“Cholesterol” has become perhaps the greatest health villain of the past 2 decades. However, it is really like Robin Hood in many ways. Like Robin Hood, cholesterol does many good things, but it can have a “bad” aspect in some cases.
As we discussed in the prior blog, cholesterol is an essential molecule in humans. We have been given the impression that it is an evil invader that breaks into the body through diet. This is an erroneous assumption that any well-versed physiologist will explain by reminding us that about 80-85% of the circulating cholesterol in the body is made in the liver and only 15-20% comes directly from food. A large change in dietary cholesterol, let’s say 50%, can only affect our circulating level by 7-9%. It is a much more meaningful objective to know why one’s body is choosing to make too much cholesterol and why cholesterol, an essential part of human function, sometimes get in trouble.
The making too much issue requires examination of the regulatory factors in cholesterol production. Basically, when the things the body does with cholesterol need to be done to a greater extent, a regulatory signal to the liver occurs to increase production. A common one is decline in hormone production such as by fatigued adrenal glands. To resolve this, the body increases the signal to produce more “raw material” for production, cholesterol. However, if the adrenal glands cannot do that because they are imbalanced, the cholesterol is not used and builds up. The task here is to figure out why the adrenal glands are fatigued and to revive “them”.
The second issue is the “misbehaving” aspect. Not all cholesterol causes problems when it is too high in the circulation. LDL or “bad cholesterol” is not a single type of cholesterol but rather a group with some members who are not much of a problem and others who cause all of the trouble. A little bit about how to read a panel of blood lipids helps to understand this. The typical readings include:
The LDL molecule is built around two different protein cores, apo B or apo A1. The core around which a cholesterol particle is built is the primary determinant of how harmful or harmless the LDL molecule is. Apo B molecules are very small and highly associated with causing vascular disease. Apo A1 molecules are large and fluffy and much less likely to cause problems.
Any given persons total LDL pool is a mix of some apo B particles and some apo A1 particles.
There is relatively weak correlation between simple LDL cholesterol levels and vascular disease risk such as coronary artery disease. The simple LDL cholesterol value is only about 50-60% predictive of risk meaning that it tells us only slightly more than the toss of a coin. Knowing the LDL particle size is much more valuable. The example below is of two persons both with the same LDL cholesterol readings of 120 mgs/dL.
The 120 mgs/dL simply means that the total weight of LDL cholesterol in a fixed volume of blood (dL or deciliter) is 120 mgs. As the diagram above shows, the same weight of cholesterol can be on fewer, larger apo A particles or on greater numbers of more small apo B particles. Same total amount of LDL but very different risks.
There is another type of “bad” cholesterol, VLDL. This type of LDL is always apo B or small particle LDL so when it is elevated, it always suggest a more dangerous small particle LDL pattern. Sometimes a “cholesterol panel” will be done which does not include VLDL. Without it, one only knows half the story of risk. The true total “bad” cholesterol is LDL + VLDL which is called “non-HDL cholesterol”. This is a better indicator of positive or negative effects of therapy than is the LDL reading alone. Making more VLDL will usually decrease the levels of HDL or good cholesterol so it is like a double whammy..
All of this can be sorted out with a more comprehensive test that measures the number and type of LDL cholesterol called a VAP profile. This test will show the majority pattern of LDL particles (large, fluffy, or small and dense). Dietary changes may produce only a small drop in “LDL” but VLDL may drop dramatically causing a very good decrease in total non-HDL cholesterol. Without looking at total non-HDL or “total bad cholesterol” it is hard to tell if risk is improved or worsened.
Although our tendency to make larger or smaller particles is partly set based on genetics, it is also partly determined by lifestyle and diet. Eating a high carbohydrate/sugar diet will cause a shift towards smaller, more dangerous LDL particles. This is typical of the standard “low fat” diet. Fat calories are replaced with carbohydrates which cause a shift towards more dangerous particles. There is no “one diet fits all” because different people by the genetic type tolerate different nutrient diet contents. Looking at the different factors in a cholesterol test will help to guide individual specific therapy.
There are also different nutrients that can be supplemented that increase particle size, that lower VLDL and total non-HDL and that raise HDL. Once one’s complete picture is understood a much more focused nutritional supplement program can be used which will produce better results.
This was a lot said to understand “why is my cholesterol misbehaving” but only looking at one piece of the problem can often lead to either inadequate realization of risks, or over treatment. It is worth a careful look!