Tag Archives: heart failure

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 and Their Influence in Heart Disease

Carbs and Their Influence in Heart Disease

With the rise in cardiovascular disease and heart disease and the deaths occurring from it, it’s a wonder that this major cause of it is still allowed to be advertised, as much as it is. With over 17,300,000 deaths alone, in 2013, our society thinks it’s more important to find new drugs to suppress the symptoms instead of finding a lasting cure, that doesn’t include any drugs at all. I guess there’s no money in it.

Carbohydrate influence in many heart diseases is clearly undeniable. Whereas cancer is a catch-all term, for a myriad of diseases, heart disease, and cardiovascular diseases are catch-all phrases for all diseases involving the heart and circulatory system. That alone makes it difficult, to nail down any one agent, source or reason for its pervasiveness in these diseases. Yet, there is one common thread that shows up in at least half of these diseases – inflammation. Inflammation’s largest contributor is glucose. Glucose’s largest contributor is carbs. They’re woven from two strands, sugar and flour – grain-based products from wheat (gluten ), corn, rice and oats in particular. This article is going to look at carbs influence on as many cardiovascular diseases as we can and I’m going to talk about carbs influence, in each one, again showing just how dangerous these food staples (flour and sugar) are. (Of course, when I mention flour, I’m talking about all wheat and grain products, because the two most prevalent, wheat and corn, are ground into flour before their preparation, to make into foods, before marketing.) It’s this grinding into flour that takes away any fiber that the food ever had. Flour and water make paste which is so quick to digest and break down to its basic form, glucose, that it loses any nutrition that it ever held. To get a better idea of the scope of cardiovascular diseases and the role carbs play in each one, I’ll list as many of them as I can, and attempt to tie each disease to what influences it most.

There are many cardiovascular diseases involving the blood vessels. They are known as vascular diseases as well as cardiovascular diseases.

Vascular diseases include:

  • Coronary artery disease(also known as coronary heart disease and ischemic heart disease)
  • Peripheral arterial disease– disease of blood vessels that supply blood to the arms and legs
  • Cerebrovascular disease– disease of blood vessels that supply blood to the brain (includes stroke)
  • Renal artery stenosis
  • Aortic aneurysm

There are also many cardiovascular diseases that involve the heart and since all vascular diseases deal with plaque in the arterial walls, we going to be looking at the ones that deal with the heart itself; “Together they resulted in 17.3 million deaths (31.5%) in 2013 up from 12.3 million (25.8%) in 1990.

With an increase like this, don’t you think it’s time for a cure?

  1. Cardiomyopathy– diseases of cardiac muscle
  2. Hypertensive heart disease– diseases of the heart secondary to high blood pressure or hypertension
  3. Heart failure
  4. Pulmonary heart disease– a failure at the right side of the heart with respiratory system involvement
  5. Cardiac dysrhythmias– abnormalities of heart rhythm
  6. Inflammatory heart disease
  7. Endocarditis– inflammation of the inner layer of the heart, the endocardium. The structures most commonly involved are the heart valves.
  8. Inflammatory cardiomegaly
  9. Myocarditis– inflammation of the myocardium, the muscular part of the heart.
  10. Valvular heart disease
  11. Congenital heart disease– heart structure malformations existing at birth
  12. Rheumatic heart disease– heart muscles and valves damage due to rheumatic fever caused by Streptococcus pyogenes a group A streptococcal infection

“There are several risk factors for heart diseases: age, gender, tobacco use, physical inactivity, excessive alcohol consumption, unhealthy diet, obesity, family history of cardiovascular disease, raised blood pressure (hypertension), raised blood sugar (diabetes mellitus), raised blood cholesterol (hyperlipidemia), psychosocial factors, poverty and low educational status, and air pollution. While the individual contribution of each risk factor varies between different communities or ethnic groups the overall contribution of these risk factors is very consistent.[18] Some of these risk factors, such as age, gender or family history, are immutable; however, many important cardiovascular risk factors are modifiable by lifestyle change, social change, drug treatment and prevention of hypertension, hyperlipidemia, and diabetes.”

To take a closer look at each one, you need to examine the risk factor I consider the most important, lifestyle. When I talk about lifestyle, I’m talking mostly about eating habits and the foods that we ingest the most, simple carbohydrates. As mentioned before, and it’s something that you all know, you are what you eat. You know that sugar kills. Carbohydrates are sugars amplified. The term carbohydrate is defined as a multiple sugars and this is what makes it so dangerous. It’s its ability to be turned into glucose, with little to no other nutritional value. That is precisely what makes it so deadly.

Just looking through the various causes of the different types of cardiovascular disease, was enlightening, to say the least. What I found to be a prevalent factor, throughout many of the causes for many of the diseases, was evidence of carbohydrate consumption, so I attempt to point out the fact that if this one factor was taken out of the equation of heart disease, that would change the end result of the equation.

Only by looking at each one individually and learning, will we know;

  • Cardiomyopathy– literally “heart muscle disease”) is the measurable deterioration for any reason of the ability of the myocardium (the heart muscle) to contract, usually leading to heart failure. Common symptoms include dyspnea (breathlessness) and peripheral edema (swelling of the legs). Those with cardiomyopathy are often at risk of dangerous forms of irregular heart rate and sudden cardiac death. The most common form of cardiomyopathy is dilated cardiomyopathy.Although the term “cardiomyopathy” could theoretically apply to almost any disease affecting the heart, it is usually reserved for “severe myocardial disease leading to heart failure.” Cardiomyopathy and Myocarditis resulted in 443,000 deaths in 2013, up from 294,000 in 1990. Of all the types shown on Wikipedia, only the last one was obesity-related, as “Obesity-associated Cardiomyopathy”. We all know what causes obesity – carbs.
  • Hypertensive heart disease– diseases of the heart secondary to high blood pressure or hypertension. Hypertension or high blood pressure affects at least 4 billion people worldwide. Hypertensive heart disease is only one of several diseases attributable to high blood pressure. Other diseases caused by high blood pressure include ischemic heart disease, stroke, peripheral arterial disease, aneurysms and kidney disease. Hypertension increases the risk of heart failure by two or three-fold[6]and probably accounts for about 25% of all cases of heart failure.[15]In addition, hypertension precedes heart failure in 90% of cases,[6] and the majority of heart failure in the elderly may be attributable to hypertension. Hypertensive heart disease was estimated to be responsible for 1.0 million deaths worldwide in 2004 (or approximately 1.7% of all deaths globally), and was ranked 13th in the leading global causes of death for all ages. A world map shows the estimated disability-adjusted life years per 100,000 inhabitants lost due to hypertensive heart disease in 2004. The risk of cardiovascular disease and death can be reduced by lifestyle modifications, including dietary advice, promotion of weight loss and regular aerobic exercise, moderation of alcohol intake and cessation of smoking. Drug treatment may also be needed to control the hypertension and reduce the risk of cardiovascular disease,[6]manage the heart failure, or control cardiac arrhythmias. Patients with hypertensive heart disease should avoid taking over the counter non-steroidal anti-inflammatory drugs (NSAIDs), or cough suppressants, and decongestants containing sympathomimetics, unless otherwise advised by their physician as these can exacerbate hypertension and heart failure.

To get an idea of how carbs influence hypertension, read article 7. My abstinence from carbs for the last two years has given me, for the first time in my adult life, absolutely perfect blood pressure, 120/60. And I attribute it to the lack of carbs in my diet plus the conversion of my diet to a ketogenic diet. My doctor told me I still have high blood pressure (it used to always run high). I just control it better now. Even she is astounded by what my diet has done for my health.  I know what causes high blood pressure more than anything else, carbs. High blood pressure is a major influence on most types of cardiovascular disease, as you’ll see in the following explanations of various forms of heart disease.

  • Heart failure often referred to as congestive heart failure(CHF), occurs when the heart is unable to pump sufficiently to maintain blood flow to meet the body’s needs. The terms chronic heart failure (CHF) or congestive cardiac failure (CCF) are often used interchangeably with congestive heart failure. Signs and symptoms commonly include shortness of breath, excessive tiredness, and leg swelling.[5] The shortness of breath is usually worse with exercise, while lying down, and may wake the person at night.[5] A limited ability to exercise is also a common feature. The underlying mechanisms vary depending on the disease in question. Coronary artery disease, stroke, and peripheral artery disease involve atherosclerosis. This may be caused by high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, and excessive alcohol consumption, among others. High blood pressure results in 13% of CVD deaths, while tobacco results in 9%, diabetes 6%, lack of exercise 6% and obesity 5%. Rheumatic heart disease may follow untreated strep throat.

“It is estimated that 90% of CVD is preventable. Prevention of atherosclerosis is best done by decreasing risk factors through; healthy eating, exercise, avoidance of tobacco smoke and limiting alcohol intake.  Treating high blood pressure and diabetes may be most beneficial.

Common causes of heart failure include coronary artery disease including a previous myocardial infarction (heart attack), high blood pressure, Atrial fibrillation, Valvular heart disease, excess alcohol use, infection, and Cardiomyopathy of an unknown cause. These cause heart failure by changing either the structure or the functioning of the heart.[5] There are two main types of heart failure: heart failure due to left ventricular dysfunction and heart failure with normal ejection fraction depending on if the ability of the left ventricle to contract is affected, or the heart’s ability to relax.  The severity of disease is usually graded by the degree of problems with exercise. Heart failure is not the same as myocardial infarction (in which part of the heart muscle dies) or cardiac arrest (in which blood flow stops altogether). Other diseases that may have symptoms similar to heart failure include obesitykidney failure, liver problems, anemia and thyroid disease.”

A majority of inflammation and plaque that builds up in the blood is directly due to oxidative stress and the byproducts it produces, free radicals in the form of cytokines that form macrophages, that wreak real havoc in all systems.

With all the cytokine activity going on in the blood, I wonder if the influence of glucose on our hormones (hormones are what influences thyroid disease), doesn’t also have an influence in thyroid disease? We know that carbs influence our hormones. We learn that in The Payoff Of Life Without Carbs, as well as Carbs, Why The Addiction Is So Hard To Break,  and touched on it in Carbs, How They Cause A.G.E.s, Your Ticket To Alzheimer’s Disease, Cancer, Heart Disease and More I don’t think too many studies were done on the influence that carbohydrates have on the hormones that affect thyroid disease. Other forms display the influence of carbs a lot more, with inflammation.

  • Pulmonary heart disease– a failure at the right side of the heart with respiratory system involvement
  • Cardiac dysrhythmias– abnormalities of heart rhythm
  • Inflammatory heart disease
  • Endocarditis– inflammation of the inner layer of the heart, the endocardium. The structures most commonly involved are the heart valves.
  • Inflammatory cardiomegaly
  • Myocarditis– inflammation of the myocardium, the muscular part of the heart.
  • Valvular heart disease is any disease process involving one or more of the four valves of the heart(the aortic and mitral valves on the left and the pulmonary and tricuspid valves on the right). These conditions occur largely as a result of aging. Most people are in their late 50s when diagnosed, and more than one in ten people over 75 have it.
  • Congenital heart disease– heart structure malformations existing at birth
  • Rheumatic heart disease– heart muscles and valves damage due to rheumatic fever caused Rheumatic fever is a disease of inflammation. Nothing more needs to be said because we know what causes inflammation.

I can see where glucose plays a major part in more than a few of these causative factors. We know that glucose is the major player in high blood pressure because of the way it’s digested into fat. We know that wheat has a propensity to cause muscle tics and spasms. The question I ask myself is, why can’t wheat affect the heart muscle as what happens with Atrial Fibrillation when the heart starts to race for no apparent reason?

“Heart failure may also occur in situations of “high output,” (termed “high output cardiac failure”) where the ventricular systolic function is normal but the heart cannot deal with an important augmentation of blood volume.  This can occur in overload situation (blood or serum infusions), kidney diseases, chronic severe anemia, Beriberi (vitamin B1/thiamine deficiency),  Thyrotoxicosis, Paget’s disease, Arteriovenous fistulae, or Arteriovenous malformations.”

“Viral infections of the heart can lead to inflammation of the muscular layer of the heart and subsequently contribute to the development of heart failure. Heart damage can predispose a person to develop heart failure later in life and has many causes including systemic viral infections (e.g., HIV), chemotherapeutic agents such as daunorubicin and trastuzumab, and abuse of drugs such as alcohol and methamphetamine. Additionally, infiltrative disorders such as amyloidosis and connective tissue diseases such as systemic lupus erythematosus have similar consequences. Obstructive sleep apnea (a condition of sleep wherein disordered breathing overlaps with obesity, hypertension, and/or diabetes) is regarded as an independent cause of heart failure.”

Inflammation is a major influence in most of the various types of heart disease as well as cancer. The number one cause of inflammation is overeating and obesity; with the closer to obese your body is, the more inflammation you get to deal with. We know that overeating is heavily influenced by carbohydrate consumption. We know that carbohydrates are the direct cause of body fat. We know that the most dangerous of these fats, is visceral fat, the kind your body deposits, from eating carbohydrates. Since we know all of the above, why haven’t we figured out that keeping this food out of our diet will eliminate 90% of the reasons for inflammation?

I remember learning about amyloids and amyloidosis when researching cancer. It’s the folding of misshaped proteins caused by glycation of cholesterol, which in turn, is caused by consumption of carbohydrates. It seems everywhere I look I see evidence of carbohydrate consumption involved in the equation too many types of cardiovascular disease. How much closer would the reduction of carbohydrate consumption bring us to controlling these epidemics? That begs the question, in whose interest is it, that we continue going down this path, we’re on. What corporate industries would rather we stay on this path?

How many more people have to die before the rest of us will heed these words? I know why the general public can’t. I know why they don’t want to pay attention to this. It’s called addiction. It’s called denial of addiction. The first people to deny this are quite often the ones who have it worst and are in complete denial that this would ever happen to them. This is a denial that we as a society need to face. I know. I was there. I denied it. Read my story in About Me, How hard it is for me to appear normal.

I weighed 205 lbs just 3 years ago. My blood pressure averaged 140/90. I controlled it with diuretics which depleted my body of potassium and calcium, both crucial micronutrients for a healthy heart. Then, I quit bread, alone. Then I quit all wheat products. That started a cascade of miraculous things that began to happen to my health. And they all happened in beneficial ways removing any side effects (from wheat consumption), that existed prior to my conversion. I’m as normal of a person as you can get. If this can happen to me, it will happen to anyone who does the same thing that I did.

I ask myself, why is this food still advertised as “healthy”?

This truly begs the question, if this food staple was replaced in our food supply, with something more nutritious and less glycemic, would we see a decline in the occurrences of these horrendous diseases? This is my biggest what if question, what if society saw the truth and reality in what is really going on when you eat high starch carbohydrate grains and foods and started to reduce their consumption of these foods, would we see a decline in these diseases? I don’t just think so, I know from experience, that it will. Science says, yes it definitively will.

The question is, will this (food) industry allow us to do that? I seriously doubt they’ll do anything about it if it’s going to hurt their business in any way. Alternatives need to be found for this food staple, not only in our diet but in our food industry as a whole. We must make it evident, to the food industrial complex that we need to reduce our consumption of these high starch foods, if we’re to remain healthy as a society. Where are the warnings: contains glucose? Where does the responsibility lie with the food industry, the grain industry, in particular, those who provide the crop seed for our farmers who grow this food for us. Isn’t it about time they took responsibility for the damage their food is responsible for, diabetes, heart disease and cancer it causes?

That’s going to be a really fun one to tackle, but I try on Carbs, Industry Concerns Of Dispelling Wheat And Grains and Carbs, Industry’s Influence In The Expansion Of Carb Production, Carbs, Why The Addiction Is So Hard To Break, and Carbs! My Life Without Them.

Editing note; Thank you immensely to Wikipedia. Even though it is an open source encyclopedia, I trust their sources to be correct, as all documents on Wikipedia are vetted by volunteer experts in that particular field. Wikipedia’s comments are italicized, while all of my comments are not. I did this to keep everything organized so people can decipher encyclopedic fact from my comments and conjecture.

Carbs, How They Create AGEs Your ticket to Alzheimer’s Disease, Cancer, Heart Disease and more

How Carbs Create AGEs Your ticket to Alzheimer’s Disease, Cancer, Heart Disease and more

AGES are the single, most influential, factor in what ages us and
are responsible for a majority of the illness and disease that we live with today. Dr. Perlmutter explains it much better in his book Grain Brain in chapter 4, starting on page 99, about Advanced Glycation End-products.

According to Wikipedia;

“In human nutrition and biology, advanced glycation end products, known as AGEs, are substances that can be a factor in the development or worsening of many degenerative diseases, such as diabetes, atherosclerosis, chronic renal failure, and Alzheimer’s disease.[1]

Before we continue on with this post, a disclaimer: all paragraphs that are blocked in quotations marks, are all copied directly from Wikipedia, Grain Brain or Wheat Belly. I did this on numerous passages on this post for the purpose of expediency. I apologize; my time is too limited to deconstruct everything I use from those indispensable sources. With that said, it’s time to get started;

Wikipedia goes on to say,

“These harmful compounds can affect nearly every type of cell and molecule in the body and are thought to be one factor in aging and in some age-related chronic diseases. They are also believed to play a causative role in the blood-vessel complications of diabetes mellitus. AGEs are seen as speeding up oxidative damage to cells and in altering their normal behavior.”

The questions this conjures, is, whatever could cause these damaging substances? They’re a normal part of aging but what amplifies their behavior is a part of our diet that’s been with us forever, carbohydrates, plain and simple. I understand why this is hard for you to accept, so we’ll go through all of the effects they cause and look at what wheat and gluten play in each part.

AGEs have a range of pathological effects, such as:[25][26]

Oxidative stress is caused by “Glycation (sometimes called non-enzymatic glycosylation) is the result of typically covalent bonding of a protein or lipid molecule with a sugar molecule, such as fructose or glucose, without the controlling action of an enzyme.”

“Some AGEs are benign, but others are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as cardiovascular diseases (the endothelium, fibrinogen, and collagen are damaged), Alzheimer’s disease (amyloid proteins are side-products of the reactions progressing to AGEs),[8][9] cancer (acrylamide and other side-products are released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination). This range of diseases is the result of the very basic level at which glycations interfere with molecular and cellular functioning throughout the body and the release of highly oxidizing side-products such as hydrogen peroxide.”

Of all the causes and effects, listed above, the two we’re going to look at are oxidative stress and cytokines. The primary reason I want to examine these factors is that these two are responsible for what makes many carboholics look 70 when they’re actually only 55. So, let’s break down each part; we’ll start with cytokines. If you haven’t checked out what Wikipedia has to say about these destroyers of life, you should do so now, right now.

“Cytokines are a broad and loose category of small proteins that are important in cell signaling. They are released by cells and affect the behavior of other cells. Cytokines are produced by a broad range of cells, including immune cells like macrophages, B lymphocytes, T lymphocytes and mast cells, as well as endothelial cells, fibroblasts, and various stromal cells; a given cytokine may be produced by more than one type of cell.[1][2][3]

“They act through receptors, and are especially important in the immune system; cytokines modulate the balance between humoral and cell-based immune responses, and they regulate the maturation, growth, and responsiveness of particular cell populations. Some cytokines enhance or inhibit the action of other cytokines in complex ways.[3]

“They are different from hormones, which are also important cell signaling molecules, in that hormones circulate in much lower concentrations and hormones tend to be made by specific kinds of cells.”

“They are important in health and disease, specifically in host responses to infection, immune responses, inflammation, trauma, sepsis, cancer, and reproduction.”

“A key focus of interest has been that cytokines in one of these two subsets tend to inhibit the effects of those in the other. Dysregulation of this tendency is under intensive study for its possible role in the pathogenesis of autoimmune disorders.”

“Several inflammatory cytokines are induced by oxidative stress.[7][8] The fact that cytokines themselves trigger the release of other cytokines[9][10][11] and also lead to increased oxidative stress makes them important in chronic inflammation, as well as other immune responses, such as fever and acute phase proteins of the liver.”

If all this is the responsibility of cytokines, and cytokines are caused by oxidative stress, what does the oxidative stress play in this equation?

“Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system’s ability to readily detoxify the reactive intermediates or to repair the resulting damage.”

“In humans, oxidative stress is thought to be involved in the development of Asperger syndrome,[2] ADHD,[3] cancer,[4] Parkinson’s disease,[5] Lafora disease,[6] Alzheimer’s disease,[7][8] atherosclerosis,[9] heart failure,[10] myocardial infarction,[11][12] fragile X syndrome,[13] Sickle Cell Disease,[14] lichen planus,[15] vitiligo,[16] autism,[17] infection,[18] and chronic fatigue syndrome.[19] However, reactive oxygen species can be beneficial, as they are used by the immune system as a way to attack and kill pathogens.[20] Short-term oxidative stress may also be important in the prevention of aging by induction of a process named mitohormesis.[21]” 

If oxidative stress is bad for you in the long term and good for you in the short term, what about the short-term benefits? We’ll come back beck to look at the short benefits of oxidative stress after we look at what it does to you in the long run.

To summarize the above paragraphs from Wikipedia, long-term oxidative can be deadly, but short-term oxidative stress is beneficial.

The short-term benefits of oxidative stress come mostly from exercise, but also from “curcumin from turmeric, green tea extract, silymarin (milk thistle), bacopa extract, DHA, sulforaphane (contained in broccoli), and ashwagandha”.

“Short-term oxidative stress may also be important in the prevention of aging by induction of a process named mitohormesis.[21]” Short term oxidative stress also helps build up Nrf2 in your brain which can supercharge your production of antioxidants. “Activation of Nrf2 results in the induction of many cytoprotective proteins.”

“One of the areas where the concept of hormesis has been explored extensively with respect to its applicability is aging.[12][13] Since the basic survival capacity of any biological system depends on its homeodynamic (homeostatic) ability, biogerontologists proposed that exposing cells and organisms to mild stress should result in the adaptive or hormetic response with various biological benefits. This idea has now gathered a large body of supportive evidence showing that repetitive mild stress exposure has anti-aging effects.[14][15] Exercise is a paradigm for hormesis in this respect.[15] Some of the mild stresses used for such studies on the application of hormesis in aging research and interventions are heat shock, irradiation, prooxidants, hypergravity and food restriction.[14][15][16]Some other natural and synthetic molecules, such as celasterols from medicinal herbs and curcumin from the spice turmeric have also been found to have hormetic beneficial effects.[17] Such compounds which bring about their health beneficial effects by stimulating or by modulating stress response pathways in cells have been termed “hormetins”.[14] Hormetic interventions have also been proposed at the clinical level,[18] with a variety of stimuli, challenges and stressful actions, that aim to increase the dynamical complexity of the biological systems in humans.[19]

Exercise is the best way to induce mitohormesis. but it can be found in curcumin also, which can be found in turmeric, an important spice used extensively on the Indian subcontinent. This one little compound is so important in the proliferation of your antioxidants, that some drug companies, are trying to copy it with their own chemical versions, like, Tecfidera, oltipraz, Bardoxolone methyl, to name a few. It’s that important.

Calorie restriction is another way to build up your anti-oxidants. This will build up more anti-oxidants in you than what you could ever drink. We’ll talk more about that later.

Effects in aging

“One of the areas where the concept of hormesis has been explored extensively with respect to its applicability is aging.[12][13] Since the basic survival capacity of any biological system depends on its homeostatic ability, biogerontologists proposed that exposing cells and organisms to mild stress should result in the adaptive or hormetic response with various biological benefits. This idea has now gathered a large body of supportive evidence showing that repetitive mild stress exposure has anti-aging effects.[14][15] Exercise is a paradigm for hormesis in this respect.[15] Some of the mild stresses used for such studies on the application of hormesis in aging research and interventions are heat shock, irradiation, prooxidants, hypergravity and food restriction.[14][15][16] Some other natural and synthetic molecules, such as medicinal herbs and curcumin from the spice turmeric have also been found to have hormetic beneficial effects.[17] Such compounds which bring about their health beneficial effects by stimulating or by modulating stress response pathways in cells have been termed “hormetins”.[14] Hormetic interventions have also been proposed at the clinical level,[18] with a variety of stimuli, challenges and stressful actions, that aim to increase the dynamical complexity of the biological systems in humans.[19]

“Epidemiological data suggest that individuals with a low-calorie intake may have a reduced risk of stroke and neurodegenerative disorders. There is a strong correlation between per capita food consumption and risk for Alzheimer’s disease and stroke. Data from population-based case-control studies showed that individuals with the lowest daily calorie intakes had the lowest risk of Alzheimer’s disease and Parkinson’s disease.”

Because “calorie restriction has been demonstrated in a variety of laboratory models to induce Nrf2 activation”, it’s as important as the exercise. Nrf2 is a basic leucine zipper (bZIP) protein that regulates the expression of antioxidant proteins that protect against oxidative damage triggered by injury and inflammation.[2]

When calories are reduced in the diets of lab animals, they not only live longer, but also become remarkably resistant to the development of several cancers.” This is according to Dr. Perlmutter, in Grain Brain. Calorie restriction is close to impossible when you are a carboholic, on a carbohydrate diet. Every two hours or so you need another infusion of glucose into your system, to keep you going. Your hunger cycles force you into this repetitive behavior. You really have little choice in it because of the drop in your sugar levels. A carboholic cannot stand the rigors and stress of fasting as easy as someone who’s been on a keto diet for of any length of time. This is one of the biggest reasons that I remain on my MCT keto diet

What else builds up Nrf2 in your brain? A diet high in fats, omega 3 fats in particular. MCT’s are the best. MCTs like coconut oil, and a diet low in carbohydrates. Why? To me, it’s simple, fats won’t glycate other fats. Glycation occurs when glucose mixes with lipoproteins (cholesterol). It’s sugars that glycate cholesterol. If, it’s the glycation of cholesterol that leads to most illness and diseases, and building up Nrf2 in your brain can help protect you from that glycation, why wouldn’t you want to build it up?

Dr. Perlmutter, says it better, in Grain Brain, of page 127 in chapter 5, where he explains the effect of antioxidant protection, and how we can generate more antioxidants, with our diet, than what we can ever ingest through drinking antioxidant beverages. He says, ”Several natural compounds that turn on antioxidant and detoxification pathways through activation of the Nrf2 system have been identified”, which we talked about above.

To summarize,

With all of these deadly consequences, AGES offer, why do people still continue to eat carbs and continue to suffer the effects of dealing with the long-term effects of these things?

Short-term effects are really beneficial, like increasing your autoimmune system by ramping up your antioxidant production, protecting from all of the above diseases. If abstaining from carbs can bring you some of the short-term effects, again, I have to ask myself, why do people still continue to eat carbs and continue to suffer the long-term effects of these things?

But then, I know the answer, Addiction which is a good reason to visit Why the addiction is so hard to break.