|Artwork of a human heart showing narrowing of the coronary arteries due to atherosclerosis on the artery wall. The narrowing causes abnormal clotting, which blocks the vessel and starves the heart muscle of blood, causing a heart attack. |
The aging process damages blood vessels, even when conventional risk factors such as cholesterol and blood pressure are within normal ranges.
Despite aggressive intervention with diet, exercise, supplements, and drugs, pathological changes still occur in the arterial wall that predispose aging adults to vascular diseases. The encouraging news is that a non-prescription method has been developed to address the underlying reason why arteries become occluded as people reach the later stages of their lives.
For the past 35 years, the standard way to treat coronary athero-sclerosis has been to bypass the blocked arteries. Recuperation from coronary bypass surgery can take months, and some patients are afflicted with lifetime impairments such as memory loss, chronic inflammation, and depression.1,2
The scientific literature reveals that atherosclerosis is associated with high blood levels of homocysteine, C-reactive protein, insulin, iron, low-density lipoprotein (LDL), and triglycerides, along with low levels of high-density lipoprotein (HDL) and testosterone. Optimizing blood levels of these substances can dramatically reduce heart attack and stroke risk.3-14
Prescribing a “statin” drug is what today’s doctors typically do to prevent and treat coronary atherosclerosis. Cholesterol and LDL, however, are only partial players in the atherosclerosis process.
Mainstream cardiologists fail to appreciate that coronary atherosclerosis is a sign of systemic arterial dysfunction requiring aggressive therapy to correct. Health-conscious adults have grown impatient with doctors who do not translate research findings into improved therapies. More than ever before, people are taking responsibility for the health of their arteries by correcting as many of the known risk factors as possible.
Anatomy of the Artery
Arteries are the blood vessels that bear the full force of each heartbeat. Laypeople often think of arteries as flexible tubes whose only function is to carry blood that flows continuously throughout the body. In reality, arteries are dynamic, functioning muscular structures that in good health expand and contract to facilitate circulation and maintain optimal blood pressure.
The artery’s outer layer mostly consists of connective tissue and provides structural containment for the two layers beneath. The middle arterial area comprises elastic smooth muscle that provides the contractile strength to make possible the artery’s expansion and contraction with each heartbeat. The inner layer—known as the endothelium—consists of a thin area of endothelial cells whose integrity is crucial if atherosclerosis is to be prevented.
A vital function of the endothelium is to form a barrier to prevent toxic substances in the blood from entering the elastic smooth muscle in the middle vessel wall. Another specialized function of the endothelium is to react to mechanical forces such as blood pressure and blood flow generated by the heart’s beating action. The endothelium releases substances into cells of the middle layer smooth muscle that changes the tone or firmness of the artery.
When endothelial cells sense an injury, they produce signals that prompt smooth muscle cells in the middle arterial wall to change. These changes result in the smooth muscle cells moving toward the site of vascular injury, where they reposition themselves just beneath the endothelial cell layer. In reaction to injury, endothelial cells also produce substances that signal circulating blood cells to stick to the endothelium (instead of effortlessly flowing through the vessel). Atherosclerosis gradually forms in response to this initial injury to the endothelium.
|Cross-section of a narrowed coronary artery partially blocked by atherosclerotic plaque. [enlarge image] |
Changes in the Aging Endothelium
As we grow older, some of the specialized functions of our endothelial cells become blunted. The self-renewal process weakens. The endothelial barrier becomes leaky. Signals to the middle wall smooth muscle cells that regulate their function become altered.
Smooth muscle cells behave as if in reaction to endothelial injury, migrating to the endothelium, where they multiply and produce matrix proteins that gradually occlude the blood vessel. The addition of these smooth muscle cells and matrix proteins within the sub-endothelial space results in thickening of the artery’s inner wall. In older arteries, the inner wall becomes a battleground where multiple reactions occur that are similar to the process of chronic injury. The inner wall dysfunction that occurs in the aging artery provides fertile soil for the seeds of atherosclerosis. All of these processes whereby normal endothelial function is compromised are collectively referred to as endothelial dysfunction.
How Atherosclerosis Develops
Atherosclerosis is so common in older adults that some experts used to think it was part of normal aging. An alternative view is that atherosclerosis is a disease process that takes advantage of changes that occur within the aging artery.
The vascular aging process and atherosclerotic process influence each other and become intertwined as we age. The more severe vascular aging is, the easier it is for atherosclerosis to take hold. The more severe atherosclerosis is, the greater its impact on diseases associated with vascular aging, such as stroke and heart attack. Thus, it appears that with advancing age, atherosclerosis and the aging process combine forces.
An often-used analogy for atherosclerosis is a “clogged pipe.” This misguided perception either leads to bypass surgery or a procedure in which the blocked coronary artery is forced opened with a balloon catheter (angioplasty) and a stent is implanted to keep the artery open. While these surgical procedures have become necessary for many people, the “clogged pipe” analogy is an inaccurate way to view the process of atherosclerosis.
Atherosclerosis begins with changes in endothelial cell function that cause white blood cells moving through the blood to stick to the endothelium instead of flowing by normally. The endothelium becomes weakened, which allows blood cells and toxic substances circulating in the blood to pass through the endothelium and enter the artery’s sub-endothelial compartment. Lipid or fat cell-like substances in the blood, such as LDL and triglycerides, then accumulate in this area.
|Cross-section through an artery obstructed with atheroma plaque. The muscular wall of the artery (orange) takes up much of the image. At center, fatty deposits of plaque (gray) are seen on the inner arterial wall; the lumen (black) has been severely reduced for the flow of blood. Narrowing of the artery disrupts blood flow and may result in clot formation or severe artery blockage that can prompt a heart attack. [enlarge image] |
The lipids that accumulate in the broken endothelium become oxidized. This causes them to signal the endothelial cells, which then alert smooth muscle cells to begin a “repair” process that eventually results in an atherosclerotic lesion. Depending on a person’s individual risk factors (such as poor diet, lack of exercise, smoking, high blood pressure, and the aging process itself), fat accumulation continues and the atherosclerotic process accelerates.
White blood cells called macrophages then invade the area to digest the fat. Smooth muscle cells that have migrated to the area have already changed their nature to also scavenge fat. These fat-laden white blood cells and smooth muscle cells, which are called “foam cells,” induce chronic inflammatory attack by various immune components. Smooth muscle cells try to curtail the injury to the endothelium by producing collagen, which forms a cap over the injury site. Then calcium accumulates and forms a material resembling bone. This is why atherosclerosis used to be referred to as “hardening of the arteries.”
This complex array of foam cells, calcification, and lipid accumulation is called an atherosclerotic plaque. The plaque grows, and if it becomes unstable, is vulnerable to acute rupture that exposes its contents to the blood. Platelets can then rapidly accumulate around this ruptured plaque, resulting in a blockage (or blood clot) on the inner surface of the blood vessel wall. This clot can become very large and occlude the vessel. Even small plaques, if they rupture, can interfere with blood flow and cause an acute heart attack.
Alternatively, atherosclerotic plaques can enlarge to such a degree as to completely block blood flow. When blood flow within an artery is severely compromised by a large plaque or blood clot, the cells of tissues that depend on blood flow from that artery become damaged or die. Coronary atherosclerosis cuts off the heart’s blood supply by occluding the heart’s arteries, thus stopping the oxygen supply to the heart and causing a heart attack. A stroke results when atherosclerosis processes cut off the oxygen supply to a portion of the brain.
|Colored scanning electron micrograph of endothelial cells lining the inside of a blood vessel. |
The Arterial Wall Under Attack
High blood pressure, elevated LDL and triglycerides, low HDL, cigarette smoking, diabetes, obesity, and lack of exercise contribute to endothelial dysfunction and the subsequent development of atherosclerosis.15-25
Additional endothelial-damaging factors include excess levels of glucose, insulin, iron, homocysteine, fibrinogen, and C-reactive protein, as well as low HDL and free testosterone (in men).3,9,10,24,26-28
Homocysteine is particularly dangerous because it can induce the initial injury to the endothelium. Homocysteine then facilitates oxidation of the fat/LDL that accumulates beneath the damaged endothelium, and finally contributes to the abnormal accumulation of blood components around the atherosclerotic lesion.29
Fibrinogen is a clotting factor that accumulates at the site of the endothelial lesion. Fibrinogen may contribute to plaque buildup or participate in blood clot-induced blockage of an artery after an unstable atherosclerotic plaque ruptures.30
Glucose at even high-normal levels may accelerate the glycation process that causes arterial stiffening, while high-normal fasting insulin inflicts direct damage to the endothelium.31-36
High levels of iron promote LDL oxidation in the damaged endothelium, while low levels of testosterone appear to interfere with normal endothelial function.9,11,14
C-reactive protein is not only an inflammatory marker, but also directly damages the endothelium. Chronic inflammation, as evidenced by persistent high levels of C-reactive protein, creates initial injuries to the endothelium and also accelerates the progression of existing atherosclerotic lesions.3,27
In response to numerous published studies, health-conscious people are altering their diets, taking drugs, hormones, and dietary supplements, and trying to exercise regularly in order to reduce these atherosclerosis risk factors. However, these efforts alone cannot be completely successful because age itself is a major risk factor for atherosclerosis.
Atherosclerotic risk conferred by age is attributable in large measure to pathological endothelial dysfunction.37,38 As noted earlier, endothelial dysfunction is not synonymous with atherosclerosis, but the two processes are increasingly intertwined with advancing age.