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This post was edited by E.T. at 2012-5-15 11:23|
Life Extension Magazine May 2012
Blood Testing That Can Save Your Life
By Michael Ozner, MD
In his new book, HEART ATTACK PROOF, cardiologist and researcher, Michael Ozner, MD, presents a proven program to help you avoid the devastation of heart disease. One critical component of his unique protocol is the use of specific blood tests to help you and your physician clearly assess your risk for heart attacks. From these tests, you can move yourself into the safety zone by incorporating lifestyle changes, high-level nutrients, and when necessary, pharmaceuticals to make yourself virtually heart attack proof. In this excerpt, Dr. Ozner explains why a blood test that utilizes an expanded cardiovascular risk profile can save your life.
Excerpted with permission from HEART ATTACK PROOF by Michael Ozner, MD, published by Benbella Books 2012.
Why It’s Important to Get Cardiovascular Blood Tests
The best way to detect metabolic abnormalities, like elevated (bad) LDL cholesterol particles or increased vascular inflammation (which may be present even if you feel well) is through a blood test. Detecting metabolic disorders is particularly important for uncovering hidden risk for heart attack, stroke, and vascular disease, thereby allowing physicians to individualize treatment programs that will lower patients’ risk of disability and death from cardiovascular disease. Simply using a standard lipid or cholesterol profile (total cholesterol, [bad] LDL cholesterol, [good] HDL cholesterol, and triglycerides) uncovers 40 percent of heart attack risk*, whereas an expanded cardiovascular risk profile, with tests such as LDL particle number and hs-CRP, can uncover 90 percent of heart attack risk. Performing regular blood tests is also essential for effectively monitoring already diagnosed conditions and ensuring that medical treatment and lifestyle changes are working.
The cost of comprehensive blood tests has decreased significantly over the past several years. And compared to the cost of treating heart attack, stroke, or peripheral vascular disease—that is, compared to the potential cost of not knowing what’s going on in your body and only being able to treat these conditions once they strike—it’s a steal!
The best time to have a comprehensive laboratory evaluation is when you are feeling well. If you wait until a heart attack (or stroke) strikes, you’ve waited too long. One-third of men and women do not survive their first heart attack, and those who do have to undergo expensive interventional procedures and lengthy hospital stays that can cost between $50,000 and $100,000. Long-term care can be very expensive, and the loss of your future earning potential can be significant. Prevention of atherosclerosis and heart attack or stroke is one of the most cost-effective strategies available—not to mention the nonfinancial benefits of staying healthy and productive and enjoying life.
The Genesis of a Heart Attack
Having these tests done regularly is crucially important. The next step is to understand what all the numbers mean. To do so, we first need to take a step back and look at the development and progression of cardiovascular disease, and how metabolic abnormalities can lead to a heart attack.
A heart attack occurs when the blood supply to the heart is cut off. We used to think that heart attacks were caused by the buildup of cholesterol and fat that ultimately choked off the artery causing a heart attack; we now know that the culprit is not cholesterol itself but the particles that carry it.
There are two types of these particles, characterized by the protein on their surfaces. The first type contains an apoB protein on the surface, which means they have the potential to enter the artery wall and lead to atherosclerotic plaque formation. Ninety percent of particles with apoB proteins are LDL particles. LDL particles are often referred to as “bad” particles, though they are not always bad. They play a beneficial role—they deliver cholesterol throughout the body where it is needed (cholesterol is an essential component of cell membranes, and is also necessary for the body to produce hormones such as cortisol, aldosterone, estrogen, and testosterone, as well as bile acids and vitamin D). But they also have the potential to enter the arterial wall and wreak havoc. The second type is HDL particles. These have a different protein on their surface called apoA1. HDL particles are often referred to as “good” cholesterol particles, because their job is to enter the arterial wall, remove cholesterol, and carry it to the liver for processing.
So, in short, LDL’s job is to carry cholesterol to the areas of the body where it’s needed, and HDL’s job is to pick up excess cholesterol inside the artery wall from the places it isn’t needed. All of this is necessary for proper functioning of the body. Problems arise when there is an excess number of LDL particles in the blood and these particles enter the artery wall. Once there, the particles can lead to the formation of atherosclerotic plaques, which are like pimples in the blood vessel wall. And just like pimples, these plaques can become inflamed and rupture.
The Formation of Atherosclerotic Plaques
Once inside the artery wall, cholesterol particles come into contact with something called free radicals. Free radical is the term used for any molecule with an uneven number of electrons. You may remember from chemistry class that molecules with uneven numbers of electrons don’t like to stay that way. They’ll do whatever they can to beg, borrow, or steal another electron so they can have an even number. This theft by free radicals is referred to as oxidation. When a free radical steals an electron from a cholesterol-carrying particle, the particle then becomes oxidized, and the body views it as a foreign invader. As a result, our natural defense system—inflammation—kicks in. Our immune system goes on the attack and sends white blood cells to the scene to engulf the oxidized cholesterol particles, and this leads to the formation of an atherosclerotic plaque.
After engulfing the cholesterol particles, the white blood cells, called macrophages, begin to release proteinases, which are designed to break down the plaque’s fibrous cap, ultimately leading the plaque to rupture. When blood comes into contact with tissue factor (a clot-promoting molecule) inside the plaque, it forms a clot at the rupture site. If that clot is large enough, it can completely block the artery, leading to a heart attack.
Reversing Heart Disease
There are a number of complex factors at work in causing a heart attack. The good news is, it’s possible to not only halt the progression of atherosclerosis, but to actually reverse it. With the proper lifestyle and optimal medical therapy, it is possible to stabilize and even get rid of the atherosclerotic plaques that lead to heart attacks. Regression of atherosclerosis is an achievable goal.
When I started my cardiology practice in 1979, a normal cholesterol level was up to 300 mg/dL! Today we know better. It is now recommended that your cholesterol level should remain under 200 mg/dL. And thanks to research like the Framingham Study, we know the optimal total cholesterol is actually less than 150 mg/dL*. Yet the average total cholesterol for Americans is still greater than 200 mg/dL (208 mg/dL). Knowing your total cholesterol is an important part of understanding your risk for a heart attack. But it doesn’t tell the whole story of what’s happening inside your body.
The next important factor in heart attack prevention—possibly the most important factor—is your particle number. Decreasing the number of (bad) LDL particles in your blood and increasing the number of (good) HDL particles is key.
Cholesterol is transported through the bloodstream by particles, and atherosclerotic plaques occur when LDL particles enter the artery wall, get retained, and become oxidized. You can think of the particles as cars and cholesterol molecules as passengers in the cars. Just as too many cars can cause a traffic jam, too many LDL particles can lead to a heart attack. It is the number of particles, not the amount of cholesterol in the particles, that is the problem.