Preventing Atherosclerosis by Dr. Jonn Matsen 2

Preventing Atherosclerosis

by Dr. Jonn Matsen

Atherosclerosis is the hardening and narrowing of the arteries which results from a slow buildup of plaque on the inner walls of the arteries. Diseases caused by atherosclerosis­heart disease and strokes­are the leading cause of illness and death in North America.

 Atherosclerotic plaques consist mainly of cholesterol. The deposits that protrude into your arteries are called plaques; they can be seen on an angiogram, an x-ray of your arteries. However, the angiogram is only seeing a very late stage of the development of atherosclerosis. By the time 25 percent of the artery flow has been blocked by hard plaque, 85 percent of the unseen inner artery is filled with soft fatty plaque, which is actually the more dangerous of the two and it doesn’t show up on an angiogram.

The hard plaque may cause discomfort by gradually clogging up your arteries and decreasing oxygen supply, creating angina or brain dysfunction. But the soft, hidden plaque underneath is more likely to suddenly break off and enter the bloodstream. The resulting clot may partially or totally block the flow of oxygen-carrying blood. If the blood supply to the heart is cut off, a heart attack can occur. Blocked blood supply to the brain may result in a stroke. When blood supply to the legs, arms or pelvis is affected, you may have symptoms of peripheral arterial disease. If the arteries to your kidneys are blocked, you may suffer from renovascular hypertension.
 
Scientists believe that cholesterol buildup results from damage or injury to the lining of arteries. A probable cause of this damage to the arterial inner walls is lipid peroxides. Your liver cells have two sets of enzymes for detoxification: the Phase I and Phase II enzymes. The Phase I enzymes create peroxides­a normal biochemical step­which should be quickly neutralized by the Phase II enzymes. Ideally, the Phase I and Phase II enzymes should work at the same speed. If the Phase I enzymes make peroxides faster than the Phase II enzymes can neutralize them, the peroxides may bind to cholesterol or fatty acids (lipids) creating lipid peroxides.

 Lipid peroxides damage cell membranes on contact, including those that make up the inner lining of your arteries. To repair the damage, the blood will immediately deliver a convoy of fats­such as lipoprotein(a), LDL cholesterol, and HDL cholesterol­to the membrane.

Lipoprotein(a) is like the hospital ship of the blood, carrying apoprotein, a sticky substance used to hold the damaged area together, much as you would use a sticky bandage to hold the sides of a wound together. LDL cholesterol is the freighter that carries the cholesterol needed to repair the damaged membrane. To protect its cholesterol cargo from oxidation (rancidity), LDL cholesterol is only lightly armed with weak antioxidants. HDL cholesterol is a more heavily armed destroyer, sent to protect both the freighter (LDL) and the damaged membrane from further lipid peroxide damage. HDL carries peroxide-damaged fats back to the liver for detoxification.

A well-equipped membrane repair crew consisting of these three important fats is more than capable of patching up lipid peroxide damage to your membranes. However, if lipid peroxides continue to bombard your membranes over and over again, your weakly protected LDL cholesterol can get torpedoed by the peroxides.

With ongoing lipid peroxide damage to your membranes, your liver will have to increase its production of fats into the blood to meet the demand. The increased levels of LDL cholesterol­if not given adequate antioxidant protection in the face of a barrage of lipid peroxides­will quickly get oxidized and run aground in your arteries, giving it the unjust nickname “bad” cholesterol. While high levels of LDL have long been considered a sign of pending heart attack or stroke, high levels of lipoprotein(a) are ten times more dangerous because its stickiness can cause clots.
 
An Oxford University study found that people with high levels of lipoprotein(a) were 70 percent more likely to have a stroke or heart attack because, due to lipoprotein(a)’s stickiness, high levels begin to deposit plaque in the arteries. In fact, Linus Pauling, who won the 1985 Nobel Prize in Medicine for his research on lipoprotein(a), theorized that vitamin C deficiency weakens the connective tissue­particularly collagen­of the arteries. This deficiency leaves the arteries more prone to damage, and to patch them up requires more lipoprotein(a).

The problem in the arteries can become much worse when your immune system gets involved. For one thing, your macrophages go in to rescue the damaged LDL. The macrophages eat the damaged LDL, but the rancidity can be so severe that the macrophages themselves can bloat up and die, becoming foam cells. This triggers a further immune response, causing even more damage to the artery membranes.

 
Atherosclerosis doesn’t begin when your heart bothers you when you shovel snow at age 65, or when your legs start cramping up after you turn 60. Atherosclerosis is a slow, progressive disease that can start during childhood and that usually does not cause symptoms until it’s often too late; namely when your arteries are severely narrowed or totally blocked. It is, however, is a reversible disease, particularly in the earlier stages.
 
To reduce your risk of atherosclerosis it’s important to decrease your liver’s production of lipid peroxides by slowing Phase I enzymes while increasing the activity of the Phase II enzymes. Some of the factors that make your liver work harder and should therefore be avoided as much as possible are:

Sugars and refined carbohydrates: these slow down your Phase II enzymes and lack the nutrients that your body needs to stay healthy.

Alcohol and tobacco: these increase Phase I enzymes.

Coffee: has recently been touted as having healthy antioxidants, but clinical experience shows that coffee increases peroxide activity in most consumers.

“Bad” fats: these include hydrogenated oils, trans fats and too many saturated fats.

Chemicals such as pesticides, additives and preservatives.

Toxic heavy metals, such as mercury which is present in silver dental fillings and some vaccinations.

Overgrowth of yeast in the small intestine: this creates even more toxins for your liver to handle.

Healthy eating, controlling your weight, exercising, getting the sleep you need, handling stress, taking vitamins and supplements that your body needs, and following the other guidelines of the Eating Alive Program will also help to reduce your risk of atherosclerosis.

9/1/2006

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