Cholesterol Testing – What’s New

The New Gold Standard of Cholesterol and Lipid Analysis

The standard lipid tests that most doctors order for you really belong to the age of the dinosaurs. They tell you the level of your total cholesterol, LDL and HDL. New testing breaks cholesterol down into fractions, appearances, and patterns, giving a much more accurate picture of what may or may not be a problem.


This test is the Lipoprotein Particle Profile (LPP) test offered by SpectraCell Laboratories in Houston, as developed by Texas A&M University.


This more comprehensive and detailed test helps doctors and patients make sense out of the cholesterol confusion. They break down the major cholesterol components and take you light-years beyond generalizations like “LDL cholesterol is the bad cholesterol and HDL cholesterol is the good cholesterol.” The reality is much more complex. It is not just about how high the LDL is, but what kind it is and how much of it you have. The same with HDL. Keep in mind that the liver – where a good chunk of your cholesterol is produced – dispatches cholesterol throughout the circulatory system in the form of protein-wrapped fatty bundles called LDL. As LDL travels through the system, the cholesterol is accessed and used by cells as needed. Similarly, spent and oxidized cholesterol is picked up by HDL particles for return to the liver and subsequent excretion.


The SpectraCell test, originally developed at Texas A & M University, hones in on research that has introduced the medical community to subgroups of lipoprotein particles and how their different sizes and numbers can play a role in the inflammatory destruction of arteries.


LDL particles, for instance, can be large or small. It is the small, dense LDL particles that can readily enter into compromised arterial walls and stoke the inflammatory process. Higher numbers of these LDL particles represent a higher risk. Genetics play a major role here, and not diet, as most people have been erroneously led to believe. If you have significant numbers of these factors present, in the presence of cigarette smoke, mercury, lead, trans-fatty acids, insulin, homocysteine, or radiation, the potential for arterial damage increases. This is where doctors and patients become concerned, and particularly when there is a significant presence of Lp(a) – the most dangerous of these lipids and truly what we can refer to as “ugly cholesterol.” This small, dense LDL entity is a major thrombotic factor. It inflames the blood and makes it sticky. Another small, dense particle that has emerged with an inflammatory reputation is called RLP (remnant lipoprotein). It plays a role in the formation of plaque.


You want to have fewer of these subtypes and instead have more of what are called large, buoyant LDL. That kind of result suggests less of a risk. With this kind of advanced testing, two people with the same total measurement of LDL cholesterol may be at opposite ends of risk. One, with a predominance of small, dense LDL particles, may have three times the risk of someone with mostly large, buoyant LDL.


Similarly, there are significant differences among subgroups of HDL that relate to how well or not they carry out their removal of excess lipids. You want to be high in the most functional HDL subgroup, labeled 2b. Not all HDL is created equal.


The worse scenario, with this kind of testing, would be to have a predominance of small, dense LDL particles and low HDL 2b.


What about your total cholesterol? you may be asking. Well, it doesn’t mean much unless you have a level over 320 or so, which increases the risk of stroke; and then it certainly behooves you to bring it down.


What about your total LDL level, according to standard tests? If your doctor thinks it is too high, I suggest having the advanced testing done.


Here’s what you have to remember if your standard cholesterol numbers are “high” and your doctor tells you to take a statin:

  • Don’t do it. Ask your doctor to follow up with a VAP or LPP test that determines your individual cholesterol fractions.

  • If you are a male between the ages of 50 and 75 and have coronary artery disease, and the advanced test shows you have a predominance of small, dense LDL, go for the statin drug. It’s a good idea. Statin drugs are also anti-inflammatory, and that’s the powerful effect you are looking for, not the cholesterol-lowering activity. I say thumbs down on statins over the age of 75.

  • If you are a woman, and do not have unhealthy levels of inflammatory types of cholesterol and inflammatory substances such as homocysteine, fibrinogen, and C-reactive protein, I would pass on statins. I’ve been disappointed with the results. However, if you are a woman with arterial disease and have a profile of high inflammatory cholesterol and other substances, a statin may provide you benefit as an anti-inflammatory agent.

  • Male or female, do not take a statin on the basis of high Lp(a). Statins do not lower Lp(a). Your best bet to neutralize the inflammatory activity of Lp(a) is the B-complex vitamin niacin (500 mg–2 g daily) of the type that causes a flushing sensation, along with 2–3 g of fish oil and 100 mg of nattokinase. That’s my most potent cocktail for neutralizing Lp(a).


Please read below for further information on the breakdown of cholesterol products that can be measured with a Lipoprotein Particle Profile.



LDL Cholesterol – the LDL protein is the major carrier of cholesterol. Consuming omega 3 fatty acids helps lower total LDL levels.


HDL Cholesterol – High Density Lipoprotein (HDL) has two important subgroups: the larger, more buoyant HDL2 and the smaller, denser HDL3. These subgroups are important indicators of the efficiency of reverse cholesterol transport by HDL, or how well HDL is clearing excess cholesterol from the body. HDL is formed in the liver as dense HDL3 and as it travels through the body and accumulates cholesterol, it becomes the larger and lipd enriched HDL2b, the largest and most buoyant HDL.  Since HDL2b is an indicator of how well excess lipid are removed from cells, it positively correlates with heart health.


How is Low HDL 2b Treated? -A low HDL count indicates potential for atherogenic dyslipidemia.  Beneficial therapies are similar to those which raise HDL and reduce elevated TG, such as exercise, niacin, omega-3’s. Certain nutritional deficiencies are associated with a low HDL, such as zinc and selenium.

  • Large Buoyant HDL 2b – if this HDL particle is low, it represents a reverse transport system that is not working well to remove excess cholesterol.

  • Large Buoyant HDL 2a, 3 – this value represents the remainder of the HDL fraction, and is less beneficial than HDL 2b.


Triglycerides – Triglycerides are the major transporters of dietary fats throughout the bloodstream.  Specifically, it is composed of one glycerol molecule that is attached to three fatty acids, hence the term triglyceride. VLDL (very low density lipoproteins) and chylomicrons are made up largely of triglycerides. Besides transporting fat throughout the bloodstream so that it can be used for fuel, triglycerides also store fat in adipose tissue (fat cells) when the body’s demand for fuel is less than what is ingested from diet.


Why Measure Triglycerides?  Elevated triglycerides are a major risk factor for heart disease and diabetes because high serum levels of triglycerides are indicative of abnormal lipoprotein metabolism. Extremely high triglyceride levels (0ver 500mg/dl) can cause pancreatitis. Triglyceride level should fall below 150mg/dl. SInce triglycerides do go up after a meal, they are typically measure after 12 hours of fasting.


Why Are High Triglycerides Harmful?  High triglycerides negatively affect LDL particle size.  Through a complex metabolic interaction, triglycerides promote the formation of small, dense LDL particles, which are particularly atherogenic. Even in the presence of normal LDL cholesterol, patients with high triglycerides typically have endothelial dysfunction, where their blood vessels do not dilate and constrict properly,  In addition, excess triglycerides lower nitric oxide levels and increase many inflammatory compounds further contributing to vascular injury and endothelial dysfunction.


Elevated triglycerides set off a cascade of events that negatively alters a patient’s lipoprotein profile.  For example, elevated triglycerides cause higher excretion rates of apolipoprotein A1 through the kidneys, thus leading to low HDL levels.  This explains the strong inverse relationship between triglycerides and HDL.


How Are Triglycerides Treated?  Diets high in carbohydrates increase triglyceride levels, particularly in those with insulin resistance or obesity.  The glucose from simple carbohydrates is converted to glycerol to form a triglyceride molecule. Specifically, decreasing the amount of ingested simple sugars will usually lower triglyceride levels. Decreasing fat consumption can lower triglyceride level, but not without also decreasing your simple sugar intake.  An increase in the consumption of omega 3 fatty acids, whether from food or supplements can reduce triglyceride level substantially in a dose dependent manner.  Regular exercise also reduces triglyceride levels leading to better energy metabolism overall.  Pharmaceuticals commonly used to lower triglycerides include fenofibrates (such as Tricor or Trilipix) and omega 3 fatty acids.


Non HDL Cholesterol – the non-HDL particle numbers are the best overall indicator of cardiovascular risk.  The lower the better. Non HDL is comprised of LDL and VLDL levels.


RLP (Remnant Lipoprotein) – RLP is a very atherogenic lipoprotein composed primarily of very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL). RLP is considered to be one of the most harmful lipoproteins, RLP is very highly correlated  with cardiovascular disease. In fact, studies show that the composition of arterial plaque closely resembles composition and density of RLP.   Omega-3 fatty acids (fish oils) have been shown to reduce triglycerides and RLP.


Why is RLP So Harmful? Although the RLP is relatively large compared to most LDL particles, it is particularly harmful because unlike LDL particles, which have to undergo oxidation before they can be taken into the arterial intima by macrophage cells, RLP can be readily scavenged by macrophage cell even when they are not oxidized. Once scavenged by a macrophage, RLP is transformed into foam cells which are the building blocks of arterial plaque. In fact, elevated RLP has been found in the survivors of myocardial infarction and persons with significant coronary atherosclerosis.