What the News Media Did Not Reveal About Bill Clinton's Heart ProblemNovember 2004
By William Faloon
LE Magazine November 2004
|What the News Media Did Not Reveal About Bill Clinton's Heart Problem|
How Atherosclerosis Develops
Atherosclerosis begins with changes in endothelial cell function that cause white blood cells moving through the blood to stick to the endothelium (inner arterial wall) instead of flowing by normally. The endothelium then becomes weakened. This 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 such as LDL and triglycerides in the blood then accumulate in this area.
The lipids that accumulate in the broken endothelium become oxidized, causing the smooth muscle cells to try to “repair” the damaged endothelium. The result of this repair process is smooth muscle cell infiltration into the endothelium causing the formation of the initial atherosclerotic lesion. Depending on an individual’s 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.
Immune cells called macro-phages then invade the damaged arterial area to digest the fat. But smooth muscle cells that have migrated to the area have already changed their nature to scavenge fat. These fat-laden white blood cells and smooth muscle cells are called “foam cells,” and provoke a 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. Calcium then accumulates over the injury site to form 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, it is vulnerable to acute rupture that exposes the contents of the plaque to blood. Platelets can then rapidly accumulate around this ruptured plaque, resulting in an acute 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 grow to such a degree as to restrict blood flow severely, as was the case with former President Clinton. When blood flow within an artery is gravely 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 atherosclerotic processes cut off the oxygen supply to a portion of the brain.
As you can see, therefore, much more is involved in the development of atherosclerosis than just high cholesterol and LDL. We must emphasize, however, that maintaining optimal LDL and cholesterol levels is an important component of an atherosclerosis-prevention program.
Protecting Your Arterial Walls
Other significant artery-damaging factors are high-normal levels of glucose, insulin, iron, homocysteine,16-24 and fibrinogen,25-28 and any level of C-reactive protein29-36 that is higher than optimal.
Homocysteine is particularly dangerous because it can induce the initial atherosclerotic injury to the endothelium, then facilitate the oxidation of the fat and LDL that accumulate beneath the damaged endothelium, and finally contribute to the abnormal accumulation of blood components around the atherosclerotic plaque.
Fibrinogen is a clotting factor that accumulates at the site of the endothelial lesion. Fibrinogen contributes to plaque buildup and can participate in the arterial blockage after an unstable atherosclerotic plaque ruptures.
Glucose at high-normal levels may accelerate the glycation process that causes arterial stiffening, while high-normal fasting insulin inflicts direct damage to the endothelium. High levels of iron promote oxidation of LDL in the damaged endothelium, while low levels of testosterone (in men) appear to interfere with normal endothelial function.
C-reactive protein is an inflammatory marker and directly damages the endothelium. Chronic inflammation, as evidenced by persistent high levels of C-reactive protein, not only creates initial injuries to the endothelium, but also accelerates the progression of existing atherosclerotic lesions.
In response to a large number of published studies, enlightened people are taking charge of the health of their arteries. They are eating better, exercising regularly, and undergoing regular blood testing to identify the specific drugs, hormones, and dietary supplements they need to reduce their atherosclerotic risk factors.
The News Media Can Endanger Your Arteries
We do not want any of our members to become victims of news media hype about what may have caused Clinton’s arteries to clog. We suspect the former president’s heart problems were due to many of the atherogenic factors discussed in this editorial. Sad to say, most cardiologists are not even familiar with the multiple heart-attack risk factors that were long ago identified by the Life Extension Foundation.
In this issue of Life Extension, we examine the pros and cons of statin drugs and provide rational strategies for using these drugs if natural approaches fail. We know that many Life Extension members with elevated LDL or cholesterol levels refuse to take statin drugs because of concern about side effects. The good news is that a patented dietary supplement has been developed that has shown remarkable effects in reducing LDL and cholesterol without side effects. For members who have excess LDL or cholesterol, this new supplement could help lower these artery-clogging factors to safe levels.
For longer life,