After a 1 week diversion, I’m returning to the topic of advanced cardiovascular testing. I began discussing cholesterol transport as it relates to vascular disease first seeking to resolve confusion about cholesterol itself which is a critical factor in good health. Cholesterol was contrasted with the lipoprotein particles which carry it through the bloodstream to a destination. These particles can become harmful to arterial walls if excessive in number, especially in small dense form, or when “rusted” by oxygen or caramelized by sugar. Inflamed vessel walls are also more readily entered by these particles. In considering risk, we balance low density lipoprotein (LDL) against high density lipoprotein (HDL), the so called “good cholesterol”. HDL acts as a scavenger of cholesterol, removing it from tissues and carrying it back to the liver for recycling or elimination in the bile. Apparently not all HDL serves this protective function. HDL2 is larger and more buoyant and is indicative of lower risk. Many now believe that the overall best measure of risk is total cholesterol/HDL with <3.5 being desirable and <3 being optimal. (Or better yet is Apo B/Apo A with Apo B representing LDL related particles and Apo A representing HDL related particles.) We have long told patients that HDL can be raised modestly by exercise, eating omega 3 fats and eliminating trans fats. In recent years, we have been astounded by the rise in HDL when carbohydrate consumption is dropped to healthy levels especially when correcting insulin resistance. High intensity interval training also seems to have a much more potent effect on HDL than long distance running or other less intense forms of exercise. Drinking wine raises HDL but has more of an effect on smaller, denser HDL3. All of this is yet another reason to lower dietary carbs and eat more healthy fats as well as eliminating processed foods with additives which increase oxidative stress. Will cover the fascinating topic of triglycerides on Wednesday!