I’m sure this seems like a straight-forward question but from a medical perspective, it is not.
The connection between cholesterol levels and atherosclerosis arose from the finding that arterial plaque has a lot of cholesterol in it. The medical reasoning that came about based on this finding was that if there was less cholesterol in the blood, there would be less arterial plaque.
Initially it was assumed that the source of the excess cholesterol must be the diet. After years of low cholesterol, low fat dietary recommendations, research began to show that dietary intakes did not have much effect on blood lipids or atherosclerosis for most people.
This realization led to the next approach which was to suppress cholesterol production in the body with drugs, and eventually statin medications became the first line of treatment for this purpose.
The problem with all of this is that it treats the “what” of atherosclerosis but not the “why”.
Research over the last 10 – 15 years has shown that there are other factors that contribute to atherosclerosis, most notably inflammation, and blood sugar effects known as advanced glycation end products. These factors relate to the “why” of atherosclerosis more directly and more often than the cholesterol hypothesis did.
To complicate matters further, however, there are people for whom blood lipids are a central issue in plaque production. This is why you need to review your personal and family medical history with your doctor to understand what your individual risks are with respect to stopping your cholesterol drug.
