Most people have probably been told that to assess their individual risk for coronary heart disease (CHD) then calculated laboratory measurements of LDL-C, HDL-C and total cholesterol must be taken. Ironically, despite established evidence that these are no longer useful or predictive tests, they are still the most commonly used markers to assess CHD risk today.
The lowering of LDL-C, the so-called “bad” cholesterol, has traditionally been used as a target to reduce the incidence of CHD.
By this time in history, we should be asking ourselves (and our physicians) why coronary heart disease (one of the top causes of death in the United States) cannot be prevented with all of the current knowledge and technology we have at our disposal today.
The answer lies in the type of cardiovascular biomarker testing being utilized…or the lack thereof.
It can be argued that premature death from CHD could be prevented with the right biomarker testing and the subsequent diet, lifestyle and supplement interventions needed to improve these biomarkers.
This is what we do at the Drs. Wolfson and we have successful case study after case study to prove the efficacy of this approach.
The true cause of a heart attack is not always what people think.
A heart attack is most often due to small, oxidized cholesterol found in plaques that breaks off and ruptures causing a blood clot. The blood clot then obstructs the artery and impairs blood flow to the heart.
This type of “damaged” (oxidized) cholesterol is not tested for in the majority of the conventional medicine offices today.
Cholesterol that is circulating in the blood does not cause plaque formation unless it lodges itself into arterial walls. This is why traditional cholesterol testing metrics are inaccurate and misleading. There are so many individuals who have died from CHD whose pre-death cholesterol levels were considered “normal”.
To understand the importance of all of this, we must first distinguish between the outdated testing used (LDL-C) and the testing that should be utilized (LDL particle number, or LDL-P).
LDL-C, or calculated LDL cholesterol level, is a measurement of the mass of cholesterol within an LDL particle. It is considered a traditional test and we view it as no longer useful or reliable.
LDL-P refers to the amount of LDL particles, or particle number. LDL-P is the sum of large LDL-P plus small LDL-P. Total LDL-P is therefore most greatly influenced by small LDL-P (the smaller they are, the more particles you will have, which drives up total LDL-P number).
Due to the fact that LDL-C has long been the go-to measurement, LDL-C (calculated low density lipoprotein cholesterol) and LDL (low density lipoprotein) have become synonymous. This is inaccurate and misleading, however, because the amount of cholesterol in LDL varies significantly and is therefore not a reliable marker of true low-density lipoprotein levels.
Thus, LDL-C is only a proxy for true LDL levels. Additionally, LDL particles also carry triglycerides. So, if an LDL particle is rich in extra triglycerides, it could have lesser amounts of cholesterol. If this was the case, then the body would need more LDL particles to carry the cholesterol-depleted but triglyceride-rich LDL’s. Research has shown that if there are excess triglycerides, the result is increased amounts of smaller LDL particles (and increased risk of CVD).
Scientific evidence has therefore revealed that the risk for cardiovascular disease is more accurately predicted by the number of LDL particles as opposed to the total amount of cholesterol within these particles. This makes sense. If there is an increased amount of smaller LDL particles, then there is a much greater chance of these small molecules lodging themselves into the arterial wall.
Other markers of great importance would be Apo B. Apo B is the main structural protein found on the surface of beta-lipoproteins including chylomicrons, VLDL, IDL and LDL. Beta-lipoproteins are capable of moving cholesterol into the artery wall. So, high numbers of Apo B are very predictive of atherosclerotic risk.
Both Apo B and LDL-P are indicative of atherogenic lipoprotein particles and risk and should be utilized together.
The most common condition underlying elevated LDL particle number and Apo B is insulin resistance (IR).
In patients who have IR, excess sugar gets converted to triglycerides and triglycerides begin to make up the majority of the LDL particle. This significantly elevates LDL-P (as stated earlier). Again, if triglycerides are high, it means that it takes many more LDL particles to transport a given cholesterol molecule, thus driving up LDL particle number.
A patient cannot have atherosclerosis unless they have a buildup of cholesterol in their artery wall. So, the question therefore should be: how does cholesterol get into artery walls?
In order to understand this mechanism, we must first understand that cholesterol is a lipid (or fat) and therefore it does not like water. Cholesterol must be packaged into protein-wrapped “transport vehicles” called lipoproteins to move through the watery blood.
Atherosclerosis is very much a lipoprotein-mediated disease.
Cholesterol can come out of cells, travel in lipoproteins and settle into arterial walls. This is the only way that cholesterol gets into arteries.
Therefore, the best testing to predict CVD risk is to assess the number of lipoproteins that can collide into the artery wall. Again, this would be LDL-P testing and Apo B testing. Why? The more particles you have (and the smaller they are) the greater the chances they can crash into arterial walls.
This is the testing that should now be a standard of care used by all physicians.
At the Drs. Wolfson, we know that in order to prevent and treat CHD, this advanced cardiovascular biomarker testing must be utilized. If you’re interested in learning more about our heart attack prevention and recovery testing panel, click here.
Discordance occurs when there is a lack of consistency between LDL-C (traditional) testing and LDL-P testing. When LDL-C is high, and LDL-P is low, this is discordance (and vice versa).
This is why it is imperative to not “trust” conventional testing. If LDL-C is high, and your cardiologist puts you on a statin then you’ve got a problem. You should be asking your cardiologist to verify what your particle number is. And if LDL-P is still elevated, then seek out appropriate treatments.
It should be noted that statins tend to lower LDL-C more greatly than LDL-P (aka they don’t really have an effect on LDL particle number). Therefore, many people who have their LDL-C levels lowered with statins could still have high LDL-P and have a significant cardiac risk.
This is why we see individuals who are on statins still experiencing cardiovascular events. The therapies to treat these two are different. Therapeutic interventions that best reduce LDL-P include omega 3 fatty acids, niacin, the Paleo diet (a low carbohydrate diet), healing insulin resistance and physical activity.
Carbohydrate restriction (found on a Paleo diet) reduces LDL-P and Apo B. Carbohydrate restriction is one of the best tools to reduce LDL-P number.
Fatty fish like wild salmon. sardines, and anchovies are superfoods for heart, brain and total body health. We recommend 3-5 servings or MORE per week. We trust Vital Choice for our seafood needs.
Fasting is a proven method to lower LDL particle number and Apo B. Read more about the heart health benefits of fasting here.
High dose your omega 3 fatty acids! Our Omega DHA 2-4 caps per day does wonders.
Physical activity can help to lower LDL-P and Apo B.
The sun’s rays convert excess cholesterol in skin to vitamin D. Get a minimum of 30 minutes of sunshine daily for your cardiovascular health.
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