When that life-giving ‘pipe’ fills up with dirt
By Dr. Harold Gunatillake
We talk, we joke, we laugh, we read on topics like cholesterol, obesity, diabetes, heart attacks, but we don't seem to talk or know much about 'atherosclerosis' - maybe because it is not a word that could be remembered and pronounced easily, in particular after that stuff we drink to boost our good cholesterol (HDL)- the alcoholic beverages!

The term "athero-sclerosis"(literally, "hardening of the arteries") is a disease that starts in the inner lining (intima) of large blood vessels due to a variety of insults. Then as a result, a fatty/wax-like substance, is deposited. These appear as fatty streaks in the early stages. They appear even during the early years of life, and have even been reported in toddlers.

These fatty streaks get built up from blood cholesterol (LDL), cellular waste products, white cells, inflammatory cells, and calcium in the blood. They gradually grow into the lumen, and sometimes through the vessel wall, becoming firmer, solid and more stable. This rubbish build up is called fibrous plaques, which cause the arteries to narrow, preventing the blood from flowing properly and depriving the tissues of oxygen and nutrients, necessary for normal functions.

"Atheros" means "gruel", porridge", or "grits". Think of the appearance of the outlet pipe in your kitchen sink, the yellowish dirty waxy grits that accumulate on the inner surface. That would be the same appearance in the blood vessels affected by atherosclerosis.

Normally, the inner wall lined by cells (endothelial cells) is smooth, and non-sticky. It is possible that these cells are damaged by free radicals, causing oxidative stress, associated with inflammation. Another reason could be that the inner lining cracks due to the turbulence of the blood flow. Then free radicals cause the inflammatory reactions. Inflammation is the response to the injury; there is redness, swelling, heat and dysfunction of the inner lining.

Inflammation is now recognized as an important factor to atherosclerosis. Recruitment of white blood cells from the neighbourhood, oxidation of innocent LDL (bad cholesterol) to become active, eating up of these oxidized cholesterol by the white cells (macrophages) giving rise to foam cells initiates the development of atherosclerotic lesions.

At this stage, I must give some information about 'oxidation'. Oxygen is essential for body functions. It is inhaled through the wind- pipes (trachea, bronchi, bronchioles), into the lungs, from the atmospheric air. This is carried through the bloodstream to the central and peripheral areas of the body. This very essential lifesaver, also acts detrimentally within the body.

The molecule of oxygen will give out an electron from its pair and become free, just like a marriage break-up and becoming free again. The free electron replaces another paired electron in a neighbouring oxygen molecule making that a free radical. This chain reaction causes millions of free radicals to be liberated within the body. This process is referred to as "oxidation", a situation where an oxygen molecule is waiting to be oxidized. Our survival and gradual dying process is due to oxidation through free radical intervention, within the body, and from without.

One puff of a cigarette liberates over a million free radicals into the lungs. The rusting of the metal on your front gate is also due to oxidation. Rancidity of cooking oils is also due to oxidation.

Atherosclerosis was believed to be in the past a progressive disease characterized by the accumulation of lipids (fatty material, including bad cholesterol) and fibrous elements in the larger arteries. This is where it was once believed that eating too much of cholesterol containing foods, including saturated fat (atherogenic food), was considered as causing the thickening of the blood vessels. So, doctors advised we reduced eating such food, and checked our blood lipid levels frequently.

Over the past decade, however, we have come to appreciate a prominent role of inflammation in atherosclerosis and its complications. So, we believe that bad cholesterol (LDL), though a main constituent of the atheromatous plaques is only a bystander. Today we believe that there is a link between artery damage, the inflammatory process and atherosclerosis of blood vessels.

One of the indications of inflammation in the arteries is the presence of a substance called "C reactive protein"(CRP) in the blood, produced by the liver. In heart disease due to the atheromatous blockage, inflammation, and the presence of inflammatory cells, marked elevation of CRP level in blood is observed.

So, recent research shows that having a high C-reactive Protein test means you are at increased risk of suffering a heart attack or stroke, irrespective of whether the cholesterol level is elevated or not. C-Reactive Protein levels fluctuate from day to day, and levels increase with aging, high blood pressure, alcohol use, smoking, low levels of physical activity, chronic fatigue, coffee consumption, having elevated triglycerides, insulin resistance and diabetes, taking oestrogen pills, eating a high protein diet and suffering sleep disturbances, and depression. Gabe Mirkin, M.D. research worker, says, "At this time, the best ways we know to reduce C-reactive protein levels are exercise and a diet that includes omega-3 fatty acids.

Statins appear to protect against inflammation as well as cholesterol, but they can cause nerve and muscle damage and deplete the body of co-enzyme Q10". (Co-enzyme Q10 is produced in the heart muscle and brain tissue, and provides energy for their functions)
Now that we know some information about 'atherosclerosis', let us look at the warning signs.

The specific symptoms depend on what arteries are affected. When arteries to the brain are affected, atherosclerosis warnings include; Headaches, dizzy spells, ringing of ears, memory problems, poor concentration and mood changes.
When the arteries to the heart are affected with atherosclerosis- warning signs are; chest pain and elevated blood pressure.

When the arteries of the arms or legs are affected, the warning signs are; aching muscles, fatigue, cramping pains in the calves, and pain in the hips and thighs. Cramping of the calf after walking a certain distance is called "intermittent claudicating". The radiologists are now able to diagnose the site of atherosclerotic stenosis (obstruction) by arteriographic dye studies.

High blood pressure damages the inner lining of blood vessels and leads to atherosclerosis. Regular blood pressure checks are very important to delay such damage. Hormone produced by the kidneys named "Angiotensin11 is now one of the usual suspects of atherogenesis. Doctors prescribe "ACE inhibitors" to prevent damage of vessels.

Smoking too damages the intima. Smoke oxidizes LDL, and leads to plaque formation. Diabetes from any cause leads to atherogenesis. This can be controlled with proper diet and medication. Raising the good cholesterol (HDL) helps to delay atherogenesis. HDL is composed of A1 and A2. There is talk of using A1 instead of HDL as your measure of "good" cholesterol. Mice fed with lots of A1 get less atherosclerosis; those fed with lots of A2 paradoxically get more.

There are more factors that lead to atherogenesis, including elevation of homo-cysteine levels, but the bottom line is, if you control your weight, exercise, and eat healthy nutritious food, you have a good chance of delaying this dreaded disease. One must get laboratory blood tests done regularly to assess the risk of atherogenesis and heart disease.

Heart attack risk can be assessed by measuring a wide range of markers including CRP, homocysteine, total cholesterol, HDL and LDL, fibrinogen, and apolipoproteins B (apo B) and apolipoproteinA-1(apoA-1) levels, as well as apo ratios.