What I Tell My Patients With High Cholesterol
In a Nutshell
High cholesterol is often a signal of underlying metabolic disease and inflammation rather than the direct cause of plaque. The key tests are fasting insulin, high-sensitivity CRP, and LDL particle fractionation to identify whether arteries are inflamed before focusing on cholesterol numbers. Prioritize fixing insulin resistance and inflammation through diet and exercise first, as treating LDL alone while metabolic damage continues fails to stop heart attacks.
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When a patient comes with high cholesterol, the first statement is often that cholesterol may not be the first problem to focus on. This surprises many patients. The speaker lived through the same confusion personally, having run marathons, followed a strict low-fat diet, and done everything the guidelines recommended while teaching the same advice to patients. A scan later revealed plaque was still building inside the arteries despite decades of following standard recommendations. This experience showed that the standard model was not designed to catch what was actually happening.
A study of 136,000 people hospitalized for heart attack found that nearly three quarters had LDL levels that their doctors considered fine, acceptable, or very good. Almost half had LDL cholesterol levels under 100, which guidelines at the time called optimal. Most of these people were already on lipid-lowering treatment, typically a statin. They had good cholesterol numbers, were being treated, and still had a heart attack.
Cholesterol is often a signal, not a source or primary cause. The mechanism that drives plaque begins with metabolic disease, including insulin resistance, pre-diabetes, and excess visceral fat around the organs. Chronic blood sugar elevation triggers systemic inflammation. Inflammation, not fat or cholesterol by itself, damages the artery wall. Once the wall is damaged and inflamed, particles become trapped inside. Immune cells called macrophages consume these particles and turn into foam cells, and the foam cell build-up forms the plaque.
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