Tag Archives: LDL cholesterol

Is Your Type of Heart Disease Curable of Just Treatable?

Can Your Type of Heart Disease be Cured or Just Treated?

Because of the growing list on the Real Poisoning of America – Glycation, it’s become evident that I need to display a different post for the different types of damage that glycation induces. From atherosclerosis and other heart-related diseases, I’ll reserve this notice for that purpose only. All cancer reports will be located on the cancer page.  Dementia will be in a separate post as well with all other diseases and disorders inflammation is responsible for.

The whole premise behind these posts is to prove that the only way you can prevent these horrendous diseases, is to stop the glycation that is responsible for them and the only way you can stop the glycation is to stop feeding it. It’s really a simple solution, just not an easy one because of the addiction factor. However, YOU and only YOU have control over this and it all depends on what YOU put in your mouth when you eat.

I’ll admit that that can be hard when you have a whole industry trying to get you to eat more of what it is that glycates. This is because they are connected to another industry that feeds off of the unsuspected that buy into this ruse, all those whom the glycation affects, the public.                                               Get the whole story!

Listed below from PubMed or PMC or the FDA are reports of studies done on the effects of glycation and its influence in any CVD or disease influenced by inflammation, which is a direct cause of glycation.

Advanced glycation endproducts induce apoptosis of endothelial progenitor cells by activating receptor RAGE and NADPH oxidase/JNK signaling axis.

Elevated levels of advanced glycation endproducts (AGEs) is an important risk factor for atherosclerosis. Dysfunction of endothelial progenitor cells (EPCs), which is essential for re-endothelialization and neovascularization, is a hallmark of atherosclerosis. However, it remains unclear whether and how AGEs acts on EPCs to promote pathogenesis of atherosclerosis. In this study, EPCs were exposed to different concentrations of AGEs. The expression of NADPH and Rac1 was measured to investigate the involvement of NADPH oxidase pathway. ROS was examined to indicate the level of oxidative stress in EPCs. Total JNK and p-JNK were determined by Western blotting. Cell apoptosis was evaluated by both TUNEL staining and flow cytometry. Cell proliferation was measured by (3)H thymidine uptake. The results showed that treatment of EPCs with AGEs increased the levels of ROS in EPCs. Mechanistically, AGEs increased the activity of NADPH oxidase and the expression of Rac1, a major component of NADPH. Importantly, treatment of EPCs with AGEs activated the JNK signaling pathway, which was closely associated with cell apoptosis and inhibition of proliferation. Our results suggest that the RAGE activation by AGEs in EPCs upregulates intracellular ROS levels, which contributes to increased activity of NADPH oxidase and expression of Rac1, thus promoting cellular apoptosis and inhibiting proliferation. Mechanistically, AGEs binding to the receptor RAGE in EPCs is associated with hyperactivity of JNK signaling pathway, which is downstream of ROS. Our findings suggest that dysregulation of the AGEs/RAGE axis in EPCs may promote atherosclerosis and identify the NADPH/ROS/JNK signaling axis as a potential target for therapeutic intervention.

With the list growing past 17,729 studies on the effects of glycation, I think this message about the process of glycation should be wider known. This is the basis of all modern disease. Why has it been kept hidden? Is it due to industrial concerns? What would happen if you wiped 98% of all illness?

This report dictates how the modification of proteins (glycation) is involved in atherosclerosis. Is this the smoking gun that carbs are dangerous foods to eat? Even though this report is from Dec 2016, it only says, again, what hundreds if not thousands of other reports dictate. They all dictate glycation is dangerous. What causes glycation should be avoided at all costs, to ensure optimal health.

Post-translational modification of proteins imparts diversity to protein functions. The process of glycation represents a complex set of pathways that mediates advanced glycation endproduct (AGE) formation, detoxification, intracellular disposition, extracellular release, and induction of signal transduction. These processes modulate the response to hyperglycemia, obesity, aging, inflammation, and renal failure, in which AGE formation and accumulation is facilitated. It has been shown that endogenous anti-AGE protective mechanisms are thwarted in chronic disease, thereby amplifying accumulation and detrimental cellular actions of these species. Atop these considerations, receptor for advanced glycation endproducts (RAGE)-mediated pathways down regulate expression and activity of the key anti-AGE detoxification enzyme, glyoxalase-1 (GLO1), thereby setting in motion an interminable feed-forward loop in which AGE-mediated cellular perturbation is not readily extinguished. In this review, we consider recent work in the field highlighting roles for glycation in obesity and atherosclerosis and discuss emerging strategies to block the adverse consequences of AGEs. This article is part of a Special Issue entitled: The role of post-translational protein modifications on heart and vascular metabolism edited by Jason R.B. Dyck & Jan F.C. Glatz.

This is the smoking gun that proves what glucose consumption does to the body in the form of atherosclerosis. How long before the FDA or the USDA will admit that this is what happens after ingesting grains? Will the Heart Association say anything about this? What about the American Diabetic Association? I wonder if this news will reach any regulatory agency. My guess is if Monsanto has anything to say about it, they’ll say “where’s the money in it.”

This report from Aug 1, 1989, reveals how aware we were then, that glycation is a damaging process that is caused by excess glucose in your system. One would think that 27 and a half years would be long enough to reveal this information. Apparently, it isn’t.

We studied 11 diabetic patients, all of whom had severe atherothrombotic disease, and 11 normal controls. Overall glycation was assessed by the extent of incorporation of [3H]-NaBH4 into fructosyl lysine separated from whole platelet proteins following amino acid analysis. Fructosyl lysine represented 5.7% +/- 1.0 S.D. of the total radioactivity in the normal whole platelet samples. Increased glycation was observed in platelets from 5 of the 11 diabetics. Platelet glycation did not correlate with glycation of hemoglobin or albumin. The pattern of glycation of various platelet proteins in whole platelets, as determined by the incorporation of [3H]-NaBH4 into electrophoretically separated proteins did not display selectivity, although myosin and glycoproteins IIb and IIIa showed relatively increased levels of [3H]-NaBH4 incorporation. Artificially glycated platelet membranes exhibited glycation mainly in proteins corresponding to the electrophoretic mobility of myosin, glycoproteins IIb and IIIa.

The previous report was published in 1989 yet have you heard anything about it? Didn’t they have idea, at that time, what carbs were doing to the body, when ingested? I guess they needed more studies. Over 17,000 of them have been filed as of yet. Why has it taken until 2010 to learn any of this? Even today, they still are reluctant to admit such, that carbs are dangerous foods to be eating.

  • Advanced glycation end products: An emerging biomarker for adverse outcome in patients with peripheral artery disease.

Patients with peripheral artery disease (PAD) suffer from widespread atherosclerosis. Partly due to the growing awareness of cardiovascular disease, the incidence of PAD has increased considerably during the past decade. It is anticipated that algorithms to identify high-risk patients for cardiovascular events require being updated, making use of novel biomarkers. Advanced glycation end products (AGEs) are moieties formed non-enzymatically on long-lived proteins under influence of glycemic and oxidative stress reactions. We elaborate on the formation and effects of AGEs, and the methods to measure AGEs. Several studies have been performed with AGEs in PAD. In this review, we evaluate the emerging evidence of AGEs as a clinical biomarker for patients with PAD.

Peripheral Artery disease is often the start of Atherosclerosis and all CVDs. They are a direct cause of glycation. Glycation is controllable by controlling the number of carbs you put in your mouth every time you eat.

This following study shows how your body reacts to the glucose infusion by sending out macrophages to counteract the damage presented by the glucose. The modified LDL particles are the glycated endproducts of what happens to your cholesterol with glucose in your system.

How do macrophages sense modified low-density lipoproteins?


In atherosclerosis, serum lipoproteins undergo various chemical modifications that impair their normal function. Modification of low density lipoprotein (LDL) such as oxidation, glycation, carbamylation, glucooxidation, etc. makes LDL particles more proatherogenic. Macrophages are responsible for clearance of modified LDL to prevent cytotoxicity, tissue injury, inflammation, and metabolic disturbances. They develop an advanced sensing arsenal composed of various pattern recognition receptors (PRRs) capable of recognizing and binding foreign or altered-self targets for further inactivation and degradation. Modified LDL can be sensed and taken up by macrophages with a battery of scavenger receptors (SRs), of which SR-A1, CD36, and LOX1 play a major role. However, in atherosclerosis, lipid balance is deregulated that induces inability of macrophages to completely recycle modified LDL and leads to lipid deposition and transformation of macrophages to foam cells. SRs also mediate various pathogenic effects of modified LDL on macrophages through activation of the intracellular signaling network. Other PRRs such Toll-like receptors can also interact with modified LDL and mediate their effects independently or in cooperation with SRs.

What you should think about, is what would happen if the glucose weren’t there. The cholesterol can do what it’s supposed to do, feed your body.

From Dec 2016, Coronary Heart Disease and Ischemic stroke are shown to be influenced by another RAGE Gly82ser. How many more of these do they have to find before they realize that you can prevent this by keeping carbs out of the diet?

Association of RAGE gene Gly82Ser polymorphism with coronary artery disease and ischemic stroke: A systematic review and meta-analysis.



The receptor for advanced glycosylation end products (RAGE) has been widely linked to diabetic atherosclerosis, but its effects on coronary artery disease (CAD) and ischemic stroke (IS) remain controversial. The Gly82Ser polymorphism is located in the ligand-binding V domain of RAGE, suggesting a possible influence of this variant on RAGE function. The aim of the present study is to clarify the association between the RAGE Gly82Ser polymorphism and susceptibility to CAD and IS.


The current meta-analysis suggests that the RAGE Gly82Ser polymorphism is associated with an increased risk of CAD and IS, especially in the Chinese population. However, better-designed studies with larger sample sizes are needed to validate the results.

The following report submitted Sep 31, 2011 shows the influence of RAGE in VRD ;

RAGE-dependent activation of the onco-protein Pim1 plays a critical role in systemic vascular remodeling processes.



Vascular remodeling diseases (VRD) are mainly characterized by inflammation and a vascular smooth muscle cells (VSMCs) proproliferative and anti-apoptotic phenotype. Recently, the activation of the advanced glycation endproducts receptor (RAGE) has been shown to promote VSMC proliferation and resistance to apoptosis in VRD in a signal transducer and activator of transcription (STAT)3-dependant manner. Interestingly, we previously described in both cancer and VRD that the sustainability of this proproliferative and antiapoptotic phenotype requires activation of the transcription factor NFAT (nuclear factor of activated T-cells). In cancer, NFAT activation is dependent of the oncoprotein provirus integration site for Moloney murine leukemia virus (Pim1), which is regulated by STAT3 and activated in VRD. Therefore, we hypothesized that RAGE/STAT3 activation in VSMC activates Pim1, promoting NFAT and thus VSMC proliferation and resistance to apoptosis. Methods/Results- In vitro, freshly isolated human carotid VSMCs exposed to RAGE activator Nε-(carboxymethyl)lysine (CML) for 48 hours had (1) activated STAT3 (increased P-STAT3/STAT3 ratio and P-STAT3 nuclear translocation); (2) increased STAT3-dependent Pim1 expression resulting in NFATc1 activation; and (3) increased Pim1/NFAT-dependent VSMC proliferation (PCNA, Ki67) and resistance to mitochondrial-dependent apoptosis (TMRM, Annexin V, TUNEL). Similarly to RAGE inhibition (small interfering RNA [siRNA]), Pim1, STAT3 and NFATc1 inhibition (siRNA) reversed these abnormalities in human carotid VSMC. Moreover, carotid artery VSMCs isolated from Pim1 knockout mice were resistant to CML-induced VSMC proliferation and resistance to apoptosis. In vivo, RAGE inhibition decreases STAT3/Pim1/NFAT activation, reversing vascular remodeling in the rat carotid artery-injured model.


RAGE activation accounts for many features of VRD including VSMC proliferation and resistance to apoptosis by the activation of STAT3/Pim1/NFAT axis. Molecules aimed to inhibit RAGE could be of a great therapeutic interest for the treatment of VRD.

Advanced glycation end products increase lipids accumulation in macrophages through upregulation of receptor of advanced glycation end products: increasing uptake, esterification and decreasing efflux of cholesterol.

Advanced glycation end products increase lipids accumulation in macrophages through upregulation of receptor of advanced glycation end products: increasing uptake, esterification and decreasing efflux of cholesterol.


Previous reports have suggested that advanced glycation end products (AGEs) participate in the pathogenesis of diabetic macroangiopathy. Our previous study have found that AGEs can increase the lipid droplets accumulation in aortas of diabetic rats, but the current understanding of the mechanisms remains incomplete by which AGEs affect lipids accumulation in macrophages and accelerate atherosclerosis. In this study, we investigated the role of AGEs on lipids accumulation in macrophages and the possible molecular mechanisms including cholesterol influx, esterification and efflux of macrophages.


THP-1 cells were incubated with PMA to differentiate to be macrophages which were treated with AGEs in the concentration of 300 μg/ml and 600 μg/ml with or without anti-RAGE (receptor for AGEs) antibody and then stimulated by oxidized-LDL (oxLDL) or Dil-oxLDL. Lipids accumulation was examined by oil red staining. The cholesterol uptake, esterification and efflux were detected respectively by fluorescence microscope, enzymatic assay kit and fluorescence microplate. Quantitative RT-PCR and Western blot were used to measure expression of the moleculars involved in cholesterol uptake, synthesis/esterification and efflux.


AGEs increased lipids accumulation in macrophages in a concentration-dependent manner. 600 μg/ml AGEs obviously unregulated oxLDL uptake, increased levels of cholesterol ester in macrophages, and decreased the HDL-mediated cholesterol efflux by regulating the main molecular expression including CD36, Scavenger receptors (SR) A2, HMG-CoA reductase (HMGCR), ACAT1 and ATP-binding cassette transporter G1 (ABCG1). The changes above were inversed when the cells were pretreated with anti-RAGE antibody.


The current study suggest that AGEs can increase lipids accumulation in macrophages by regulating cholesterol uptake, esterification and efflux mainly through binding with RAGE, which provide a deep understanding of mechanisms how AGEs accelerating diabetic atherogenesis.

This is the proof that AGEs inhibit proper cell nutrition by preventing the flow of cholesterol into the cell. This allows accumulation of LDL particles in your blood. Usually, with a carbohydrate diet, those LDL particles are going to be ApoB particles and those are the most proliferate in all disease. Again, this is something you have full control over, as you don’t have to eat this food. There are plenty of healthier alternatives.

The next study details how glycol-AGEs work their way into the cellular wall of your arteries creating Atherosclerosis. What you should think about is, could this happen without glucose in your system? Can you live without glucose? If you answered YES to both of those questions, you’re on your way to a healthier body.

Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium.

Advanced glycation end-products (AGEs) are involved in the development of vascular smooth muscle cell (VSMC) dysfunction and the progression of atherosclerosis. However, AGEs may indirectly affect VSMCs via AGEs-induced signal transduction between monocytes and human umbilical endothelial cells (HUVECs), rather than having a direct influence. This study was designed to elucidate the signaling pathway underlying AGEs-RAGE axis influence on VSMC dysfunction using a co-culture system with monocytes, HUVECs and VSMCs. AGEs stimulated production of reactive oxygen species and pro-inflammatory mediators such as tumor necrosis factor-α and interleukin-1β via extracellular-signal-regulated kinases phosphorylation and nuclear factor-κB activation in HUVECs. It was observed that AGEs-induced pro-inflammatory cytokines increase VSMC proliferation, inflammation and vascular remodeling in the co-culture system. This result implies that RAGE plays a role in AGEs-induced VSMC dysfunction. We suggest that the regulation of signal transduction via the AGEs-RAGE axis in the endothelium can be a therapeutic target for preventing atherosclerosis.

Do you have any idea of how to regulate the transduction of AGEs? It’s simple, go keto. Will an industry that depends on your illness, tell you that? I seriously doubt it. Since it’s this industry that regulates the regulatory agencies, I doubt that you’ll ever hear it from them. That’s why it’s so important to follow your own advice to stay healthy, stay away from unhealthy substances. Now you know how unhealthy glucose is, simply due to its glycative effects.

Are these enough reports to prove how directly influence diabetes? After reading this can you see the logic in controlling your diabetes by controlling your carb intake? Where are the warnings from the FDA and the USDA? Don’t they care about what they’re recommending? Don’t they understand because of their recommendations, they’re sending millions of Moms and Dads, sisters and brothers, husbands and wives to their slow, expensive, painful deaths?

These are free reports that are available to everyone. All you have to do is search for them at the National Library of Medicine in the National Institute of Health. There are literally 100s of thousands of reports on the effects of glycation that remain hidden in the PubMed and PMC databases except to the few who look through them.  The only ones looking through this database are the drug companies looking for more ways to make money. Nobody is looking to warn anyone of the dangers of this food.

My question is why? The answer I get is, “there’s no money in it”. That’s is why I said in my first book, it would be a shame if profits and money weren’t the primary motivating factors in our society, but they are, and we have to live with it. That’s why I choose not to buy into it. It’s the same choice you have.





Carbs, The Foundation of LDL Cholesterol

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.

LDL cholesterolIn 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.

“Apolipoproteins are proteins that bind lipids (oil-soluble substances such as fat and cholesterol) to form lipoproteins. They transport the lipids through the lymphatic and circulatory systems.:

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., bloodlymph).”

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

“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.[3]

“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 (insulinglucagonthyroxinestrogensandrogens), alcohol intake, and various drugs (statinsniacin, 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 chylomicronsVLDLIDL, 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.1114 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 diseasestroke & many other body wide complications after decades of progression. There is considerable evidence that concentrations of ApoB[1][2] and especially the NMR assay[3] (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.”

“Overproduction of apolipoprotein B can result in lipid-induced endoplasmic reticulum stress and insulin resistance in the liver.[8]

“Mice overexpressing mApoB have increased levels of LDL “bad cholesterol” and decreased levels of HDL “good cholesterol”.[4] 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.[5]

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 (VLDLIDLLDL[9]). 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.

In conclusion,
  • 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.

Curbing Carbs for Diabetes Control

Curbing Carbs for Diabetes Control

As carbs are the major influence in type 2 diabetes, this post deals entirely with type 2 diabetes.health-care-diabetes-info-text-23318754

Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced.[5] There are three main types of diabetes mellitus:

  • Type 1 DM results from the pancreas’s failure to produce enough insulin. This form was previously referred to as “insulin-dependent diabetes mellitus” (IDDM) or “juvenile diabetes”. The cause is unknown.[3]It’s thought that glucose may trigger an auto-immune response that tells the pancreas to not produce insulin, but this was only theory when I last checked.
  • Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[3] As the disease progresses a lack of insulin may also develop.[6] This form was previously referred to as “non insulin-dependent diabetes mellitus” (NIDDM) or “adult-onset diabetes”. The primary cause is excessive body weight and not enough exercise.[3]
  • Gestational diabetes is the third main form and occurs when pregnant women without a previous history of diabetes develop high blood-sugar levels.[3]

Only because of the extra glucose in the bloodstream, is type 2 diabetes called diabetes called diabetes. In all actuality,  is the result of carbohydrate overload, and should be called carbolism. I call it carbolism, simply because of its addictive nature, and how it acts upon the body in the same that alcohol does. Alcohol is, after all, a carbohydrate. As this post is only concerned with type 2 diabetes, gestational diabetes isn’t even looked at in this article.

As described on the Carbs, The Newly Found Death Sentence;

  • Diabetic Lancet Device In Hand Stock Photo
    Is Diabetes Your Goal?

    Type 2 diabetes is caused primarily by carrying extra fat on the body and carbs play a major part in that. Carbs cause diabetes because of their need for insulin to be turned into fat so the body can use it. This is the beginning of a downhill spiral that forces the body to make adjustments that it would never have to do if it were on a diet of protein and fats instead of carbohydrates. Because carbs have to be broken down to their most basic sugar, glucose to be used as a fuel, the glucose flows through your bloodstream before it can be metabolized on a cellular level, to be used for that fuel. Glucose needs insulin, to be turned into fat to be digested, to use for energy. Glucose cannot enter the cell without insulin to turn it into fat. The problem is, most of the glucose after it gets turned into fat, it gets stored as fat in any one of the multitude of fat cells on your body. This takes place in the visceral fat (fat around the internal organs) first and foremost, where it’s the most dangerous. The more carbs you eat, the more insulin your body needs to metabolize those carbs and with a body full of sugar (carbs), you need a lot of insulin to turn all those sugars into fat. After processing a diet full of high carbohydrate food over your lifetime, your body starts to have problems, manufacturing enough insulin, so you can continue to digest the carbs you continue to eat. Because your insulin production can’t keep up with your carb intake, the sugar doesn’t get turned into fat and stays in your bloodstream as sugar. It begins to build up in your blood system and you become diabetic. Hence the name insulin-dependent diabetes or type two diabetes. Remove the carbs, remove the excess blood glucose. If you remove the glucose from the equation, you remove diabetes. If you take away the carbs, you take away the obesity and excess glucose. Can it really be that simple? Duh!

Insulin induces HMG-CoA reductase activity, whereas glucagon diminishes HMG-CoA reductase activity.[42] While glucagon production is stimulated by dietary protein ingestion, insulin production is stimulated by dietary carbohydrate ingestion. The rise of insulin is, in general, determined by the digestion of carbohydrates into glucose and subsequent increase in serum glucose levels. In non-diabetics, glucagon levels are very low when insulin levels are high; however, those who have become diabetic no longer suppress glucagon output after eating.”

I would have used a better choice of words when describing “the digestion of carbohydrates into glucose”, I would have said, “breakdown of carbohydrates into glucose”, as the glucose at this point isn’t digested. It’s just broken down. It doesn’t get digested. Not until it can find a little hormone known as insulin, can it get digested. If it can’t find any insulin, it continues to float around in your bloodstream as glucose, looking for something to attach to.

This is why this disorder is called type 2 diabetes and it has little to do with type 1 diabetes except that it allows glucose to continue to flow in your blood with being turned into fat  Type 1 diabetes is an auto-immune disease that shuts down the manufacture of insulin by the pancreas by destroying the cells where insulin is produced.

The fact that carbs are the major cause of type 2 diabetes, should be a warning to all who continue to eat this food. But what should alarm everyone, is what the excess glucose does, that carbs put into your system because it’s this excess glucose that’s so deadly.

Glucose and cholesterol are the basic building blocks of plaque buildup in your system and it’s this plaque, that kills.

Cholesterol is formed by lipids (fat) clinging to protein cells called apolipoproteins. They come basically in two forms that make up high density and low-density particles, the foundation of cholesterol in your blood. You can read about that on the page about The Foundation of LDL Cholesterol; apolipoprotein B.

It’s excess fat in our bodies that form excess cholesterol in our bodies by providing the fat to be formed into cholesterol, and it’s this excess cholesterol in the form of LDL particles that drives fuel necessary to manifest any one of a multitude of illnesses, disorders, and diseases.

When you combine these two destructive forces of glucose and fat in the body, it’s like two weather systems colliding. Havoc ensues. 

Plaque is by far the worst manifestation of diabetes and a carbohydrate diet. It happens when glucose molecules combine with fat, cholesterol or protein molecules, before they can be utilized by your cells, and displays the true destructive force of glucose on your body.

According to Wikipedia, there are seven different kinds of plaque, AmyloidAtheromaDental plaqueMucoid plaquePleural plaqueSenile plaquesViral plaque. We’re going to look at only 4 of these though.

By far the worst of the plaques caused by digesting wheat and gluten is amyloid plaque, because of all the diseases it has a role in. According to Wikipedia;

  1. Amyloids are insoluble fibrous protein aggregates sharing specific structural traits. They are insoluble and arise from at least 18 inappropriately folded versions of proteins and polypeptides present naturally in the body.[1] These misfolded structures alter their proper configuration such that they erroneously interact with one another or other cell components forming insoluble fibrils. They have been associated with the pathology of more than 20 serious human diseases in that abnormal accumulation of amyloid fibrils in organs may lead to amyloidosis, and may play a role in various neurodegenerative disorders.[2]” The list of diseases caused by amyloid plaque is quite extensive, ranging from Alzheimer’s disease to Diabetes, Parkinson’s and Huntington’s diseases and more. the list on Wikipedia is 21 diseases and disorders or conditions associated with amyloid plaque. In my opinion, amyloid plaque is caused by the digestion of gluten from any source, whether it be wheat, barley or rye. Wikipedia says; “Studies have shown that amyloid deposition is associated with mitochondrial dysfunction and a resulting generation of reactive oxygen species (ROS), which can initiate a signaling pathway leading to apoptosis.[46]” In short amyloid plaque is caused by oxidative stress and cell death, both of which are caused by consumption of gluten and other high starch foods.
  2. Atheromatous Plaques are basically plaques from fats and is the type of plaque that clogs up your artery walls. This is the type of plaque that causes atherosclerosis and leads to heart and cardiovascular disease.
  3. Dental plaque is caused by the excessive amount of sugar on the teeth, creating bacteria, causing decay. (Remember, carbs = sugar.)
  4. Senile plaques (also known as neuritic plaques, senile druse and brain druse) are extracellular deposits of amyloid beta in the grey matter of the brain.[1][2]” 

They cause Alzheimer’s disease and dementia and play a role in most every other cognitive disorder due to the way this plaque gums of the neurons in your brain.

This is why Type 3 diabetes is considered dementia or brain damage and this is the major reason you don’t want to play around with type 2 diabetes, the next step is a loss of your senses, and you won’t even know it, as you won’t realize it as it happens.

Sugar and fat are what cause the plaque buildup

You need both glucose and lipids flowing through your body to create plaque. The glucose attaches itself to a lipid (fat) molecule that has yet to be utilized for energy and glycates that lipid molecule. The lipids, in this case, are LDL cholesterol. Low-density lipoproteins particles.

Because they float around in such loose form, they’re easily attacked by any free-flowing glucose in the system. This is the doom of maintaining a high amount of glucose in the body.

This is the beginning of plaque. Multiply this by the number of carbohydrates you ingest every day. The result is exponentially worse than you would ever want to believe.

So, how do you stop diabetes? It’s actually a simple decision, stop eating foods that contain wheat. The problem is that following through on this decision is it’s the hardest thing you’ll ever have to achieve. The biggest problem is that the worse your addiction is, the harder it is to break the addiction, but also, the more important it is to break the addiction. This could be the worst concern with carbohydrate addiction, there are different degrees of addiction, unlike that of heroin, cocaine, and alcohol. This problem manifests itself when trying to cut back as the greater your addiction is, the harder it will be to eliminate this food from your diet. But, it’s essential that you eliminate it, because if you don’t, the world of hurt described on Carbs, The Newly Found Death Sentence, will follow you until you either die or quit eating that which causes it.

The easiest path to this goal is explained at Carbs, How To Cut Back.