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
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:
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.
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.
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.
Iodine – Sea Kelp
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.
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:
Being WELL in your Nutrition, Exercises, Stress Management and Structural balance.
For more information go to www.wellnesseducationfoundation.org