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 (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?"
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."
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:
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.
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:
We have already outlined Dr. Roberts’ description of the metabolic changesthe 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.
Energy depletion can come from starvationreal, 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 slowlyover 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.
His book is about prevention of ADan 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:
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. 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:
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.
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:
*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.