The Acid Alkaline Balance Diet by Felicia Kliment

Author:Felicia Kliment
Language: eng
Format: epub
Publisher: McGraw-Hill Education
Published: 2010-04-10T04:00:00+00:00

Alzheimer’s Disease

Before Rebecca developed Alzheimer’s she suffered from atherosclerosis. She said that the hardening of her arteries started when she was a child. At the age of four she had severe pains in her feet; in her teens the pain had crept up into her legs. Then in her early forties she developed chest pains. At the age of seventy, she was showing symptoms of Alzheimer’s. I believe the same condition that caused the hardening of Rebecca’s arteries when she was a child also hardened the protein strands in her brain in older age.

Modern science views Alzheimer’s and cardiovascular disease as two different pathologies presumably because calcified plaques that trigger the development of blood clots adhere to the arteries whereas the beta-amyloid plaques that characterize Alzheimer’s float in the watery lymphlike fluid surrounding the neurons in the brain.

However, before the onset of Alzheimer’s, the protein strands inside the neurons that extend beyond the neurons’ cellular membranes perform the same function for the brain as arteries do for the rest of the body: they transport materials to and from their destination. Furthermore, the protein strands in the brain harden (and are deposited in amyloid plaques) just as arteries harden. It makes sense that both the arteries in the circulatory system and the protein strands that grow through the brain’s neurons are exposed to acidic wastes—the protein strands from the acidic by-products of the metabolic processes that go on inside the brain, and the arteries from the acidic waste by-products the blood picks up from the various organ systems in the body.

The efforts of mainstream medicine to eliminate amyloid plaque in the brains of Alzheimer’s patients, if successful, might very well interfere with normal brain function. The protease enzymes that cut the protein strands into segments so they can be deposited in amyloid plaques are programmed to get rid of old protein strands. Amyloid plaques may therefore act as waste deposit sites for protein strands that have outworn their usefulness. The fact that these plaques are held together by a protective structure of metals and a waxy, cholesterol-like substance reinforces this possibility and makes the prevention of amyloid plaques tantamount to interfering with the brain’s waste disposal system. The most convincing evidence against eliminating these plaques is that only those beta-amyloid plaques that have become inflamed destroy brain cells.

The important question then is how amyloid plaques become inflamed in the first place. Here is a likely scenario. The highly selective blood-brain barrier in the brain’s micro blood vessels develops leaks. These leaks exude harmful substances such as acid waste, which depletes oxygen. In the absence of oxygen amyloid plaques become inflamed. When brain cells come in contact with these inflamed plaques, they also become inflamed and die off. With the death of a critical number of brain cells, Alzheimer’s becomes symptomatic.

One plausible reason that acidic wastes inflame amyloid plaques is that a brain injury has disabled the respiratory machinery so that there isn’t enough energy to dispose of acidic waste debris in the brain.

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