A Cure for Alzheimer's

While recently scanning the internet I came across a site which proclaims: “One of the best ways to prevent Alzheimer’s disease (AD) is with a cocktail. A specific cocktail, in fact.” It then describes a substance claimed to include “curcumin, an ingredient from green tea, and several vitamins and antioxidants,” suggesting “this specific cocktail was capable of improving mental function.”

It concludes with both an offer to sell bottles of this extract formulation and a request for donations, with the assurance “Now you can do something about your memory and help fund cutting-edge scientific research on AD prevention.”

Before you rush to buy a bottle of anything or make your donation to a questionable worthy cause, you’ll need to know a few facts about this frightening ailment. For most of the 20th Century, the diagnosis of Alzheimer’s disease, named for the German neuropathologist Alois Alzheimer who first described the condition in 1902, was relegated to individuals who displayed symptoms of senile dementia between the ages of 45 and 65.

The terminology changed in 1977 following a conference of professionals in the field, who concluded the symptoms observed were much the same independent of age. Thereafter the term Alzheimer’s disease became universally used.

Today the dominant Alzheimer’s organization is the National Institute of Neurological Disorders and Stroke (NINDS), a division of the National Institutes of Health (NIH), established and funded by the U.S. government. NIH is divided into two parts: the “Extramural” parts are responsible for the funding of biomedical research outside of NIH, while the “Intramural” parts conduct research. It works toward that mission by conducting research in its own laboratories, supporting the research of non-Federal scientists (in universities, medical schools, hospitals, and research institutions throughout the country and abroad), helping in the training of research investigators, and fostering communication of medical and health sciences information.

NINDS also funds clinical research related to diseases and disorders of the brain and nervous system. By necessity, NIH and NINDS are closely allied with the medical industry, and particularly the psychiatric community. As you can understand, with massive sums of money regularly distributed, intense political pressures and lobbying are at work in every aspect of operation.

This gets us to the subject at hand: Alzheimer’s disease. Reports on the research, studies, and tests conducted on this malady are virtually limitless. However, the results of these reports can be concisely summarized:

1) Although the course of the disease is unique for each individual, there are many common symptoms.

2) The early stages of the condition are difficult to diagnose.

3) Numerous competing hypotheses exist trying to explain the cause of the disease.

4) Experimental vaccines have been tried, but none with any significant effect.

5) To date, the safety and efficacy of countless pharmaceutical treatments have been investigated. None have shown particularly favorable results.

6) At present, there’s no definitive evidence to support that any particular measure is effective in preventing the ailment.

7) There’s no cure for Alzheimer’s disease; available treatments offer relatively small symptomatic benefit but remain palliative in nature.

8) The cause and progression of the ailment are not well understood. Currently used treatments arguably offer a small symptomatic benefit; no treatments to delay or halt its progression are yet available … with but one almost unnoticed sentence in a NINDS report: “Physical activity is associated with a reduced risk of AD.” Please take note: A comprehensive analysis of this sentence will follow, but first I must broach a somewhat unrelated subject.

There’s a well-known medical impairment known as cerebral hypoxia; it refers to a reduced supply of oxygen to the brain. Its effect on the body is impairment of brain function. One common cause is stroke, categorized by the severity and location of the brain’s oxygen deprivation, the most serious and often fatal being total oxygen deprivation known as cerebral anoxia.

Other abnormalities can also cause cerebral hypoxia or anoxia: severe asthma, various sorts of anemia, ascent from a deep water dive, flying at high altitudes in an un-pressurized cabin, and various traumatic events such as choking, drowning, strangulation, drug overdoses and shock. Brain damage can occur both during and after oxygen deprivation.

During deprivation, cells die due to an increasing acidity in the brain tissue, and these cells are very sensitive to reduced oxygen levels. Once deprived of oxygen they will begin to die off within five minutes.

The physiological effects of oxygen deprivation are also well documented. When localized to a specific part of the brain, brain damage will be localized to that region. Damage to the left side typically causes problems with speech and language. Damage to the right side may interfere with the ability to express emotions or interpret what one sees.

The final observation on this subject of oxygen deprivation comes from an Internet blog I stumbled upon: My Crohn’s and Colitis Blog. It included this inquiry by J. Burgess: “Can anyone tell me what the effects of long-term oxygen deprivation are, as in mild chronic untreated allergic asthma?”

The response from another participant said: “Dear J. Burgess, I can’t claim to be an expert on this, but my fiancée was a chronic and unstable asthmatic for many years. The effects I recognize as being directly linked to oxygen deficiency were: 1. Clubbing of fingers and toes 2. Confusion and mental ‘fog’ 3. Poor circulation, particularly to the extremities”

With the preceding information, documentary evidence, and a lone testimonial as my input, I’m now prepared to offer a theory as to one possible cause of Alzheimer’s disease as well as pose a pair of hypothetical questions relating to its prevention.

First, the theory: It’s abundantly clear many of the symptoms commonly associated with dementia of all sorts can be related to oxygen deprivation. Let’s take a closer look at the normal aging process. As persons get older they become less physically active. Singles tennis played in the 20s is replaced by doubles in the 50s and finally by observing the grandchildren at play in the 70s.

The 4-mile run performed three times weekly by a fit 36-year-old is no longer possible when, at 53, the knee joint fails. The aches and pains which come in the later years dissuade many from taking that exhilarating five mile round-trip hike to the post office. It’s quicker and easier by auto.

Another factor changes as the years progress. With a reduction in physical activity is added a slowdown in metabolism, particularly the body’s failure to burn fats which otherwise end up lining the artery walls. As the deposits accumulate, the blood vessels narrow and the flow of blood – and with it oxygen it carries to all parts of the body – is reduced.

We must now ask a pointed question: What is one notable result of this more sedentary lifestyle? It is less blood flows through the arteries – and particularly through the two carotid arteries which supply oxygen to the brain. As physical activity lessens, supply of oxygen to the brain must similarly lessen. In an otherwise healthy senior, is this reduction sufficient to bring on the effects of dementia? Perhaps it is; perhaps it isn’t. But it’s time for the two hypothetical questions, designed to focus on a single aspect of Alzheimer’s disease: prevention.

1. If the flow of blood to the brain, and with it the oxygen it carries, can be sustained, through regular cardiovascular exercise, into a person’s senior years, might it result in an effective preventative to dementia?

2. Is it plausible, given a favorable answer to question 1, that a sufficient number of persons in their 50s, 60s, 70s, and beyond can be induced to regularly engage in activities necessary to effect a positive result?

I‘ll add, these questions are not hypothetical to me. Over the past fifty years I’ve regularly engaged in the sort of exercises which speed the heart rate. Although the running, tennis and bicycling I once engaged in pretty well ended years ago, I’ve maintained, now into my 80s, a daily schedule of an hour of continuous swimming and 30 minutes of weights. I don’t know whether this is one of the major reasons nothing seriously afflicts me. Perhaps I’m just lucky. And as for dementia, I didn’t need a ghostwriter to compose this article. I’ll leave it to you to decide whether Alzheimer’s has set in.

A rhetorical question is now in order. Why did NIH and its NINDS division never pose the questions I just asked? Is it because my theory is so outlandish as to be rejected out of hand? Though it may sound conspiratorial, I can think of another reason. For the many organizations which work closely with NINDS, there are fortunes to be garnered in studies conducted, research reports, testing and retesting, drug experimentation, and all the allied activity to be lobbied through Congress. On the other hand, there isn’t much profit to be reaped by encouraging oldsters to vigorously walk four miles at a clip or visit the local YMCA for a daily swim. Perhaps for these governmental agencies it’s simply business as usual.

Al Jacobs, a professional investor for nearly a half-century, issues a monthly newsletter in which he shares his financial knowledge and experience. You may view it on http://www.roadwaytoprosperity.com

al@beachcomber.news