If you want to understand the true cause of heart disease and many diseases related to poor vascular health, this is a "must-read."
Here are the highlights.
LEWIS COMMENT: The small particles are the problem - or are they? It's clear they are formed and respond to an "insult," a.k .a. toxicity of some type. What are the toxins, and what is the way to reduce heart disease? THIS IS VERY IMPORTANT...
LOWER YOUR SUGARS - LOWER YOUR HEART DISEASE RISK
LOWER INFECTION - LOWER YOUR HEART DISEASE RISK
LOWER LDL - RAISE YOUR HEART DISEASE RISK.
WHY? THEY ARE THERE RESPONDING TO THESE ROOT-CAUSE PROBLEMS - SUGARS AND INFECTION (AND THESE 2 GO HAND-IN-HAND. THE SMALL PARTICLES ARE NOT THE ROOT CAUSE - SUGARS AND INFECTIONS ARE.
INTRODUCTION
Because lipids (fats), such as cholesterol and triglycerides, are insoluble in water, these lipids must be transported in association with proteins (lipoproteins - LDL, HDL) in the circulation.
To avoid toxicity, large quantities of fatty acids from meals must be transported as triglycerides.
These lipoproteins play a key role in the absorption and transport of dietary lipids by the small intestine, in the transport of lipids from the liver to peripheral tissues, and the transport of lipids from peripheral tissues to the liver and intestine (reverse cholesterol transport).
LEWIS COMMENT: LDL transports fats from the liver - HDL transports fats back to the liver
A secondary function is transporting toxic foreign hydrophobic and amphipathic compounds, such as bacterial toxins, from areas of invasion and infection (1).
LEWIS COMMENT: This is why HDL is so important - it detoxifies your body from what is called LPS.
LEWIS COMMENT: LDL is important because bacterial toxins create cellular damage, and LDL carries fats that repair and build new cell membranes destroyed by the toxins.
For example, lipoproteins bind endotoxin (LPS) from gram-negative bacteria and lipoteichoic acid from gram-positive bacteria, thereby reducing their toxic effects (1). In addition, apolipoprotein L1, associated with HDL particles, has lytic activity against the parasite Trypanosoma brucei brucei and lipoproteins can neutralize viruses (2,3).
LEWIS COMMENT: If you saw testing results on people I work with, you would see that viral burden is prolific, especially in people with chronic fatigue and sleeplessness.
Thus, while this article will focus on the transport properties of lipoproteins, the reader should recognize that lipoproteins may have other important roles.
STRUCTURE OF LIPOPROTEINS (4)
Lipoproteins are complex particles with a central hydrophobic core of non-polar lipids, primarily cholesterol esters and triglycerides. This hydrophobic core is surrounded by a hydrophilic membrane consisting of phospholipids, free cholesterol, and apolipoproteins (Figure 1). Plasma lipoproteins are divided into seven classes based on size, lipid composition, and apolipoproteins (Table 1 and Figure 2).
Chylomicrons (5)
These are large triglyceride-rich particles made by the intestine, which transport dietary triglycerides and cholesterol to peripheral tissues and the liver. These particles contain apolipoproteins A-I, A-II, A-IV, A-V, B-48, C-II, C-III, and E. Apo B-48 is the core structural protein and each chylomicron particle contains one Apo B-48 molecule. The size of chylomicrons varies depending on the amount of fat ingested. A high-fat meal forms large chylomicron particles due to the increased amount of triglyceride being transported. In contrast, the chylomicron particles are small in the fasting state, carrying decreased triglyceride quantities. The quantity of cholesterol carried by chylomicrons also can vary depending on dietary intake.
LEWIS COMMENT: Medicine worries about "cholesterol" but NOT the actual cholesterol molecule. They measure lipoproteins to assert you have "high cholesterol." However, it is quite clear that The quantity of cholesterol carried by chylomicrons can also vary depending on dietary intake.
INTERPRETATION: Medicine does NOT have a clue as to your real cholesterol value.
Very Low-Density Lipoproteins (VLDL)
These particles are produced by the liver and are triglyceride rich. They contain apolipoprotein B-100, C-I, C-II, C-III, and E. Apo B-100 is the core structural protein and each VLDL particle contains one Apo B-100 molecule. Similar to chylomicrons the size of the VLDL particles can vary depending on the quantity of triglyceride carried in the particle. When triglyceride production in the liver is increased, the secreted VLDL particles are large. However, VLDL particles are smaller than chylomicrons.
LEWIS COMMENT: LabCorp presents the VLDL value (sometimes), but the triglyceride value is essentially the same - they track 1 for 1.
Removing triglycerides from VLDL by muscle and adipose tissue forms IDL particles, which are enriched in cholesterol.
LEWIS COMMENT: Hmmm... I wonder why the cholesterol would be high in muscle tissue. I believe in God and nature; they are there for a reason. Could this be why statins cause muscle pain? Could it be beyond the reduction of CoQ10? Cholesterol repairs. If you cannot repair muscle due to a lack of cholesterol, then an energy crisis results (like the pain you experience when your body is repairing a wound). Statins cause muscle pain - and lowering LDL may be part of the reason.
Low-Density Lipoproteins (LDL)
These particles are derived from VLDL and IDL particles and they are even further enriched in cholesterol. LDL carries the majority of the cholesterol that is in the circulation. The predominant apolipoprotein is B-100 and each LDL particle contains one Apo B-100 molecule. LDL consists of a spectrum of particles varying in size and density.
An abundance of small dense LDL particles are seen in association with hypertriglyceridemia, low HDL levels, obesity, type 2 diabetes (i.e., patients with metabolic syndrome), and infectious and inflammatory states. These small, dense LDL particles are considered to be more pro-atherogenic than large LDL particles for a number of reasons (8). Small dense LDL particles have a decreased affinity for the LDL receptor, resulting in a prolonged retention time in the circulation. Additionally, they more easily enter the arterial wall and bind more avidly to intra-arterial proteoglycans, which trap them in the arterial wall. Finally, small, dense LDL particles are more susceptible to oxidation, which could enhance macrophage uptake.
LEWIS COMMENT: The small particles are the problem - or are they? It's clear they are formed and respond to an "insult," a.k .a. toxicity of some type. What are the toxins, and what is the way to reduce heart disease? THIS IS VERY IMPORTANT...
LOWER YOUR SUGARS - LOWER YOUR HEART DISEASE RISK
LOWER INFECTION - LOWER YOUR HEART DISEASE RISK
LOWER LDL - RAISE YOUR HEART DISEASE RISK.
WHY? THEY ARE THERE RESPONDING TO THESE ROOT-CAUSE PROBLEMS - SUGARS AND INFECTION (AND THESE 2 GO HAND-IN-HAND. THE SMALL PARTICLES ARE NOT THE ROOT CAUSE - SUGARS AND INFECTIONS ARE.
High-Density Lipoproteins (HDL) (9-11)
These particles play an important role in reverse cholesterol transport from peripheral tissues to the liver, which is one potential mechanism by which HDL may be anti-atherogenic.
In addition, HDL particles have anti-oxidant, anti-inflammatory, anti-thrombotic, and anti-apoptotic properties, which may also contribute to their ability to inhibit atherosclerosis.
LEWIS COMMENT: Is it the HDL that protects your heart or is it the contents of the HDL particles - particularly the cholesterol? This paper may convince you that it is the cholesterol contents.
HDL particles are enriched in cholesterol and phospholipids. Apolipoproteins A-I, A-II, A-IV, C-I, C-II, C-III, and E are associated with these particles. Apo A-I is the core structural protein and each HDL particle may contain multiple Apo A-I molecules.
In addition, using mass spectrometry, proteins involved in proteinase inhibition, complement activation, and the acute-phase response are associated with HDL particles (12).
There is much more information on lipids and lipoproteins to unpack, but this is enough for one blog. More to come in future blogs.
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