|
 Chapter
1
The False Promise
Today is the first day of the new year. My wife,
Talat, and I returned from Greece yesterday afternoon and stayed up late last night
watching CNN cover the New Year celebrations from New Zealand to New York. Oh, what a
global party! What a view of the good life! Humankind wore a face I had never seen before.
The excitement was immense and infectious—both for the stunning achievements of the
past as well as for the predictions for the future that stretched credibility. What a
feeling to be human on a day like that!
As I write this chapter, I hear two celebrated futurists on
CNN share their great visions of the future. One of them holds an adopted Chinese baby in
her arms and her face glows with joy. "She will live to be 115. All her needs will be
met," she beams, then goes on to salute medical science and the projected miracles of
gene therapy. The second futurist chimes in, "She will retire at age 29." Next,
he goes on to wonder wistfully what else she might want to do with her life. It is easy to
over
look the enthusiasm of the CNN futurists. They are not
biologists. I recalled the words of a physicist-friend, "Medicine advances by trial
and error. So far, gene therapies have only killed people. But I see a brilliant future.
Don't you?" he asked. I shrugged but did not explain why I do not share his
enthusiasm about gene therapy extending human life span to 115.
OF LIVING MARBLE AND DYING FROGS
The day before yesterday in Athens,
Talat and I stood before the massive gleaming marble columns of the Parthenon, mesmerized
by the temple's majesty. The remaining columns of Athena's temple are as alive today as
when built over 2,500 years ago by the Greek goddess' cult. Some days earlier, in Istanbul
I had read a short piece about red-legged frogs that have not been seen in Calveras
County, California, for several decades. It had struck me odd then that Turkish Daily
News was curious about why Mark Twain's frogs had disappeared without leaving any
clues to their demise. My thoughts drifted from how much the ancients knew about the life
span of marble to how little we know about the life span of frogs.
Of course, we humans are not the only
victims of dysfunctional oxygen metabolism. We can learn much about oxygen metabolism by
examining how excessive oxidation and dysfunctional oxygen metabolism cause disease and
death in the animal kingdom. To underscore that point and to further illustrate my theme,
I also explore disturbances in oxygen dynamics in the large bodies of waters and
consequences of oxidosis suffered by many forms of life in fresh waters as well as in
coastal waters, bays, and open seas. Below, I include some text from one of my articles
published in The Journal of Integrative Medicine1 to show that we can learn much
about dysfunctional oxygen metabolism from disappearing frogs, shrimp, oysters, and other
living beings.
What do alpine meadows of Yosemite National
Park, piney woods of South Carolina, and plains of Laramie, Wyoming, have in common?
Answer: The warm summers there are unusually hushed. The reason for this is that the frog
population in those areas—and many others in the world—has been decimated. By
some estimates, up to a third of the nation's amphibians—frogs, toads, and
salamanders —have disappeared. In 1988, in Costa Rica on a Monteverde ridge, half of
the 40 amphibian species simply vanished. Some wags have speculated that those amphibians
were stolen by aliens—a global whodunit!
In Chesapeake Bay, during some summers,
nearly all Eastern oysters are parasitized by dermo. Up to one-half of the total
population succumbs. Similarly, grass shrimp suffer from heavy parasitic
infestation. In Alaska, ten years after one of the largest oil spills in history, the
Valdez accident, species which have failed to recover include the common loon, cormorant,
harbor seal, harlequin duck, and pigeon guillemot.
Marine biologists report "mass
mortalities" among plants and aquatic life forms. Consider the following quote from a
recent issue of Science2:
In the past few decades, there has been a
worldwide increase in reports of diseases affecting marine organisms. In the Caribbean,
mass mortalities among plants, invertebrates, and vertebrates have resulted in dramatic
shifts in community structure. Recent outbreaks of coralline algae lethal orange disease
have affected Indo-Pacific communities on unprecedented scale.
The CNN futurists did not seem to know any
of that. None of them so far this morning have broached the subject of dying frogs and
vanishing marine life forms. Who wants to be a skunk in a garden party?
Did the CNN futurist who predicted a
115-year life span for her adopted daughter ever bother to study human genetics?
Did the second futurist who foretold her retirement at age 29 ever bother to talk to
millions of children all over the world whose lives have been severely diminished by
chronic fatigue syndrome,
fibromyalgia, and chemical sensitivity syndrome? I have seen
hundreds of young people who were disabled by age 29, not retired by that age!
Their active lives are truncated by excessive oxidation—a process of loss of
energy through loss of electrons.
FROM GENOMICS TO PROTEOMICS
Gene researchers have spent billions of
dollars of tax money and are coming close to mapping out the full human genome (gene
structure). They have little, if anything, to show for all that money. Gene therapies
simply have not helped the sick to date. Their claims to the contrary are superficial,
deceptive, or both. Now they are changing the party line. Now the buzz word is proteomics.
They want many more billions of dollars for mapping out all the proteins of cells. In its
December 16, 1999, issue, Nature ran two remarkable editorials. Both pieces are
very relevant to my subject of oxygen and aging. Consider the two headings and two direct
quotes from the texts:
Gene Therapy for the Public3
The case of Jesse Gelsinger, whose
death during a gene-therapy trial led to last week's hearing, reveals how poorly
understood are the body's responses to those vectors [viruses that carry genes] in
particular. But the uncertainties and violations revealed by the hearing should not halt
pursuit of the adenovirus approach.
The Promise of Proteomics4
Analyzing the entire set of proteins of
an organism is a far bigger challenge than anything in genomics...The inside of a cell is
a crowded and dynamic place, where proteins are perpetually being created and
discarded...Indeed, there is no such thing as proteomics—it will differ significantly
not only between individuals (much more than do their genome), but also within one
individual before and after, say, a millennium party.
Later, it was reported that "hundreds
of gene-therapy deaths had gone unreported." A doctor on TV tried to defend such
deaths by claiming that the persons who had received such therapies had no options. Was
that really true? Had any of those patients been given vigorous oxygenative and nutrient
therapies before deciding that there were no other options? My problem here is not that
geneticists are twisting our arms for hundreds of billions of additional dollars of our
tax money. My frustration is that they do not allow integrative physicians to apply for
minimal grants of several thousand dollars to study the oxygen order of human life and how
inexpensive oxygenative therapies outlined in this book can help hundreds of millions of
people with chronic disorders. In their ignorance, they dismiss all such research as
"unscientific."
A PREDICTION:
Gene Therapies Will Not Increase the
Human Life span
It is generally believed that the
structure of human DNA ( genome) will be completely mapped out by 2002, and that such
knowledge will open the way for genetic repair of damaged brain cells, weakened heart
muscle, injured liver tissue, and bad backs. I hear of gene cures for cancer. Indeed, I
often hear some geneticists exult that soon they will begin to toss out nonfunctioning
body parts and insert genetically engineered new ones, just as car mechanics do now. I am
much amused by such predictions. Nature did not build the human frame quite the same way
carmakers makers build their machines.
I do agree that genes set the limits on the
life span for an individual. But I strongly disagree with those who think gene therapies
will soon let everyone live to the ripe old age of 115 years or more. I will make a clear
prediction here: Gene therapies for extending human life span, whenever such therapies
become available, will contribute to longevity and healthful aging only if oxygen
metabolism can be maintained within the healthy range. As long as we continue to violate
the oxygen metabolism of our children and young, no gene therapies will be able to correct
their dysfunctional oxygen metabolism.
In the context of the
dysoxygenosis theory
of aging, there are two essential points:
1. Within the limits set by genes, the
lifespan of an individual is governed by oxygen metabolism.
2. Genes function well only when oxygen
metabolism is normal.
MUTANT MICE AND LIFE SPAN GENES
This is a time of great expectations in
the world of genetics. Every week in my copies of Nature and Science, I read
about fascinating discoveries of new genes and new behaviors of old genes. A paper by
Italian researchers in the November 18, 1999, issue of Nature5 reported that mutant
mice live longer than mice in the wild. A longer life in mutant worms,
yeast, and fruit
flies was reported earlier. What distinguished the Italian report is that it was the very
first time that life extension by a gene (p66shc) modification was demonstrated in a
mammal, hitting close to home for us humans. Heady times for geneticists!
Are there other things we should know about
gene research? Did the yeast, worm, and fruit fly pay a price for their longer lives? Of
course, they did, in smaller size and loss of fertility. Did the mutant Italian mice pay a
price? Of course, they did, in abnormal lung tissue. Would such mice have reduced
fertility? Most likely, yes. Are there likely to be many more long-term adverse effects?
Almost certainly, in my opinion. There are yet other problems.
GENES THAT DO NOT FOLLOW OUR SCRIPTS
Gene enthusiasts seldom, if ever, temper
their wild claims with the issues of genes affecting the structure and function of other
genes. When I hear talk of production of genes to "mass cure" human diseases, my
mind often drifts to the subject of 'gene silencers.' An interesting experiment was
reported about ten years ago. Some geneticists came up with the idea of improving the
color of flowers by inserting additional copies of pigment genes to petunias. The results
startled them: Rather than showing the expected darker purple color, the flowers showed
complete bleaching of the color in the form of white stripes.6 My purpose in citing the
preceding study is not to propose that gene therapy will not be valuable in any
situations. Rather, it is to point out the possibility of the same happening to people
receiving gene therapies. What genes will be silenced in people? What will those silenced
genes do to them? What genes will take over when others are silenced? What will be the
consequences of such a happenstance? Time alone will provide the answers. For now, I see
the clear possibility of gene therapies playing out as antibiotics did: many short-term
important benefits and many, many more long-term serious problems. It also seems likely to
me that the problems created by silenced or silencing genes may be far worse than those of
overgrowth of dangerous microbes created by antibiotics.
Another subject of interest in this context
is that of " genome instability," in which genetic alterations are seen in
cancer cells far in excess of what would be expected from random mutations alone. It has
long been known that genes respond to environmental changes. The concept of genome
instability, however, puts that in a much more sinister perspective since it indicates a
dangerous instability of a growing part of the genome. For example, in the case of colon
cancer it is increasingly recognized that such gene instability is related more to
acquired genetic defects and less to inherited abnormalities. 7
Human genes simply do not work well except
when cellular oxygen metabolism is normal. This is my primary reason for believing
that progress in gene therapy will be achieved only after we have learned how to maintain
a healthful oxygen metabolism.
GENES AND DIABETES
Loser-Gainer Games and Diabetes- Cancer
Trade-Off
Another good example to illustrate my
reservation about the views of the gene therapy enthusiasts is the case of type II
diabetes.
Type II is a widespread and growing
problem in the United States, which puts an individual's lifespan in serious jeopardy. It
usually develops slowly in older persons with a family history of diabetes and who have
normal or high blood insulin levels. The reason that persons with type II diabetes have
high blood sugar levels even though they have normal or high blood insulin levels
is insulin resistance. In health, insulin is the primary hormone that facilitates entry of
glucose into cells and its utilization there. Insulin resistance develops when the insulin
receptors on the cell membranes fail to respond to insulin and blood sugar level rises.
The pancreas produces more insulin to overcome the resistant insulin receptors, but to no
avail. The blood sugar level continues to rise and type II diabetes is diagnosed.
Insulin resistance, in essence, is a
cell membrane dysfunction.
In 1987, I introduced the term oxidative
cell membrane dysfunction for a state in which oxidative injury to the cell membrane
results in leaky cell membrane.8 The result: What is outside the cell floods the cell
innards and what is inside the cell hemorrhages out. For example, calcium enters the cell
in excess through the leaky cell membrane and potassium leaks out. Other substances
present in excess in or outside the cell are also affected by the increased
"leakiness" (permeability) of the cells. All such changes put the cellular
function and structure in serious jeopardy. In later chapters of this book, I present
evidence for my view that all acquired cell membrane dysfunctions are
oxidative-dysoxygenative in nature.
Doctors prescribe various drugs to lower
the blood sugar level by increasing its entry and utilization in cells. However, none of
those drugs address the fundamental issue of what causes the cell membrane to malfunction
in genetically susceptible persons.
Enter gene therapy enthusiasts. Their
approach is conceptually simple and seems logical on the surface: Find the culprit gene
and replace it. That, of course, is easier said than done. I cite an example. One type of
cell membrane receptor that plays an important role in insulin activity is called PPARy.9,10
This receptor controls both the entry of glucose in cells and its metabolism there. Recent
research has identified three different groups of mutations involving that receptor in a
small number of type II diabetics: (1) a group of loss-of-function mutations; (2) a
group of gain-of-function mutations; and (3) a group of other mutations that are
associated with variable effects on insulin sensitivity. It can be safely predicted
that many more mutations in each of those and other categories will be found in the
future. In gene therapies, how will we assure that when we need a gainer gene, we
will not end up with a loser gene? How will we tell both groups from the variable
loss-gain genes? How will we know what genes will silence which genes to play havoc on the
person? To date mutations of only PPARy receptors have been identified in a small
number of type II diabetics. How many other receptors are there which affect insulin
activity? How many other groups of mutations involving those receptors lurk behind the
visible tip of the iceberg? The enthusiasm about curing diabetes by replacing the faulty
genes must be tempered with the sobering thoughts concerning those questions.
WILL THERE BE A DIABETES-CANCER TRADE OFF?
The loser-gainer gene games in diabetes do not
end there. The PPARy receptors are also involved in production of substances for
immune cells and cells lining the blood vessels. Mutations in those functions are thought
to contribute to cancer and obesity. Will there be a diabetes- cancer trade-off? How will
we assure that while we try to cure diabetes with gene therapies, we do not cause cancer?
A different approach to the problem of
insulin-resistant cell membranes is to restore the cell membrane function by integrative
nutritional, herbal, and oxygenative therapies. It is a little known fact that many
experienced integrative physicians can successfully manage high-insulin diabetics without
prescribing drugs by focusing on all issues of cell membrane health. My colleagues and I
have several examples of such patients in our practices.
Again, the issue here is not whether we
continue to pour billions of dollars into gene therapy research. My point simply is this:
Genes therapies will not work unless oxygen metabolism is preserved in healthy subjects
and is restored in sick persons. And that restoration of oxygen metabolism calls for an
"ecologic-restorative" approach.
A MENAGERIE OF MYSTERY MALADIES
FOR THE MILLENNIUM
In matters of health, our legacy to the new
millennium is a growing menagerie of mysterious maladies. It includes chronic fatigue
syndrome, fibromyalgia, multiple che mical sensitivity syndrome,
Gulf War syndrome,
chronic Epstein-Barr syndrome, "candidiasis" syndrome, attention disorders,
learning disabilities, and others. According to The Wall Street Journal, fibromyalgia
alone disabled eight million Americans by 1999, and neurosurgeons were drilling parts of
the skull bones off to treat muscle pain caused by that condition.11 In some reports, up
to one-quarter of patients presenting to general clinics complained of chro nic fatigue.12
Over ten years ago, the Journal of the American Medical Association reported that up to
six percent of children in Baltimore County were prescribed drugs for attention and
hyperactivity disorders.13 I know of school systems in which up to nine percent of
children take Ritalin and related drugs. Holistic doctors diagnose candidiasis in most of
their patients. I return to this subject later.
The essential point I make concerning such
mystery maladies is that none of those conditions can be understood without understanding
dysfunctional oxygen metabolism (DOM). Beyond that, the readers will note that the
concept of DOM also answers many questions concerning such common diseases as coronary
heart disease, Alzheimer's disease, and rheumatoid arthritis. I refer the readers
interested in pursuing the subject of oxidosis further to the companion volume, RDA:
Rats, Drugs and Assumptions.
OXYOLOGY
Oxyology (oxy-olo-gy) is the study of
oxygen, just as gemology is the study of gems. I recently introduced this term in an
editorial published in The Journal of Integrative Medicine14 for the following two
reasons:
1. The study of oxygen deserves to be
considered as the core medical discipline; and
2. Oxygen therapies have been badly
neglected in clinical medicine.
Most doctors think of oxygen only when
someone is near death in an intensive care unit. This is most unfortunate, because oxygen is
what breathes life into all human cells at all times, in healthful aging and in
disease states.
Oxygen ushers life in. Oxygen terminates
life. As I amply demonstrate in this book, oxygen is the most important healing
substance, the most effective detox agent, the premium blood cleanser, the most potent
antibiotic, a versatile hormone, a blood clotter and declotter, and the conductor
of the orchestra of the immune system. Without oxygen, the lungs cannot breathe, the heart
cannot beat, the brain cannot think, the bowel cannot digest or absorb food, and the
muscles cannot move. That is all very basic and essential.
A cancer cell hates oxygen; an immune cell
loves it. That, in simple words, is the foundation of all oxygenative therapies my
colleagues at the Institute and I prescribe for patients with malignant tumors. Indeed, I
do not believe anyone can effectively manage any of the systemic metabolic issues
involved in cancer treatment without an unrelenting focus on issues of oxidosis and
dysoxygenosis.
Like cancer cells, primordial life forms
(PLFs) also hate oxygen. PLFs is my term for a very large group of microbial families that
include yeast-like microbes, nanobacteria, mycoplasma, the so-called stealth microbes, and
bowel anaerobes. That is the primary reason why my colleagues and I prescribe oxygenative
therapies for patients with acute and chronic infections, chro nic fatigue syndrome,
fibromyalgia, che mical sensitivity syndrome, multiple sclerosis, asthma, and many other
immune and degenerative disorders. Most doctors will raise their eyebrows when they read
this sentence, but that is because they have seldom, if ever, explored the enormous
potential of oxygenative therapies. At present, not many physicians seem interested in
oxygen metabolism in health and disease. I can confidently predict that will change in the
future as the basic facts of dysfunctional oxygen metabolism get widely recognized.
NEED FOR ECOLOGIC THINKING
For healthful aging, we need to think of
oxygen and oxidation within a larger ecological perspective. We must recognize and address
the fundamental and global threats to our oxygen supply and dysfunctional oxygen
metabolism. Or, we must prepare to watch helplessly while hundreds of millions of
chronically ill persons continue to suffer from "mystery" maladies, as our Star
Wars medical technology utterly fails to restore their health. Without an enlightened
ecologic thinking and a clear understanding of the oxygen order of human life, we are
doomed to wallow in ignorance as we encounter a growing menagerie of mystery maladies for
the millennium. From extensive experience I know that, by and large, those maladies are
reversible with broad-based, ecologic-restorative management plans. It is from the
lessons learned from such experience that we can formulate preventive plans to stem the
tide of those maladies and help people to age healthfully. That is the essential message
of this book.
References
1. Ali M. Fibromyalgia: an
oxidative-dysoxygenative disorder (ODD). J Integrative Medicine 1999;3:17-37.
2. Harvell CD, Kim K, Burkholder JM, et al.
Emerging marine diseases, climate links and anthropogenic factors. Science 1999;285:1505.
3. Editorial. Gene therapy for the public.
Nature 1999;402:703.
4. Editorial. The promise of proteomics.
Nature 1999;402:703.
5. Migliaccio E, Giogio M, Mele S, et al.
The p66 shc adapter protein controls oxidative stress response and life span in mammals.
Nature. 1999;402:309-13.
6. Candidate 'gene silencers' found. News
of the Week. Science 1999;286:886.
7. Offit K. Genetic prognostic markers for
colorectal carcinoma. N Eng J Med 2000;342:124-5.
8. Ali M. Leaky Cell Membrane Dysfunction.
Monograph. 1987. Teaneck, New Jersey.
9. Schwartz MW, Kahn SE. Insulin resistance
and obesity. Nature 1999;402:860-1.
10. PPARy (perioxisome
proliferator-activated receptor gamma) is both a receptor and a transcription factor. It
belongs to a family of nuclear-hormone receptors. When activated by ligands, such as
thiazolidinedione, it binds to specific DNA sequence in gene promoters. Next, complexed
with RXR (retinoid X receptor, another transcription factor), it activates the
transcription of specific genes.
11. Surgery on the skull for chronic
fatigue? Doctors are trying it. The Wall Street Journal, November 11, 1999. pp, A1 and A8.
12. Buchwald D, Sullivan JL, Karmaroff A.
Frequency of chronic active Epstein-barr virus infection in general medical practice. JAMA
1987;257:2303.
13 JAMA 1988;260:2256
14. Ali M. Oxyology: the need for a new
discipline in clinical medicine. J Integrative Medicine. 1999;3:1-2.
Order this book
at Amazon.com
Return to home page
|
