eat and drink and the huge number of new chemicals, many of them neurotoxic, which surround us. These two sentences summarize the thesis of NOHA speaker H. J. Roberts, MD, in his new book, Defense Against Alzheimer’s Disease: A Rational Blueprint for Prevention.*

"Alzheimer’s disease represents a type of response by the brain to injury resulting from altered nutrition and metabolism, multiple exogenous neurotoxins in food, water, air, and drugs, deficient oxygen (hypoxemia), and other forms of stress. . . ."

Alzheimer’s disease (AD) "now constitutes a medical, social, and economic scourge. This relentless and dehumanizing affliction destroys memory and personality, and ultimately causes or accelerates death." Other dementias had been described previously but lacked the specific bodily signs of Alzheimer’s disease, which is "a 20th Century phenomenon. . . . Specifically, Dr. Alois Alzheimer reported the single case of a 51-year-old German woman in 1907. The significance of this time and place relates directly to a question being universally asked by relatives and caregivers of AD patients: Why has our society been victimized by this disease?"

Two aspects of the [Alzheimer] report are noteworthy. First, the editors of [the German medical periodical] – astute physicians and scientists acknowledged as authorities in their fields – wrote the following preface: "The picture he presents is of a case so deviant even on clinical grounds alone that it does not fit into any of the known disease categories, and the anatomical findings diverge from all currently known disease processes" [italics in the original] . . . .

Second, the patient resided in Frankfurt/Main where she had been institutionalized. Because Germany was at the forefront of chemical innovation, both industrial and pharmacologic, its population doubtless became exposed to novel environmental neurotoxins. These have increased exponentially as contaminants in water, air, food, and drugs over subsequent decades – generally with little awareness or concern by the medical profession or regulatory agencies. Our society is now forced to confront one of the costs of such corporate-driven commercialism and uninhibited consumerism: an epidemic of Alzheimer’s disease.

Dr. Roberts carefully describes numerous clinical symptoms and the specific anatomical signs of AD. The latter include amyloid (starch-like) plaques, neurofibrillary tangles (NFTs), and cell death in particular areas on the brain. Some of these areas "constitute the major suppliers of neurotransmitters to higher cortical centers."

"Our society is now forced to confront one of the costs of such corporate-driven commercialism and uninhibited consumerism: an epidemic of Alzheimer’s disease."

The hard substance in the plaques is called "beta-amyloid" and is formed from a amyloid precursor protein. It exists in healthy cells and "has a normal function, presumably to protect neurons against bio-physiologic dangers (lack of glucose and oxygen), neurotoxic exposure, and physical injury – perhaps through preventing the accumulation of excessive calcium" [italics in the original]. However, when too much beta-amyloid accumulates, it:
 
  • Destabilizes calcium metabolism,
  • Is directly toxic to certain neurons, and
  • Increases the toxicity of various excitotoxins such as glutamate and calcium.
 
 

Thus, when not broken down, it exacerbates the symptoms of AD.

In Alzheimer’s disease both nerve growth factor (NGF) and the exceedingly important neurotransmitter acetylcholine become depleted. NGF stimulates the growth of projections through which our neurons can communicate, and it can promote the growth and survival of neurons that utilize acetylcholine. Adequate NGF, along with other factors, can protect areas of our brain where many neurons die in AD against damage caused by hypoglycemia (low blood sugar). Of course, NGF receptors in the brain must be present for NGF to fulfill its protective functions. However, Dr. Roberts points out an interesting relationship between diabetes and abnormal NGF metabolism: Cleavage products of the receptors for NGF are increased "in the urine of patients with diabetic neuropathy [the lack of feeling in peripheral nerves that often occurs in diabetics]. This soluble cleavage product of the NGF-receptor also is elevated in plasma and urine after nerve injury . . . and in patients with amyotrophic lateral sclerosis (ALS)." Unfortunately, the neurons that produce NGF-receptors are particularly vulnerable to injury. Thus, when its receptors are destroyed, the protective NGF becomes depleted.

. . . depletion of acetylcholine is a major factor in the development of AD. Adequate brain levels of both oxygen and glucose are essential for the normal synthesis and release of this neurotransmitter.

Hypoglycemia also disrupts the metabolism of the neurotransmitter acetylcholine. "A normal glucose concentration restrains the synthesis and release of acetylcholine. These processes become stimulated at low blood glucose levels (hypoglycemia). If excessive, convulsions can result."

Acetylcholine is exceedingly important for nerve transmission. Certain nutrients, including choline, plus a continuous supply of oxygen and glucose, which is the body sugar that supplies energy, are essential for the synthesis of acetylcholine. "In the absence of ingested choline, the choline used for synthesizing large amounts of acetylcholine probably comes from a reservoir . . . in nerve membranes, a process termed ‘autocannibalism.’" In full-blown Alzheimer’s disease there is massive depletion of the nerve fibers that liberate acetylcholine.

In setting forth his theory of the causation of Alzheimer’s disease, Dr. Roberts states:
 
  • Alzheimer’s disease represents a type of response by the brain to injury resulting from altered nutrition and metabolism, multiple exogenous neurotoxins in food, water, air, and drugs, deficient oxygen (hypoxemia), and other forms of stress. . . .
  • Such damage tends to be compounded over time by trauma, altered circulation to the brain, and immunologic reactions resulting from exposure to toxic chemicals. . . .
  • These adverse effects ultimately cumulate in a significant loss of nerve cells (neurons) within the highly integrated memory neurosystem that are unable to regenerate.
  • The same noxious influences contribute to degenerative changes (the shriveling and disappearance of cells in the absence of inflammation or an interruption of their blood supply) elsewhere in the nervous system. . . . The foregoing theory also is consistent with the evolving belief that cell-death pathways or apoptosis (from the Greek word meaning "a falling off") are inappropriately activated in AD and other neurodegenerative diseases.
 

We have already outlined Dr. Roberts’ description of the metabolic changes—the deleterious effects on the production of acetylcholine and nerve growth factor with the resulting neuron death and the formation of beta-amyloid plaques and NFTs from recurrent energy depletion, lack of oxygen, and overloads of toxins.

"In the absence of ingested choline, the choline used for synthesizing large amounts of acetylcholine probably comes from a reservoir . . . in nerve membranes, a process termed ‘autocannibalism.’"

Energy depletion can come from starvation—real, which is world-wide, and also by choice. Dr. Roberts deplores the habits of women, especially the young, who starve themselves for the sake of fashion. He describes the problems from the ubiquitous high sugar diet, which can result in insulin stimulation, a plunging blood sugar, and energy depletion in the brain.

As described above, depletion of acetylcholine is a major factor in the development of AD. Adequate brain levels of both oxygen and glucose are essential for the normal synthesis and release of this neurotransmitter. Dr. Roberts outlines many factors that can result in decreased oxygen to the brain, including smoking; prolonged sleep and narcolepsy (inappropriate sleep, which is also clinically associated with hypoglycemia); the postoperative state; heart and lung disorders; air travel; and high altitudes. Low levels of brain oxygen can favor Alzheimer plaque formation because amyloid protein precursor is stimulated by many kinds of biological injury, including inadequate oxygen. "Furthermore, the reduced pH (acidity) caused by oxygen lack may accelerate amyloid plaque formation, and prevent [its] breakdown."

Dr Roberts points out a great deal of evidence that AD develops very slowly—over periods of perhaps thirty years. We possess an abundance of neurons so the process of deterioration and cell death can proceed for a long time before actual behavioral changes and major memory deficits appear.

"The dramatic rise of this problem [the multiple chemical sensitivity syndrome] during recent decades coincides with the escalating epidemicity of AD."

His book is about prevention of AD—an urgent appeal to people to prevent the development of full-blown AD by avoiding, as much as possible, the neurotoxins in our environment, by minimizing actions that enhance susceptibility, and by avoiding the neurotoxins in our processed foods. He goes into great detail on all these subjects. His book is dedicated "in gratitude to [NOHA Honorary Member] Beatrice Trum Hunter for her invaluable insights in many areas of nutrition, health, and general culture." He quotes her on "what is happening to our entire food supply, namely a lowering of food quality, which results in nutritional shortchanging." He states:

The progressive depletion of soils is also relevant. Fruits and vegetables purchased in most markets tend to have reduced micronutrients. [NOHA speaker B. L. Smith, in a 1993 study] compared the amount in pears, apples, sweet corn, and potatoes grown in the conventional way and by "organic" gardening. Selenium, manganese, sodium, magnesium, strontium, potassium, and lithium were increased in the organically grown products. Conversely, the organic foods contained less aluminum, lead, mercury, and cadmium.

Dr. Roberts covers a vast number of changes that have resulted in additional neurotoxic exposures for us. He refers extensively to Environmental Toxins in Our Food by NOHA Professional Advisory Board member J. Gordon Millichap, MD, and to the work of the late Theron G. Randolph, MD, a founding member of our Professional Advisory Board. In writing about multiple chemical sensitivity, Dr. Roberts states:

Dr. Theron Randolph, a pioneer in this field, describes the severe effects of noxious environmental agents on susceptible individuals. They include headache (the most common symptom), hyperactivity, dizziness, anxiety attacks, severe depression, impaired thinking ("brain fag"), memory loss, flu-like symptoms, extreme fatigue, and gastrointestinal complaints (especially among children).

"Many persons have experienced severe confusion and memory loss after consuming products that contain aspartame, a low-calorie sweetener widely known as Nutrasweet® and Equal®."

The exposure of these persons even to trace amounts of chemicals in common foods or indoor air can induce or reproduce symptoms, especially the "sick building syndrome." The offending substances might be petrochemicals, MSG [monosodium glutamate], sulfites, formaldehyde, pesticide residues, paint fumes, deodorants, scented detergents, colored ink in magazines, artificial colors, sweeteners, preservatives, ripening procedures (e.g., ethylene gas), protective food waxes, plastic food wraps, other packaging materials, the phenolic resin found in some can linings, and butylated compounds used with rubber gaskets to seal food containers.

Carpeting and adhesives can emit toxic chemicals indoors. Furthermore, carpeting may act as a "sink" for pesticides, molds, and dust mites. As many as 120 chemicals have been identified in carpeting and the carpeting underlayments used for installation. Many are known to be toxic and carcinogenic – e.g., benzene, toluene, xylene, styrene, and solvent-based dyes. . . .

The dramatic rise of this problem [the multiple chemical sensitivity syndrome] during recent decades coincides with the escalating epidemicity of AD.

Using single-photon emission computed tomography (SPECT) scanning, Callender (1991) reported that 56 of 67 patients with well-defined chemical exposures evidenced decreased flow in the frontal and temporal lobes, and in the basal ganglia [areas deep in the brain, involved in motor coordination]. Similar results were found in several patients by PET scanning – i.e., reduced brain glucose metabolism involving the hippocampus, amygdala, [these first two are part of the limbic system, which is common to all mammals and controls our involuntary functions], putamen [important for movement], and thalamus [a relay center for sensory impulses to the cerebral cortex]. Comparable findings exist in "early" AD [italics in the original].

Dr. Roberts, who spoke to NOHA on aspartame in October 1992, has had a great deal of clinical experience with aspartame-consuming patients and has written extensively on the neurotoxicity of this ubiquitous sweetener. In this volume he states in italics:

Many persons have experienced severe confusion and memory loss after consuming products that contain aspartame, a low-calorie sweetener widely known as Nutrasweet® and Equal®. These reactors offer a unique "experiment in Nature" that has extraordinary relevance to AD for two reasons. First, such reactions may constitute a reversible human model for studying "early" Alzheimer’s disease. Second, this association provides fertile clues for preventing AD.

Finally, Dr. Roberts describes the role of stress and points out how the stressed condition can affect our neurotransmitters. He gives much excellent advice for reducing everyday stress.

His book is about prevention of AD – an urgent appeal to people to prevent the development of full-blown AD by avoiding, as much as possible, the neurotoxins in our environment, by minimizing actions that enhance susceptibility, and by avoiding the neurotoxins in our processed foods.

Since all the deleterious effects take place over many years, Dr. Roberts is eager for us to learn the details, which he has set forth. Thus, we can follow much of his advice and can hope to prevent Alzheimer’s disease in ourselves. In describing his urgent need for publication, he states:
 
  • AD is escalating at an alarming rate not only in the aged, but also among maturing "baby boomers." More than four million people in the United States already have this disease. . . .
  • It is unlikely that any "magic bullet" can "cure" AD in the wake of sufficient nerve cell death to have caused dementia.
  • Primary emphasis upon prevention for the population at risk must be based on reasonable attempts to avoid or correct neurotoxic influences before advanced neurological deterioration has occurred.
 
 

________________________

*Sunshine Sentinel Press, Inc., P.O. Box 8697, West Palm Beach, Florida 33407, 1995, 236 pages, hard cover, $27.95.

Article from NOHA NEWS, Vol. XXI, No. 1, Winter 1996, pages 5-7.