Posted on November 2, 2018 by Tia Lalani

Biology professor Neil Haave discusses how levels of cholesterol in our bodies act as risk factors for atherosclerosis and coronary artery disease.

In recent years, giant “fatbergs” have developed in the sewers of London, UK. These are massive build ups of household and industrial grease that fall out of solution and block the sewer tunnels, preventing the flow of waste. Fatbergs are akin to the build-up during atherosclerosis, which causes coronary artery disease: our blood vessels become blocked with fat, which prevents the blood from delivering oxygen and foodstuffs to our tissues. Without oxygen and energy, the tissues die, which typically leads to heart attack and stroke.

Atherosclerosis is a progressive disease that develops over decades. At its most basic, atherosclerosis is an inflammatory disease of the arterial wall. When blood vessel walls are injured, inflammation results. Arterial inflammation can result from high blood pressure, which may be congenital or may be the result of lifestyle (lack of exercise, presence of chronic stress). Other risk factors for developing atherosclerosis include smoking and diabetes. The resulting chronic irritation of the blood vessel wall recruits circulating immune cells that initiate the inflammatory process.

It is also important to understand how high levels of circulating bad cholesterol (LDL) and low levels of good cholesterol (HDL) increase our risk for atherosclerosis and coronary artery disease. When LDL levels are high, they can find their way under the lining of irritated blood vessels, where they are ingested by white blood cells that then accumulate, causing the vessel wall to swell and balloon.

At some point, the blood vessel becomes blocked, limiting blood flow and oxygen delivery to the tissues. When oxygen delivery becomes too slow, cells are no longer able to rapidly convert food energy (fats, carbohydrates and protein) into the common energy currency of the cell. When this happens in the coronary arteries feeding our heart, cardiac arrest—a heart attack—occurs.

Although cholesterol is often depicted as a life-threatening molecule, our bodies cannot survive without it. We need a minimal amount to maintain the integrity of cell membranes and to make steroid hormones, which regulate many of our life processes. We also need cholesterol to make bile acids that facilitate the digestion and absorption of dietary lipids. The problem with cholesterol for many North Americans is that there is typically too much of it in our blood and it must be regulated.

Our natural processes increase LDL receptors on our cells when the level of cellular cholesterol drops below a minimal level needed for cell function, which effectively removes LDL from circulation, reducing the level of bad cholesterol in our blood. Other methods of decreasing blood cholesterol include inhibiting its absorption from the intestine and promoting the recycling of LDL receptors back to the cell surface once it has delivered cholesterol to the cell from the blood.

Treatments for the prevention of coronary artery disease have focused on lifestyle changes and medical intervention, which act on LDL levels. Lifestyle changes include decreasing caloric and fat intake and also diminishing stress levels. Medical interventions may include drugs to decrease blood pressure. The most successful drug to date at decreasing the circulating bad cholesterol is the statin family of drugs (e.g. Lipitor). Statins inhibit cholesterol synthesis inside our cells and in response, our cells increase the number of LDL receptors on their surface facilitating removal of the bad cholesterol from our blood.

Another common drug intervention to decrease our risk for coronary artery disease is daily low dose aspirin therapy. Low dose aspirin tips the balance of blood clotting molecules away from clot formation, thereby favouring blood flow. This balance involves a set of molecules that help to circumvent the possibility of a blood clot forming in our arteries.

So don’t be like the city of London which is now struggling with fatberg infested innards because city officials ignored the problem for far too long. Understand and reduce the risk factors associated with coronary artery disease and speak with your doctor about what steps you can take to ensure a long and full life.

Neil Haave, Biology, Augustana Campus, University of Alberta. This column originally appeared in the Camrose Super Booster on October 23, 2018. 


Posted in Augustana Campus, Featured. | Permalink

Comments are closed.