HIGH BLOOD
heart - heart disease heart attack heart health blood vessels artery clogged lower cholesterol
Why Our Arteries Become Clogged As We AgeThe 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.
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.
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.
ANATOMY OF THE ARTERY
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.
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 dysfunctionHow 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 Arterial Wall Under Attack
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).
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.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.
High levels of iron promote LDL oxidation in the damaged endothelium, while low levels of testosterone appear to interfere with normal endothelial function.
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