Majid Ali is a
pioneer who is changing the face of medicine with his
innovative and spirited approach.
His credentials are
impeccable
Complementary Medicine Journal
"I stand in awe of Ali's
superb scientific knowledge, his insights into the nature of
the the healing process and his ability to explain hard
science."
Aubrey Worrell, MD
Past President, the American Academy of
Environmental Medicine
Majid Ali,
M.D.
Editor,
The Journal of Integrative Medicine
Formerly, Associate Professor of Pathology (adj.), College
of Physicians and Surgeons of Columbia University, NY
Formerly, President of Staff and
Chief Pathologist, Holy Name Hospital, Teaneck, NJ
Fellow, Royal College of Surgeons of England
- Diplomate,
American Board of Anatomic and Clinical Pathology
Diplomate, American Boards of Environmental Medicine
Past President Capital University of Integrative
Medicine
Oral Chelation Aging
Healthfully
proudly offers the
Oral EDTA Chelation Protocol
developed and used
by
Majid Ali, M.D.
in his practice for
over twenty
years.
The More-Plaques-Fewer-Deaths
Paradox
First of five-segment Series
Should You Say No to
Non-emergency Coronary Bypass Operation?
Majid Ali, M.D.
More arterial plaques are associated with fewer deaths from
heart attacks and strokes. No, you did not misread the
sentence. I write precisely what I mean: people with less
intense plaque formation have higher mortality from
cardiovascular diseases. I anticipate harsh frowns from
doctors on the title of this tutorial. The idea that plaques
in arteries cause heart attacks and strokes is deeply etched
in doctors’ belief systems, and through them in the
consciousness of the general public. The very notion that
more plaques are associated with fewer heart attacks and
strokes is likely to be considered preposterous.
Strong Claims Require Strong Evidence
Neglect of the scientific facts of arterial plaques leads to
more disastrous treatment errors than any other neglect
except that of insulin toxicity that sets the stage for
obesity and diabetes. This is a strong claims and requires
strong evidence. I devote this five-part series to do just
that. I present personal autopsy, microscopic, biochemical,
and clinical observations to expose the folly of both the
plaque theory and cholesterol theories of coronary heart
disease. I also cite the neglected published work of others
to further support my assertions.
In past publications, I presented extensive evidence for
debunking the "cholesterol theory" of coronary heart
disease. In this series, I marshal evidence to debunk the
"plaque theory"—the notion that plaques cause heart
attacks—to offer readers a liberating and scientifically
sound challenge to the dictums of the bypass-stent industry
for cardiac conditions that do not threaten life in crisis
setting.
The More-plaques-fewer-deaths Paradox
I introduce the term "more-plaques-fewer-deaths paradox" to
highlight six essential points.
First, in general fewer coronary heart and stroke deaths are
associated with greater degrees of arterial plaques.
Surprise!
Second, we have choice: We can keep the inner "endo region"
of the arterial wall healthy and live longer, or we can
obsess on cholesterol deposits and plaques in the outer
region of the arterial wall and live less. Another surprise!
Third, countless lives are lost when non-drug oxygen
therapies to restore "endo health" are opposed and blocker
drugs (beta blockers, calcium channel bloclers, etc) are
used to suppress symptoms caused by injury to endo cells.
Fourth, coronary bypasses and stents do not remove arterial
plaques. Stents close up with high frequency and bypasses
less often.
Fifth, many people live long healthful lives after coronary
bypasses and stents but only when they address issues of
foods, environment, an dstress that keep the inner linings
of arteries non-sticky and negatively charged.
Sixth, drugs save lives in crisis situations but do not
reverse plaque formation to any meaningful degrees. By
contrast, the focus on the inner endo region, where the
circulating blood interfaces with the arterial wall,
prevents heart attacks, strokes, and deaths.
An Iron Pipe With Inner Aluminum Lining
Imagine an iron water pipe with a delicate inner aluminum
lining. The lining is so delicate that it is easily injured
and leaks water. The lining also has a magical capacity for
self-healing. It readily plugs its own micro-holes and
prevents further water leakage. However it cannot prevent
slow and steady corrosion of the outer strong part of the
pipe made of iron by water which leaks through it before it
self-plugs.
One part of the iron-aluminum pipe is burried in the soil.
With passing years, the corroded iron part of the wall
develops microscopic holes and some water leaking through
tears in the aluminum lining,escapes into the soil
surrounding the pipe. With time, the leaked water feeds mold
spores in the soil and other microbes to create moldy,
mulch-like suds around the pipe. A CAT scan of the pipe at
this time reveals a thickened pipe wall—muddy mulch suds
appear like plaques. However, the technology of CAT scanning
is not yet advanced to reveal self-healing tears in the
inner delicate aluminum lining. When the water flowing
through the pipe is checked, it is clear.
Evolution’s Intelligent Design for Arteries
The structure of arteries is one of Nature’s marvel. It is a
self-cleansing and self-healing structure. My grandfather
forgot to die on time. I do not know whether he lived for
101, 102, or more years. My grandmother lived a similarly
long life. They did not have any heart attacks or strokes.
The Japanese in Okinawa Islands live for 120 or more years
without heart attacks or strokes. That means Nature’s
intelligent design for arteries can prevent plaque formation
for hundred or more years, if only toxicities of foods,
environment, and thoughts can be avoided.
Anatomy of the Arterial Wall
The arterial wall has the following four layers:
1. Inner endothelial (endo for short) lining composed of a
single-celled layer
2. A thin layer of loose connective tissue beneath the endo
cells.
3. A strong and resilient muscle layer
4. A thin outermost layer of loose connective tissue
The inner endo layer is smooth and has a negative charge. It
forms the "inner region" and prevents the blood cells and
plasma from sticking to it. The outer region is where muscle
and surrounding tissue develop cholesterol crystals, calcium
deposits, and plaques. The endo region directly faces the
circulating blood while the outer region is removed from it.
The endo cells have strong healing ability since they are
directly supplied by oxygen and nutrients. By contrast, the
outer part damaged by scarring and plaques have limited
ability to heal and restore their normal structure.
The "action" in events that trigger heart attacks, strokes,
and kidney failure occurs in the endo region—the "endo-blood
interface" seems an appropriate designation—and is always
regulated and preserved by factors related to oxygen
homeostasis (balance). This simple fact is readily validated
by high-resolution phase-contrast microscopy. Regrettably,
it is completely neglected by doctors controlled by the
"heart disease industrial mega-complex." Please ask
yourself, when did I last see an "endo commercial" on TV?
Or, when did The New York Times publish a large "endo
article"? Or, The New Enron Journal of Medicine fight back
the "statin monsters" who want everyone to be on drugs like
Lipitor, Crestor, Zocor, Pravaco an dothers prescribed to
lower blood cholesterol level?
What Do Arterial Plaques Really Mean?
In cardiology literature, those who profit from the plaque
preoccupation seldom, if ever, duly recognize and consider
evidence against their model of the plaque-death
relationships. Below are some quotes from recent cardiology
journals that reveal the dimension of the problem that are
seldom, if ever, duly considered in the matters of
plaque-death relationships:
1. Atherosclerotic plaques that lead to acute coronary
syndromes often occur at sites of angiographically mild
coronary-artery stenosis. Lesion-related risk factors for
such events are poorly understood (N Engl J Med 2011;
364:226-235).
2. Currently, there are no available methods that can
reliably predict when or if an atheroma will rupture. (
Journal of Invasive Cardiology 2010;22: 406-411, September
2010).
3. The study by Stone et al. provides conclusive evidence
that current morphologic assessments of vulnerable coronary
plaque do not predict major adverse cardiovascular events
4. Study4 have confirmed that positive remodeling was a
predictor of future acute coronary events, independent of
plaque characteristics.
5. In response to the comments of Maseri and colleagues
(writers of a letter to the Editor) we agree that the
lesion-specific characteristics that we identified were
sensitive but not specific for future major adverse
cardiovascular events.
6. The 13 infarctions (areas of tissue death) that were
related to culprit lesions were caused by stent thrombosis.
Robust Endo Responses Explain the
More-Plaques-Fewer-Deaths Paradox
The leaking iron-aluminum pipe analogy explains the absence
of the cholesterol-coronary connection, but not the
more-plaques-fewer deaths paradox. For this, one must
understand diverse tissue healing responses under varying
conditions. Acute injury triggers rapid but short-durated
response. Chronic ongoing tissue insult, in contrast, evoke
persistent healing responses. Such differences are well
known to pathologists. Up to a point, the more repeated the
insult, the stronger the healing response. Plaque formation
in arteries occurs as a delayed consequence of repeated
injury to the endo cells, which would be expected to mount
stronger and longer lasting "endo-healing" responses. That,
indeed, occurs. For example, a compensatory enlargement of
human coronary arteries occurs in some cases of advanced
plaque formation.
True Significance of Arterial Plaques
Are plaques in the arteries of the heart, brain, and kidneys
of no significance? No. Plaques indicate the presence of
chronic vascular injury. The longer the duration of vascular
injury, the more wide spread the plaques. The crucial
clinical importance of more-plaques-fewer-deaths paradox is:
It fundamentally challenges the prevailing view of the cause
of heart attacks and strokes. It shifts the focus from
secondary changes in the outer arterial wall—plaques,
cholesterol crystals, and calcium deposits—to the crucial
primary events involving the inner endo cells. Heart attacks
are triggered when endo cells in the coronary arteries are
injured beyond their ability to repair themselves. Strokes
are caused when the same happens to endo cells lining brain
arteries. And so begins the kidney damage that often leads
to dialysis.
In my Oxygen Model of Coronary Artery Disease, micro-clots
and micro-plaques in the circulating blood form and endo
dysfunction develops due to local dysox conditions (deranged
oxygen signals and other aspects of dysfunctional oxygen
metabolism). Dysox sets the stage for excess acidity,
increased oxyradical activity, and thickening of bodily
fluids. Simply stated, heart attacks and strokes are the
problems of the "oxygen-endo (ox-en) axis"—the centerpiece
of the Oxygen Model.
This
information is provided only to provide
information, it is never, ever to be used as a
self help guideline. Always consult your own
health care provider for information or
questions on your health!
Throughout this website, statements are made
pertaining to the properties and/or functions of
nutritional supplements.
These statements about
nutritional supplements have not been
evaluated by the Food and Drug Administration
and are not intended
to diagnose, treat, cure or prevent any disease
