I will try to demonstrate, by the use of diagrams and photographs, how the excess of cortisol and the overproduction of catecholamines impair carbohydrate metabolism and create conditions in which there is insufficient oxaloacetic acid for the oxidation of acetyl CoA, resulting in an increased plasma lipid concentration and increased cholesterol level. This is in full agreement with established biochemical principles, as shown by the following quotations: “Cortisol excess raises blood lipids and the plasma cholesterol level. This leads to arteriosclerosis” (Emphasis added. Keele and Neil 1982) — i.e., to CVD. The nonoxidated acetyl CoA will be used for the biosynthesis of cholesterol, as described by Keele and Neil (1961): “Cholesterol is synthesized from active acetate units in lieu of their conversion to fatty acids and leads to the rapid development of arteriosclerosis.” These active acetate units are the acetyl CoA not oxidated by the Krebs cycle.