Cholesterol is one of the most important molecules in the body. It is involved in the structure and function of all cell membranes; the brain itself is 25% cholesterol; it’s a raw material for many hormones; and is the precursor to vitamin D (which is made when UVB rays from the sun react with the cholesterol near the skin surface). Cholesterol is a critical component of the bile salts necessary to emulsify and digest fats. Cholesterol is so important that we evolved an elaborate system of lipoprotein transporters to deliver this critical substance throughout the bloodstream to wherever it is needed.
The main lipoprotein transporters are VLDL (very low density lipoprotein), LDL (low density lipoprotein) and HDL (high density lipoprotein) molecules. You are likely familiar with the oversimplified characterizations of HDL as “good” cholesterol and LDL as “bad” cholesterol. VLDLs are manufactured in the liver to transport mostly triglycerides (fatty acid molecules that are increased when a high-carb diet provides more glucose than can be burned or stored) and some cholesterol to cells throughout your body. After delivering their nutrients, VLDLs shrink substantially in size and convert into either large, fluffy LDLs or small, dense LDLs. Large, fluffy LDLs are generally harmless in the bloodstream, even when levels are unusually high – something that is strongly associated with genetics.
When triglycerides are high in the blood (usually through a high-carbohydrate diet and excess insulin production). VLDL production skyrockets to handle the extra load, and many of these particles can convert into small, dense LDLs. These small, dense LDL have been identified as the problematic particles of cholesterol that can become stuck in small spaces on the walls of your arteries and later become oxidized and inflamed. This artherosclerosis process is further accelerated when you consume easily oxidized PUFAs. A diet lower in carbohydrates has been shown to reduce the number of these dangerous particles.
This is the point in the story where Conventional Wisdom goes off track. While it’s true that statin drugs, or low-fat/vegetarian eating can lower the level of triglycerides and cholesterol in the bloodstream, a high insulin-producing diet can and will take whatever small, dense LDLs are still there and initiate the oxidation and inflammation process. In 2008, television journalist Tim Russet, unfortunately, illustrated the point when he succumbed to a heart attack at age 58 despite a (statin-induced) extremely low 105mg/dL level of total cholesterol in his bloodstream.
Conversely, HDLs are known as “nature’s garbage trucks” because they scavenge old “used” cholesterol in the bloodstream and return it to the liver for recycling. HDLs are very small molecules that can also easily get into the artery lining and remove small, dense LDLs lodged there, so their effect within the arterial lining is very beneficial. High blood values of HDL can be achieved with sensible (not chronic) exercise, moderating insulin production and consuming saturated fat (really!) and high-antioxidant (pesticide-free) vegetables and fruits. Nailing these four recommendations goes a long way toward making you heart attack proof.