Arteriosclerosis, or hardening of the arteries, is behind roughly half of all deaths in developed countries. And not all of them can be blamed on a cholesterol-laden diet or the life of a couch potato. The results of a new study by Natacha DePaola, a bioengineer at Rensselaer Polytechnic Institute in Troy, New York, suggest that no matter how assiduously you avoid fatty foods, or how vigorously you exercise, there is one risk factor for circulatory disease you can’t escape: cumulative wear and tear on your arteries by the impact of flowing blood. Cholesterol and fat probably only serve to hasten what is an inevitable process, says DePaola.
The problem seems to start when scavenging white blood cells stick to arterial walls and engulf cholesterol passing in the bloodstream. Precisely why the white cells do this is unknown, though some researchers think the cells may be trying to clean the blood. At any rate, after adhering to the artery walls, says DePaola, the white cells typically start burrowing between layers of tissue that make up the wall, damaging it in the process. This behavior also baffles researchers, but the results of the activity are clear: as the tissue tries to repair itself, blood clots form meshlike structures that trap cholesterol and fats flowing by, narrowing the artery. These deposits eventually constrict blood flow, reducing the oxygen supply to various tissues, which can lead to heart disease or stroke.
Autopsies show that this arterial damage doesn’t occur everywhere in the body but only where arteries branch or bend sharply. This has led researchers to suspect that changes in the force of blood flow on artery walls might trigger the disease.
To test this theory, DePaola cultured human arterial cells on glass slides. She then placed the slides in a machine that uses a saline solution to mimic various blood flow patterns. Cells subjected to a constant flow were more or less normal, she found. But cells exposed to changing flows were damaged. This damage, DePaola suspects, makes it easier for white blood cells to attach and then pass to the adjacent tissue, triggering the ultimately lethal repair process.
DePaola’s gloomy prognosis is that none of us--if we live long enough--will escape the disease. Somebody with a higher level of cholesterol will probably get sick faster, she says, but we all already have the beginning of arteriosclerosis--not to the point that it will kill us, but it’s there and it’s building up. It starts when you’re very young, in the first decade of life.