This article was stimulated by a friend who knew of my studying nutrition and asked me to interpret his lipid numbers from a recent blood test from my point of view
MORE THAN YOU EVER WANTED TO KNOW ABOUT CHOLESTEROL
Not being an MD, I would never be so bold as to offer advice. Having studied these issues, what I can offer is something for you to take up with your doctor, if you so choose. With that demurral, here’s what I see in the numbers you gave me.
The important numbers here are the triglycerides and the HDL level. The risk factor for heart disease is triglycerides/HDL>3. Your risk ratio is 1, well below the risk factor despite the flags on your report indicating high numbers. To understand why, we need to understand what triglycerides are and exactly how cholesterol is implicated in heart disease.
Triglycerides are a storage form of saturated fat, mostly palmitic acid, created by the liver from carbohydrates. When you eat carbohydrates, your body wants to get rid of them as fast as possible, so the first thing it does is burn off as much as it can. What can’t get burned gets shunted to the liver which turns the carbohydrates into saturated fat in a process known as de novo lipogenesis. The next step is to move these triglycerides to the adipose tissue for storage and later use. Here’s where the lipoprotein comes in. The only way to move fat from one place to another is through the bloodstream; the problem is that fat is not water soluble. So the liver creates a water soluble envelope for transporting non-water soluble compounds through the bloodstream, the lipoprotein.
Another non-water soluble compound that travels through the bloodstream in the lipoprotein is cholesterol. There is no such thing as good cholesterol or bad cholesterol; there is only cholesterol, an important substance for which your body has many uses. Every cell in your body requires cholesterol on a constant basis. Most cholesterol is made in the liver and sent through the bloodstream in the same lipoprotein as the triglycerides. LDL takes cholesterol to the cells that need it; HDL picks up any unused cholesterol and takes it back to the liver for recycling. Never does your body excrete cholesterol; it is too precious a substance to waste.
When there are problems with lipoproteins, it is with the LDL profile. There are about seven different sub-fractions of LDL grouped into two profiles: LDL A is a large, fluffy particle, while LDL B is a smaller denser particle. The small, dense LDL B particle can get stuck in the endothelium, the inner surface of the artery, whereupon it oxidizes and causes an inflammatory reaction from the immune system. The immune system creates a plaque under the injured endothelium which can constrict the artery if it gets big enough or break off and form an embolism.
Every lipoprotein starts out from the liver as a very low density lipoprotein, or VLDL. We can think of the VLDL as something like an airport shuttle, ferrying various passengers to various parts of the city. The two most important passengers in the VLDL are triglycerides and cholesterol. The first stop the VLDL makes is to offload the triglycerides into the adipose tissue, at which point the VLDL becomes a low density lipoprotein, or LDL, filled mostly with cholesterol. The more carbohydrates you eat, the more triglycerides your liver makes; the more triglycerides, the higher the ratio of triglycerides to cholesterol in the lipoprotein. Most of the seats in this airport shuttle will be taken up by triglycerides, and there will be little room left over for cholesterol. When this VLDL offloads its crowd of triglycerides into the adipose tissue, the resultant LDL, because of the small amount of cholesterol in it, will be a small, dense particle of LDL B, the troublemaker.
If you eat low carbohydrate, and, subsequently, have low triglycerides, there will be more cholesterol in the VLDL, and the resultant LDL particle will be the larger, fluffier LDL A. So the overall number for LDL is meaningless unless we know the LDL profile. If your LDL is primarily profile A, a high number is not harmful. If your LDL is primarily profile B, a low number will not help you; you’re in trouble. Profile A is always correlated with high HDL and low triglycerides, so the only important risk ratio is triglycerides/HDL. Your HDL level is unusually high. This is good. Ignore the flag on that number in the report.
The protein that comprises the lipoprotein is known as apolipoprotein B100. If you eat a low fat diet, your total LDL will likely go down , as will your level of HDL, but the level of apoB 100 will remain unchanged, which, of course, means that there is less cholesterol in each particle of LDL. Your LDL profile will have shifted to profile B. When you eat a low carbohydrate diet, your LDL will either stay the same or could even rise a little, but HDL will also rise. However, the level of apoB 100 will go down, signifying larger particles of LDL profile A. I see nothing but good news in your lipid panel, but don’t take my word for it; take it up with your doctor.