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Historically, LDL-cholesterol, a low-density lipoprotein (LDL) that is attached to cholesterol, has been called the “bad” cholesterol because it has the ability to collect in the walls of the blood vessels and form plaque.
Cholesterol can’t travel on its own. It relies on lipoproteins to move through the blood stream. The two main lipoprotein groups people are familiar with, are HDL (high-density lipoprotein) and LDL (low-density lipoprotein). Most people are aware that HDL is considered "the good cholesterol" and LDL is "the bad cholesterol"; however, there is a lesser-known lipoprotein group that is an important cholesterol marker: lipoprotein(a) or Lp(a). More about Lp(a) later because Lp(a) is a genetically independent risk factor for heart disease.
Low density lipoprotein (LDL) is a carrier protein that carries cholesterol to all areas of the body. Critical for life, vital cholesterol metabolites, are created all over the body in important organs such as the brain, heart, muscles, adrenal glands, gonads and adipose tissue, not to mention, every cell in our body. Once manufactured, cholesterol is transported, attached to its carrier protein, low-density lipoprotein (LDL), all over to do its job with the exception of the brain. The brain is 100% dependent upon cholesterol, BUT makes cholesterol itself, de novo, for all its responsibilities in brain function.
SO why do we think that destroying cholesterol manufacturing in our body with statins makes any sense at all?
Cholesterol - specifically the LDL-cholesterol, literally became a target for destruction for the pharmaceutical world when it was discovered in the 1970's to reside within the the hardened plaque which builds within the arteries. But, the truth then and now is that cholesterol is not the cause for hardening of the arteries, but is ATTACHED to the actual culprit for vascular plaque formation- oxidized low density lipoprotein (LDL). Due to their predisposition to become oxidized, all carrier proteins, such as LDL, are easily changed into free radicals that cause inflammation. The pivotal word here is OXIDIZE. Oxidation occurs easily and naturally inside the body and unfortunately increases with age and is a part of the aging process. In the case of lipoproteins such as LDL, the oxidized LDL attached to cholesterol begins the process of implanting this cholesterol into blood vessels to start hardening of the arteries, known as atherosclerosis, which can lead to heart disease and stroke.
By itself, cholesterol is as innocuous as it is essential for all life processes in our body. Cholesterol cannot form plaque without being altered to do so.
After all, we don’t make cholesterol or carry it around on LDL to make plaque but instead to create essential for life constituents inside our body.
Little PEARL:
Did you know that Vitamin D is made from Cholesterol in the liver and stored in the skin, where the sun activates it?
GOAL:
Reading between the lines here, it can be concluded that:
To best measure our risk of heart disease and stroke associated with cholesterol in the body, rather than finding any clinical value in the Total Cholesterol and LDL-C in the circulation, we should be measuring the LDL particles, as this value measures the risk of circulating cholesterol being oxidized and forming plaque, (hardening of the arteries).
Hence, rather than targeting the well-known LDL-C and striving to lower it with statins, why doesn't your doctor use the decades old now and much more reliable measurement of LDL which does just this:
measures the amount of carrier lipoprotein attached to cholesterol-the LDL-P, also known as the LDL- Particle number. The LDL-P counts the number of LDL particles present in the blood as a total measure of the number of LDL carrier proteins that carry cholesterol throughout the body.
The LDL carrier protein and attached cholesterol - LDL-P moieties - come in different sizes, with some being small and compact, while others are bigger and lighter. Research has demonstrated for decades that smaller, denser LDL particles can burrow themselves into arterial walls and build up plaque far more easily than larger LDL particles.
Small, dense LDL particles contain the most atherogenicity, (i.e. tendency to build plaque) due to their Apo-B protein content and dense, small diameter. More about Apo-B shortly.
Called the small LDL-P, these particles are the most dangerous for various reasons:
- The smaller particles are associated with rapid uptake into the vascular lining (endothelium)
- They are often cleared out of the circulation more slowly
- They are consequently oxidized more easily and hence accelerate the process of hardening of the arteries, known as atherosclerosis.
All I have ever used to analyze cardiovascular risk related to circulating cholesterol is the Liposcience NMR-LipoProfile, which measures the relationship between increased LDL particle number and plaque buildup in the artery wall rather than just the traditional concentration of LDL that is calculated in the blood (LDL-C). The NMR-Lipoprofile is able to measure the atherogenicity, (i.e. tendency to build plaque) of cholesterol circulating in the body. This is our GOAL above.
Dating back to 1999, LipoScience began to offer its flagship product, the NMR LipoProfile blood test, introduced for clinical research in 1997 and use in patient care in 1999. Yes, you read it right...1999.
The NMR-Lipoprofile testing is the missing link to explain the "age-old" question, why people who have low total cholesterol levels and even low total LDL-cholesterol levels can still be at high risk and DO have heart attacks and strokes. The answer lies in the results of those people's NMR-Lipoprofile report: they can and often DO still have a predominance of small - LDL particles in their blood which makes them more susceptible to plaque buildup.
The burning question that should be rising to the surface of your mind right now, is what do I do if I have this predominance of small - LDL particles in my blood which makes me more susceptible to plaque buildup?
This newsletter is already too long and before I answer that question, we need to COMPLETELY analyze your blood for all risk factors!
THEN, we address the problem naturally!
Unlike the Total Cholesterol, LDL-C and HDL as well as Triglyceride numbers that are checked by your doctor, rarely does a doctor look at the small LDL-P level in your blood.
BUT worse is that physicians are so dependent on protocol for everything that is ALL dictated by BIG PHARMA, that doctors refuse to acknowledge that decades of evidence has proven that there are several factors which contribute to cardiovascular disease (CVD) risk beyond the LDL content calculated in the blood and that lowering LDL-C itself does not lower morbity or mortality since the inception of statins in the mid 1970's.
Systemic inflammation and metabolic dysregulation such as seen in Obesity and Diabetes are huge confounding and contributing factors to the myth that the LDL-C (traditional LDL levels looked at in the blood), alone is responsible for CVD. In fact, inflammation, very difficult to directly measure in the blood, is likely the primary cause for CVD and both Diabetes and Obesity cause profound inflammation in the body. This inflammation can be very accurately, albeit indirectly measured by the small—LDL- P levels in the blood as well as the measurement of a specific surface protein on all atherogenic lipoproteins, called the Apolipoprotein B.
Apolipoprotein B
Apo-B 100
ApoB – is THE major structural protein on the surface of all potentially atherogenic lipoprotein-cholesterol particles in the blood - to include LDL, IDI and VLDL.
Years of research tells us that the more appropriate and reliable assessment method for measuring LDL cholesterol and its association with heart disease is measuring the LDL particles rather than the LDL-C in the blood. This is based on many studies over the decades that tell us that “the lipid content” circulating in the blood is secondary to the number of circulating atherogenic particles (LDL, IDL and VLDL) that are trapped within the arterial lumen. This suggests that a focus solely on the measurement of LDL-C is not complete and is at best, misleading due to the now large body of evidence to support the hypothesis that the key initiating event in atherogenesis is the retention of cholesterol-rich apolipoprotein B (apoB)-containing lipoproteins within the arterial wall.
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