Atherosclerosis
Atherosclerosis is a disease of the
arteries characterized by the deposition of fatty material on their inner
walls. It is also known as arteriosclerotic vascular disease or ASVD.
Atherosclerosis is a specific form of arteriosclerosis in which an artery wall
thickens as a result of the accumulation of fatty materials such as cholesterol
and triglycerides.
Atherosclerosis is commonly referred
to as a hardening or furring of the arteries. It is caused by the formation of
multiple plaques within the arteries. It is a syndrome affecting
arterial blood vessels, a chronic inflammatory response in the walls of
arteries, caused largely by the accumulation of macrophages and white blood
cells promoted by low density lipoproteins (LDL, plasma proteins that carry
cholesterol and triglycerides) without adequate removal of fats and cholesterol
from the macrophages by functional high-density lipoproteins (HDL).
Sometime called the “Silent Killer”,
Atherosclerosis is a chronic disease that remains asymptomatic for decades.
Atherosclerotic lesions, or atherosclerotic plaques are separated into two
broad categories: Stable and unstable (also called vulnerable).
The pathophysiology of
atherosclerotic lesions is very complicated. The progression of atherosclerosis
is generally categorized as stable and unstable in which a development of
stable atherosclerotic plaques, which tend to be asymptomatic, are rich in
extracellular matrix and smooth muscle cells, while, unstable plaques are rich
in macrophages and foam cells and the extracellular matrix separating the
lesion from the arterial lumen (also known as the fibrous cap) is usually weak
and prone to rupture.
Early atherogenesis is characterized
by the adherence of blood circulating monocytes (a type of white blood cell) to
the vascular bed lining, the endothelium, followed by their migration to the
sub-endothelial space, and further activation into monocyte-derived
macrophages.
Is it hypercholesterolemia? The
pharmaceutical industry has billions of dollars per year at stake in revenue
from cholesterol as a precipitating factor in Atherosclerosis. “Normal”
Cholesterol concentration levels have changed in the last 30 years from 240, to
220, to 200 to 180 which has introduced millions more people as customers, but
has done little to slow the progression of Atherosclerosis.
Most current research demonstrates
that dietary changes to reduce internal toxicity and inflammation have the
greatest impact on the progression of Atherosclerosis.
Other
sources of inflammation:
Oxidative stress/Free Radical Damage
Pathogens
The primary documented driver of
this process is oxidized lipoprotein particles within the wall, beneath the
endothelial cells, though upper normal or elevated concentrations of blood
glucose also plays a major role and not all factors are fully understood. Fatty
streaks may appear and disappear.
During the Oxidation process, ROS molecules
are formed that include free radicals, such as: superoxide, hydroxyl radical
and NO. ROS are generated by internal
and external stresses including vasoactive factors such as angiotensin II and
endothelin. Cellular sources such as lipoxygenases and nicotanamide adenine
dinucleotide phosphate (NADPH) oxidase.
NADPH plays a role in the physiological
respiratory burst produced by phagocytic cells such as neutrophils and
macrophages that result in large amounts of ROS production.
The process of inflammation is
caused by a number of factors, including:
Vasoactive factors
Cellular sources
Mechanical forces from shear stress
from fluid movement
Stretching forces -Activates NADPH
oxidases and ROS production
Initial damage to the endothelium
results in an inflammatory response. Monocytes enter the artery wall from the
bloodstream, with platelets adhering to the area of insult. This may be
promoted by redox signaling induction of factors such as VCAM-1, which recruit
circulating monocytes, and M-CSF, which is selectively required for the
differentiation of monocytes to macrophages.
Red Blood Cells with spiked edges in
a classic “coke bottle cap” demonstrate free radical damage which circulate and
damage the endothelial lining of the arteries. The Body attempts to heal damage
on the inner walls of the arteries in a process similar to the coagulation
cascade.
The monocytes drawn to the damaged,
inflamed arterial walls will differentiate into macrophages, which ingest
oxidized LDL, slowly turning into large "foam cells" – so-called
because of their changed appearance resulting from the numerous internal
cytoplasmic vesicles and resulting high lipid content.
Under the microscope, the lesion now
appears as a fatty streak. Foam cells eventually die, and further propagate the
inflammatory process. There is also smooth muscle proliferation and migration
from the tunica media into the intima responding to cytokines secreted by
damaged endothelial cells. This causes the formation of a fibrous capsule
covering the fatty streak. Intact endothelium could prevent the proliferation
by releasing nitric oxide.
Calcification forms among vascular
smooth muscle cells. In time, as cells die, necrosis, this leads to a
progression of the inflammatory process where extracellular calcium deposits
between the muscular wall and outer portion of the atheromatous plaques. These
capped fatty deposits (now called 'atheromas') produce enzymes that cause the
artery to swell, “tumor”, enlarge over time.
As long as the artery enlarges
sufficiently to compensate for the extra thickness of the atheroma, then no
narrowing ("stenosis") of the opening ("lumen") occurs. The
condition remains silent until an atheroma ulcerates, which leads to immediate
blood clotting at the site of atheroma ulcer.
This triggers a cascade of events
that leads to clot enlargement. The result is the formation of a thrombus
(blood clot) overlying the atheroma, which obstructs blood flow acutely. With
the obstruction of blood flow, downstream tissues are starved of oxygen and
nutrients. If this is the myocardium (heart muscle), angina (cardiac chest
pain) or myocardial infarction (heart attack) develops. The clot may also move
to the lung or brain, or cause a blockage of the extremity.
Atherosclerosis treatment, in my
opinion will not improve as long as the focus is on lowering cholesterol. Why?
because lipoproteins are found in the cell membrane – the cholesterol is a
natural stabilizer. Cholesterol is
responding to the ROS damaged epithelium – NOT a cause of atherosclerosis.
EVALUATION/DETECTION
Examples of anatomical detection
methods include (1) coronary calcium scoring by CT, (2) carotid IMT (intimal
media thickness) measurement by ultrasound, and (3) intravascular ultrasound
(IVUS).
Examples of physiologic measurement
methods include (1) lipoprotein subclass analysis, (2) HbA1c, (3) hs-CRP, and
(4) homocysteine.
Current theory of evaluation
includes a standard blood lipid profile which includes values for total
cholesterol, LDL, HDL cholesterol, and total triglycerides. Several ratios,
such as LDL/HDL ratio and the total cholesterol/HDL ratio, are used as risk predictors.
The pharmacological industry has a vested interest in keeping these tests
inexpensive as it contributes to the adding of millions of customers for the
statins.
INTERVENTION:
Pharmacological intervention - statins have been the most popular and are widely
prescribed for treating hyperlipidemia promoted by the Pharma Industry for
atherosclerosis (side effects muscle weakness and pain, neuropathy). A better
approach would seem to be the development of some product to intervene in the
positive feedback loop of the runaway inflammatory cycle.
Natural or wholistic intervention:
Niacin (vitamin B3), in pharmacologic doses
Dietary Changes to include reduction of meats and eggs has
not been shown to be effective
Dietary supplements of Omega-3 oils
Vitamin C - acts as an antioxidant in vessels and
inhibits inflammatory process.
Oats
Iodine – Sea Kelp
PALEO DIET
Chelation - Chelation therapy using EDHT showed promise, but the FDA halted
this approach. In 1999, the ACAM agreed to stop presenting EDTA chelation
therapy as effective in treating atherosclerosis in progressive heart disease,
avoiding legal proceedings from the FDA under pressure from the pharmaceutical
giants.
Surgical intervention - angioplasty procedures that may include percutaneous
transluminal angioplasty using a balloon and stents to physically expand
narrowed arteries and major invasive surgery, such as bypass surgery, to create
additional blood supply connections for the more severely narrowed areas.
SUMMARY
Cardiovascular disease is the number
one killer in the US and in most industrialized nations of the world. We
already had a presentation of hyperlipidemia. The prevalent thought is that
high LDL, Triglycerides and Cholesterol are the predisposing factors that cause
atherosclerosis. My position is that inflammation is the causative agent that
initiates atherosclerosis. If you remove the huge monetary benefit of
cholesterol lowering medications and their influence on treatment option, I
believe we can get to the source of atherosclerosis and actually do something
significant to change the course of this devastating disease.
The way to make real intervention in
the halting the development and progression of atherosclerosis is to take a holistic
approach: changing the diet to be less inflammatory, reducing global toxicity
and stress, moderate exercise. My formula would be:
WELL-N-E-S-S
Being WELL in your Nutrition,
Exercises, Stress Management and Structural balance.
For more information go to www.wellnesseducationfoundation.org
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