Lower cholesterol

Author: Mason W. Freeman (USA), Christiane Jorgensen (USA)
Publisher:
Publish Date: June 1, 2006
Features: How is your cholesterol level? This has probably become a greeting we ask when meeting, whether at family gatherings or in the endless advertisements on TV. Although people have gained more awareness of high cholesterol in the past two decades, there are still some misconceptions. The biggest misconception is that all cholesterol production is balanced, even though it is utilized by the body. In reality, as many people are beginning to understand, cholesterol in the bloodstream is carried by many different types of particles, the two most important being high-density lipoproteins (HDL) and low-density lipoproteins (LDL). These two types of particles have entirely different effects on adhering to and blocking blood flow in the vessel walls. In short, HDL can protect your heart from disease, while LDL can lead to heart disease. The two patients mentioned in the preface of this book—Peter and Mary—are examples of having the same cholesterol level but differing greatly in their risk of heart disease. When we talk about cholesterol, what we need to focus on most is not the total cholesterol level but the extent to which its balance system is disrupted. Even if a person's cholesterol level is below 200 (generally considered a safe range), they can still be at high risk for heart disease. As long as their HDL content is too low or there are other reasons that lead to blocked arteries, heart disease can occur.
Step 1: Damaging the Inner Layer
The prerequisite for heart disease caused by cholesterol is the elevation of cholesterol in the blood. Cholesterol is carried by lipoprotein particles, particularly in LDL. When there is an excess of LDL in the blood, some of them separate from the blood and adhere to the vessel walls. The more excess LDL there is, the more will adhere to the vessel walls. The artery wall consists of three layers. The innermost layer is called the intima, composed of a single layer of cells called endothelial cells. The intima acts like a plastic film, protecting the artery wall and allowing blood to flow smoothly. Endothelial cells also play a role in transmitting signals, guiding repair cells to damaged areas so they can clear dead tissue and antigens. High cholesterol, high blood pressure, smoking, and diabetes can all damage the function of endothelial cells. This damage can take various forms, affecting the regularity of blood flow and blood pressure. The endothelial cells and intima may also be damaged, creating gaps. Regardless of a person's cholesterol level, endothelial cells transport some LDL to the intima layer, and the amount transported is proportional to the amount of LDL. Cholesterol also accelerates the damage to the inner layer of the vessel and penetrates deeper into the vessel wall.
Step 2: Inflammatory Response
These changes trigger an inflammatory response. Endothelial cells play a significant role in releasing chemical signals that attract immune cells called macrophages to the site of the lesion. Macrophages engulf and encapsulate LDL, swelling and forming foam cells (so named because they resemble foam in appearance). Although macrophages attempt to clear all the LDL and other debris stuck to the vessel wall, as the amount of LDL continues to increase, the number of macrophages grows as well, ultimately leading to these excess cells blocking the artery and causing the undesirable outcome. This is because the primary function of macrophages is to engulf bacteria, kill them, and then disappear. When the body continuously produces fat particles that become targets for macrophage attack, the process is like a lifelong infection. The more LDL appears, the more macrophages there are to eliminate it, creating a chronic inflammatory response in the artery wall. Eventually, the cholesterol within the macrophages dominates, damaging them and releasing their contents along with other inflammatory substances, further accelerating the process.