Carbs, The Foundation of Dirty LDL Cholesterol
Hopefully, by now, we’re comfortable with cholesterol and its importance in the body. What we shouldn’t be comfortable with is the presence of LDL cholesterol in the body and where it comes from. If you haven’t read The value of balancing your cholesterol, you might want to read that first.
In my search to find where fat production starts in the body, what I’ve found, when it comes to LDL, tells me to be aware of Apolipoprotein_B. But before we can look at Apolipoprotein B we need to know what these apolipoproteins are.
Apolipoproteins are the foundation of all lipoproteins.
This is the start of cholesterol, these dictate how cholesterol is carried in your bloodstream. They’re the foundation for HDL particles as well as LDL particles and they also dictate how the cholesterol is going to perform in your body. Here is where it gets interesting, because it’s what kind of cholesterol they’re going to make, that dictates how they are classified. Apolipoproteins are protein cells that bind your fats cells into particles, either high density or low density.
“There are two major types of apolipoproteins. Apolipoproteins B form low-density lipoprotein (“bad cholesterol”) particles. These proteins have mostly beta-sheet structure and associate with lipid droplets irreversibly. Most of the other apolipoproteins form high-density lipoprotein (“good cholesterol”) particles. These proteins consist of alpha-helices and associate with lipid droplets reversibly. During binding to the lipid particles these proteins change their three-dimensional structure. There are also intermediate-density lipoproteins formed by Apolipoprotein E.” These are turned into VLDL.
“The lipid components of lipoproteins are insoluble in water. However, because of their detergent-like (amphipathic) properties, apolipoproteins and other amphipathic molecules (such as phospholipids) can surround the lipids, creating the lipoprotein particle that is itself water-soluble, and can thus be carried through water-based circulation (i.e., blood, lymph).”
These amphipathic or amphiphilic properties tell me why we lose weight when we exercise. Fats are water soluble in the body and the body disposes of fats by using them for energy and disposing of them with HDL particles, to be cleaned out in the liver. I think of the HDL particles as cell scrubbers, cleaning out all the used fats and dirt (foreign contents) any LDL particles might carry into the cell.
Since LDL particles are so much larger than the HDL particles and aren’t as tightly bound, so they tend to let other debris in the blood stream drift in and out the particle. This is where these particles get glycated by the excess glucose in the system. Without the glucose, nothing happens to the cholesterol except that it gets to do its job, fuel the body, create hormones, make vitamin D. But then, usually when there’s no glucose in the system, there’s fewer LDL particles and more HDL particles (the ones that are hard to glycate). This lowers the rate of glycation because of the higher concentration of the HDL particles.
This is how the body disposes of used fats, with HDL particles. It’s the LDL particles that feed the fats into the cells, and it appears that this is where the problem with Apolipoprotein B, comes into play. Apolipoprotein B is sometimes a dirty or glycated protein, meaning that it’s bent so that it can’t be used properly. This is when glucose attacks the lipid before it can be used as fuel. It’s the beginning of plaque, and it’s plaque that’s at the base of over one half of all cancers, cardiovascular diseases, and all brain diseases, like Alzheimer’s disease, Parkinson’s disease, and dementia.
“There are six classes of apolipoproteins and several sub-classes:” All are HDL building apolipoproteins except for Apolipoprotein B, E and L. They’re the ones that build LDL, with B being the one that is the genesis for so many ailments and diseases.
Most apolipoproteins are made in the intestine, however, the Apolipoprotein B is formed in the liver.
I have to wonder if this is where its problems begin. This is why Apolipoprotein B is the basis for so many diseases? Knowing that ApoB is responsible for LDL cholesterol particles tell me why ApoB is responsible for all the disease it causes. It’s that they’re more easily invaded by glucose and that is what glycates the cholesterol, and that is where most of the problems with disease begin.
There are six apolipoproteins
- A (apoA-I, apo A-II, apo A-IV, and apo A-V) – High density
- B (apo B48 and apo B100) – Low Density
- C(apo C-I, apo C-II, apo C-III, and apo C-IV) - High density
- D – High density
- E – Very Low density
- H – High density
“Exchangeable apolipoproteins (apoA, apoC and apoE) have the same genomic structure and are members of a multi-gene family that probably evolved from a common ancestral gene. ApoA1 and ApoA4 are part of the APOA1/C3/A4/A5 gene cluster on chromosome 11.
“Hundreds of genetic polymorphisms of the apolipoproteins have been described, and many of them alter their structure and function.”
“In particular, apoA1 is the major protein component of high-density lipoproteins; apoA4 is thought to act primarily in intestinal lipid absorption.” That tells me that Apolipoprotein A is manufactured in the intestine. This is where fats are digested, the small intestine. That also tells me that the Apolipoprotein B is formed in the liver, the organ that filters the blood.
“Apolipoprotein synthesis in the intestine is regulated principally by the fat content of the diet.
“Apolipoprotein synthesis in the liver is controlled by a host of factors,
including dietary composition, hormones (insulin, glucagon, thyroxin, estrogens, androgens), alcohol intake, and various drugs (statins, niacin, and fibric acids). Apo B is an integral apoprotein whereas the others are peripheral apoproteins.”
It appears that the foundation of HDL type cholesterol particles or Apolipoproteins A, C, D, and H come from the fat you eat, whereas the foundation of LDL type of particles (Apolipoprotein B), comes from many sources, as it’s made in the liver. Maybe it’s polluted Ribosomes that make the protein calls, since they’re made in the liver, rather than in the intestine, like the Apolipoprotein A. Because the liver cleans all the toxins out of the blood, maybe some of the toxins get deposited in some of the Ribosomes the liver manufactures for protein. I don’t know if this is the start of “bad cholesterol” or not, but that’s not the point. The point is that there are too many variables in the manufacture of Apolipoprotein B, from dietary choices to alcohol consumption to hormones and drugs that you take, to make it a steady source of reliable apolipoproteins for consistently healthy cholesterol, thus, “Bad Cholesterol”. This is why, when it comes to LDL, what I have discovered tells me to be aware of Apolipoprotein B and what creates it. So, what does create Apolipoprotein B?
The biggest factor in regulating Apolipoprotein B, it dietary choices, including alcohol consumption. This would entail all consumption of sugars, since we know that fats are responsible for Apolipoprotein A,C, E and H. Since there are only three basic food groups, fats, proteins and carbohydrates, we know that fats are good because they create Apolipoprotein A, proteins are good because they are the basic building blocks or our bodies, leaving sugars or carbohydrates to create Apolipoprotein B….the foundation of most diseases.
Apolipoprotein B and
LDL cholesterol tell me
why it’s so important to
Stay Away From Sugar
Dietary choices and Alcohol consumption both have to deal with sugar in the diet, because the fats in your diet go to make the foundation of HDL particles. It’s the sugar in the diet or the carbs in the diet that make up the Ribosomes that make the proteins that are the foundation of LDL particles. Put plainly, carbs create LDL particles, fat creates HDL particles. That explains why the LDL is so dangerous, its base proteins are apolipoproteins made in an organ that filters blood for the body. As explained by Wikipedia;
“Apo lipoprotein B (ApoB) is a protein that in humans is encoded by the APOB gene. “Apolipoprotein B is the primary apolipoprotein of chylomicrons, VLDL, IDL, and LDL particles (LDL – known commonly by the misnomer “bad cholesterol” when in reference to both heart disease and vascular disease in general), which is responsible for carrying fat molecules (lipids), including cholesterol, around the body (within the water outside cells) to all cells within all tissues. While all the functional roles of ApoB within the LDL (and all larger) particles remains somewhat unclear, it is the primary organizing protein (of the entire complex shell enclosing/carrying fat molecules within) component of the particles and is absolutely required for the formation of these particles. What is also clear is that the ApoB on the LDL particle acts as a ligand for LDL receptors in various cells throughout the body (i.e., less formally, ApoB indicates fat carrying particles are ready to enter any cells with ApoB receptors and deliver fats carried within into the cells).”
The National Institute of Health says about Apolipoprotein B;
“Apolipoprotein (apo) B represents most of the protein content in LDL and is also present in intermediate-density lipoproteins (IDL) and VLDL. ApoA-I is the principal apolipoprotein in HDL. Both apolipoproteins, therefore, separately provide information for detecting high-risk individuals. ApoA-I is also believed to be a more reliable parameter for measuring HDL than cholesterol content since it is not subject to variation. Therefore, the apoB/apoA-I ratio is also highly valuable for detecting atherogenic risk, and there is currently sufficient evidence to demonstrate that it is better for estimating vascular risk than the total/HDL cholesterol ratio.11–14 The apoB/apoA-I ratio was stronger than the total cholesterol/HDL cholesterol and LDL/HDL cholesterol ratios in predicting risk.11 ” Are you beginning to see the value of balance, in your cholesterol?
“This ratio reflects the balance between two completely opposite processes (Figure 1): transport of cholesterol to peripheral tissues, with its subsequent arterial internalization, and reverse transport to the liver.15 Figure 2shows that the greater the apoB/apoA-I ratio, the larger will be the amount of cholesterol from atherogenic lipoproteins circulating through the plasma compartment and likely to induce endothelial dysfunction and trigger the atherogenic process. On the other hand, a lower apoB/apoA-I ratio will lead to less vascular aggression by plasma cholesterol and increased and more effective reverse transport of cholesterol, as well as other beneficial effects, thereby reducing the risk of cardiovascular disease.”
Wikipedia continues to state;
“Through mechanisms only partially understood, high levels of ApoB, especially associated with the higher LDL particle concentrations, are the primary driver of plaques that cause vascular disease (atherosclerosis), commonly first becoming obviously symptomatic as heart disease, stroke & many other body wide complications after decades of progression. There is considerable evidence that concentrations of ApoB and especially the NMR assay (specific for LDL-particle concentrations) are superior indicators of vascular/heart disease driving physiology than either total cholesterol or LDL-cholesterol (as long promoted by the NIH starting in the early 1970s). However, primarily for historic cost/complexity reasons, cholesterol, and estimated LDL-cholesterol by calculation, remains the most commonly promoted lipid test for the risk factor of atherosclerosis. ApoB is routinely measured using immunoassays such as ELISA or nephelometry. Refined and automated NMR methods allow measurement distinctions between the many different ApoB particles.”
“High levels of ApoB are related to heart disease.
Hypobetalipoproteinemia is a genetic disorder that can be caused by a mutation in the ApoB gene, APOB. Abetalipoproteinaemia is usually caused by a mutation in the MTP gene, MTP.
Mutations in gene APOB100 can also cause familial hypercholesterolemia, a hereditary (autosomal dominant) form of metabolic disorder Hypercholesterolemia.”
“Mice overexpressing mApoB have increased levels of LDL “bad cholesterol” and decreased levels of HDL “good cholesterol”. Mice containing only one functional copy of the mApoB gene show the opposite effect, being resistant to hypercholesterolemia. Mice containing no functional copies of the gene are not viable.“
It is well established that ApoB100 levels are associated with coronary heart disease, and are even a better predictor of it than is LDL level. A naive way of explaining this observation is to use the idea that ApoB100 reflects lipoprotein particle number (independent of their cholesterol content). In this way, one can infer that the number of ApoB100-containing lipoprotein particles is a determinant of atherosclerosis and heart disease.”
“ApoB100 is found in lipoproteins originating from the liver (VLDL, IDL, LDL). Importantly, there is one ApoB100 molecule per hepatic-derived lipoprotein. Hence, using that fact, one can quantify the number of lipoprotein particles by noting the total ApoB100 concentration in the circulation. Since there is one and only one ApoB100 per particle, the number of particles is reflected by the ApoB100 concentration. The same technique can be applied to individual lipoprotein classes (e.g. LDL) and thereby enable one to count them as well.”
This tells me that it’s not the amount of cholesterol in your body that’s important. It’s the number of ApoB100 lipoproteins floating around regardless of how much cholesterol is in each individual LDL particle, that’s important. So, what do I need to look out for to keep from building this ApoB100, in my system? What causes ApoB?
“Apolipoproteins are of great physiological importance and are associated with different diseases such as dyslipidemia, cardiovascular and neurodegenerative diseases. Apolipoproteins have therefore emerged as key risk markers and important research targets yet the function of apolipoproteins has not been fully elucidated.” That’s according to Mabtech, they go on to say, “Apolipoproteins are proteins that bind hydrophobic lipids in the blood and help solubilize them. Together with phospholipids, apolipoproteins form lipoprotein particles into which different lipids can be packed. Apolipoproteins have pivotal functions as structural components in lipoprotein particles, ligands to receptors and co-factors to enzymes. Lipoprotein particles are necessary for transportation of lipids used for energy supply and for synthesis of hormones, vitamins and bile acids. ApoB and apoE are important in the transport of dietary and endogenous lipids to peripheral tissues for energy supply, whereas apoA1 is crucial for the returning of excess cholesterol from peripheral tissues back to the liver. Apolipoproteins such as apoE and apoJ are also important for the transportation of lipids in the brain.”
They also added; “There are two major types of apolipoproteins: non-exchangeable and exchangeable. Apolipoprotein B (apoB) is non-exchangeable and anchored in the lipoprotein particle whereas apolipoproteins A, E, D, J and H are exchangeable and can be transferred between different lipoprotein particles. ApoA1 and apoB represent the main protein components of HDL and LDL, respectively.”
With all the different kinds of cholesterol, just lowering it seems to me, to be a little counterproductive. There are just too many good uses for cholesterol to just lower it. In my opinion, that’s like signing your death warrant. One would think that concentrating on the cause of LDL particles would be much more productive than focusing on lowering LDL cholesterol after its arrival.
- Apolipoprotein A, C, D, E, H, L – the genesis of HDL, healthy cholesterol, comes from fats
- Apolipoprotein B – the foundation of LDL cholesterol, comes from primary carbs, and cause too many diseases to list
All cholesterol is so important for fat transportation in our bodies as well as hormone balance, vitamin D production and removing fats from the body, my question is, why would anyone in their right mind, want to lower it when a good balance of cholesterol is so much more important.
Again, I have to thank Wikipedia for their extensive help in putting together this post, Their entries are in quotations marks. I also have an entry directly from the NIH National Library of Medicine website, PubMed. A lot of what is on Wikipedia has shown to be the same as that on PubMed.