What’s Your Number?
If you have had a health checkup lately, chances are you had your cholesterol measured. In fact, you probably had a Lipid Profile done, which measures not only Total Cholesterol, but also Triglycerides (TG) and either measures or calculates a level for 3 important carrier molecules, namely High Density Lipoprotein (HDL), Low Density Lipoprotein (LDL) and Very Low Density Lipoprotein (VLDL). A typical lipid panel measures cholesterol, HDL and triglycerides and then calculates LDL. The problem here is that the calculation for LDL assumes your total cholesterol and triglycerides are fairly low. So your calculated LDL number may be highly inaccurate. And as we will see, not all LDL is the same.
HDL is often referred to as the “good cholesterol” and LDL the “bad cholesterol”, but in reality neither is made of cholesterol. HDL and LDL (as well as VLDL) are protein and fat (lipid) based carrier molecules for cholesterol. You see cholesterol is technically a high molecular weight organic alcohol (sterol). Your body uses these water soluble carrier molecules (HDL, LDL, VLDL) to move cholesterol and triglycerides from the liver to the tissues and then back again.
Cholesterol is an extremely important molecule. It forms the basic structure of vitamins A, D, E and K and many hormones including estrogen, testosterone and progesterone to name just a few. Cholesterol is also is used in the formation of cell membranes. Your liver produces 1-2 grams of it every day. A “regular” diet will typically contain about 200-300 mg of cholesterol daily. So roughly 80% of your daily cholesterol requirement is manufactured each day by the liver, and about 20% is ingested. Liver production of cholesterol involves an enzyme called HMG CO-A Reductase. This is the enzyme that is inhibited by statin drugs such as Lipitor, Crestor and Zocor.
Triglycerides are formed in the liver in response to carbohydrate ingestion (such as table sugar, wheat, flour, rice, high fructose corn syrup, or potatoes). Triglycerides can be a vital source of quickly accessed energy, but if they are not consumed soon after production any excess is transported to and stored in your fat cells. Triglycerides are also a stimulus to the liver to make more VLDL carrier molecules. All LDL starts as VLDL. VLDL carries both cholesterol and TG and donates these to other molecules and tissues for use. As VLDL loses the cholesterol and TG it is carrying it becomes smaller and denser and eventually becomes LDL. So LDL can be either large and fluffy or small and dense.
While the difference in size between large LDL and small LDL may be only a few billionths of a meter, the clinical importance is huge. You see small dense LDL is much more likely to cause blockages in arteries than large and fluffy (less dense) LDL. It also hangs around in your blood stream 40% longer and is easier to oxidize (think of this as rusting of the molecule). So you want as few small dense LDL particles as possible to help reduce your risk of cardiovascular blockages. Conversely, the larger and fluffier your LDL is, then the lower the risk for blockages.
Think of LDL as a truck, and TG and cholesterol as the cargo that needs to be moved. If you greatly increase the number of trucks then by definition there will be smaller loads per truck. High TG production ( driven by carbohydrate ingestion) stimulates the liver to make more trucks than is needed, so the total number of LDL particles goes up and the amount of TG and cholesterol per particle goes down. It becomes smaller and denser LDL – the truly “bad cholesterol”.
Diet has a significant effect on both LDL size and triglyceride levels. As noted above TG production is strongly influenced by carbohydrate consumption. Saturated fat consumption inhibits liver production of triglycerides. At least 7 clinical trials have consistently shown that the lower the fat content in the diet and the higher the carbohydrate, the smaller and denser your LDL will be.
Conversely diets low in carbohydrates will reduce TG production, lower insulin levels (which also reduces liver production of lipids) and thus lower production of small dense LDL. Studies at UC Berkley have demonstrated an average 26% drop in LDL levels when subjects were placed on a 12 week diet that limited carbohydrates to 10% of total daily calories.
Low carbohydrate diets also lower insulin levels and average blood glucose levels. Weight loss, sometimes significant, can also be achieved through carbohydrate restriction. This is because the body will stop storing new fat in your cells, and start burning the currently stored fat to make up for the decreased carbohydrate ingestion. In his book “Wheat Belly”, cardiologist William Davis references a Mayo Clinic study of overweight subjects who went gluten (wheat) free for 6 months and lost an average of 27 ½ pounds.
Knowing your true LDL number is an important measure of your cardiovascular risk. Your doctor can order an NMR profile, or do a VAP study to get accurately measured results. It is clear that sugar in any form raises TG and eventually increases small dense LDL (the truly “bad” cholesterol). So the next time you see that tray of jelly doughnuts in the break room you might want to think twice before snagging one of them.
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Recommended Reading: “Wheat Belly” by William Davis
You Tube video “Why We Get Fat” by Gary Taubes (please start at the 6 minute mark).
