Tag Archives: inflammation

Is Your Diabetes Curable or Just Treatable?

Can Your Diabetes be Cured or Just Treated?

Diabetes can be the worst scourge to ever hit mankind. It’s complications have magnified in the last 30 years or so and have set more souls up for shortened lives, than any other disorder, as this disorder is the gateway to future drug use and continued treatments, ultimately until death. The death is always premature. The grain industry and the pharmaceutical industry has made certain of this with a passion seldom matched by even our greatest artists, athletes and musicians, they are inflicting their will upon an unsuspecting public.

The desire of these industries to dominate our food supply and our pharmaceutical supply is ginormous. Their motivation has pushed them to force as many farmers as they can to grow their GMO seed, simply to sell more of their Roundup Herbicide. You know how dangerous that is by now. You should know that 1.3 million tons of it has been sprayed on your food or on feed for feed lots that goes directly into your meat. It’s this desire that has made carbs more glycemic today than they’ve ever been in history. This is what’s driving the diabetes pandemic today.              Get the book now!

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 you 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!

With over 123,250 studies and reports available when I searched for diabetes and carbs on PubMed, it appears that this has been known for some time. There are studies on diabetes and carbohydrates dating from 1946. How could it have taken this long to put these pieces together?

The good news here, is that there is a cure for diabetes. Thank you Dr Davis for pointing it out for us. If you’re tired of treating your diabetes and poking yourself all the time, all one has to do to cure it or avoid it in the first place, is to not eat the food that is responsible for creating it and that is the starchy carbohydrates.

From PMC and PubMed,

Evidence of your carb intake and Diabetes

The only way out of this dilemma is to curb the carb usage completely. The following reports detail how carb ingestion leads directly to type2 diabetes, which ultimately leads to every modern disorder or disease;

The first one I looked at was from 1952; This study was so old, they still called glucose dextrose;

This was a difficult study to read and it only showed 8 diabetic patients. It didn’t mention which type they were either. It basically showed that an increase in carbohydrate consumption led to added glycogen and far stored in the body, clearly showing the link between carbs and fat. This study is older than I. Why have I not heard anything about it? Where were the warnings? Where they too afraid of upsetting an industry, so safeguard the public’s health?

This again is evidence that carbs and diabetes were being researched in 1945, as this report is from May,1945.

This is PubMed’s explanation of carbohydrates and how the glycemic index works. It helps to know how diabetics are thinking and how they need to keep track of the glucose levels in their blood.

  • Issues in Nutrition:Carbohydrates.

Carbohydrates include sugars, starches, and dietary fibers. Resistant starches resemble fiber in their behavior in the intestinal tract, and may have positive effects on blood glucose levels and the gut microbiome. Fibers are classified as soluble and insoluble, but most fiber-containing foods contain a mixture of soluble and insoluble fiber. Soluble fiber has been shown to lower low-density lipoprotein cholesterol levels. Many artificial sweeteners and other sugar substitutes are available. Most natural sources of sweeteners also are energy sources. Many artificial sweeteners contain no kilocalories in the amounts typically used. Sugar alcohols may have a laxative effect when consumed in large amounts. Glycemic index and glycemic load are measurements that help quantify serum glucose response after ingestion of particular foods. These measurements may be affected by the combination of foods consumed in a given meal, and the glycemic index may vary among individuals eating the same meal. Eating foods with a low glycemic index may help prevent development of type 2 diabetes. There is no definitive evidence to recommend low-carbohydrate diets over low-fat diets for long-term weight loss; they are equally effective.

They stop short of say that if you don’t eat carbs you can avoid diabetes, so let me be the first to tell you, you don’t need to eat carbohydrates. Carbs, the way they’re grown today, makes them as dangerous as arsenic.

This article published online on Dec 10, 2016 disputes the importance large amounts of carbohydrates in the diet;

Carbohydrates are essential nutrients that are used as a primary source of energy. Carbohydrate utilization should be properly controlled, as abnormal regulation of carbohydrate metabolism is associated with diseases, such as diabetes, cardiovascular diseases, and stroke. These metabolic syndromes have become a serious problem in developed countries, and there is an increased need for research examining the influence of carbohydrates on animal physiology. Diets enriched in glucose, a major carbohydrate, are also associated with accelerated aging in several model organisms, including yeast and Caenorhabditis elegans (C. elegans). Genetic factors that mediate the effects of high glucose diets on aging have been identified during the last decade, mostly through the use of C. elegans. In this review, we describe studies that determine the effects of carbohydrate-enriched diets on aging by focusing on the mechanisms through which evolutionarily conserved pathways mediate the lifespan-altering effects of glucose in C. elegans. These include the insulin/insulin-like growth factor-1, sterol-regulatory element-binding protein, and AMP-activated protein kinase signaling pathways. We also discuss the effects of various carbohydrates and carbohydrate-derived metabolites on aging in model organisms and cultured mammalian cells. Finally, we discuss how dietary carbohydrates influence health and aging in humans.

Would you consider this evidence that carbs should be, for the most part, limited to small portions…as small as possible.

  • Effect of type and amount of dietary carbohydrate on biomarkers of glucose homeostasis and C reactive protein in overweight or obese adults: results from the OmniCarb trial.


The glycemic index (GI) of dietary carbohydrate is thought to affect glucose homeostasis. Recently, the Effect of Amount and Type of Dietary Carbohydrates on Risk for Cardiovascular Heart Disease and Diabetes Study (OmniCarb) trial reported that a low-GI diet did not improve insulin sensitivity. We conducted this ancillary study of the OmniCarb trial to determine the effects of GI and carbohydrate content on glucose homeostasis and inflammation.


OmniCarb was a randomized cross-over feeding study conducted in overweight or obese adults without diabetes (N=163). Participants were fed each of 4 diets for 5 weeks with 2-week washout periods. Weight was held constant. Diets were: high GI (GI≥65) with high carbohydrate (58% kcal), low GI (GI≤45) with low carbohydrate (40% kcal), low GI with high carbohydrate, and high GI with low carbohydrate. We measured glycated albumin (GA), fructosamine, and high sensitivity C reactive protein (CRP) at baseline and following each dietary period. These biomarkers were compared within-person between diets.


The study population was 52% female and 50% black. Mean age was 53 (SD, 11) years; mean body mass index was 32 (SD 6) kg/m2. Reducing GI had no effect on GA or fructosamine, but increased fasting glucose in the setting of a high-carbohydrate diet (+2.2 mg/dL; p=0.02). Reducing carbohydrate content decreased GA in the setting of a high-GI diet (-0.2%; p=0.03) and decreased fructosamine in the setting of a low-GI diet (-4 µmol/L; p=0.003). Reducing carbohydrate while simultaneously increasing GI significantly reduced both GA (-0.2%; p=0.04) and fructosamine (-4 µmol/L; p=0.009). Neither reducing GI nor amount of carbohydrate affected insulin or CRP.


Reducing carbohydrate, regardless of high or low GI, decreased GA and fructosamine. This suggests that reducing carbohydrate content, rather than GI, is a better strategy for lowering glycemia in adults at risk for diabetes.

Would you consider this as evidence that carbs should be, for the most part, limited to small portions…as small as possible. Need I say more?

  • [Composition of macronutrients in the diabetic diet].

The diabetic diet is one of the pillars of diabetes treatment. The rapid development of knowledge relating to the treatment of diabetes also includes diet. The paper focuses on the importance of a diet in the treatment of type 2 diabetes and prevention of atherosclerosis. Its main goal is to assess the impact of a composition of macronutrients on individuals with type 2 diabetes. The paper is divided into several parts, each of which ends with a conclusion. The first part examines weight reduction. The diet aimed at a weight loss is effective, it can effectively prevent diabetes, it leads to improvements in glucose control and reduction of the risk factors for atherosclerosis, however it will not impact on cardiovascular morbidity and mortality until after more than 20 years. The second part deals with “healthy” foods. The studies exploring this area are not convincing. The only really rational component of food in relation to atherosclerosis is dietary fibres. Important is a balanced diet combined with regular physical activities. The third part focuses on the composition of macronutrients. It turns out that, considering a low-calorie diet, the effects of high- and low-carbohydrate diets on people with diabetes are similar with regard to weight loss and lowering of HbA1c, however the low-carbohydrate diet is associated with lower glycemic variability and a reduced need for anti-diabetic drugs. We do not know how the comparison of the two extreme diets would come out regarding individuals with a high energy diet. Currently it is useful to focus on the quality of individual macronutrients. Choose foods containing carbohydrates with a low glycemic index and high fibre foods, prefer fats that contain a low proportion of saturated fatty acids. The fourth part discusses the recent recommendation of the Czech Diabetes Society regarding the composition of macronutrients in the diabetic diet. As compared with the diet proposed earlier, lower intake of fibre-rich carbohydrates and higher intake of proteins and fats with a low content of saturated fatty acids is now recommended. Experts’ recommendations on this subject are included. Key words: atherosclerosis – diabetic diet – HbA1c – macronutrients – low-carbohydrate diet – obesity – dietary fibres – high-carbohydrate diet – health food.

  • Adverse effects on insulin secretion of replacing saturated fat with refined carbohydrate but not with monounsaturated fat: A randomized controlled trial in centrally obese subjects.


Current dietary guidelines recommend the replacement of saturated fatty acids (SAFAs) with carbohydrates or monounsaturated fatty acids (MUFAs) based on evidence on lipid profile alone, the chronic effects of the mentioned replacements on insulin secretion and insulin sensitivity are however unclear.


To assess the chronic effects of the substitution of refined carbohydrate or MUFA for SAFA on insulin secretion and insulin sensitivity in centrally obese subjects.


Using a crossover design, randomized controlled trial in abdominally overweight men and women, we compared the effects of substitution of 7% energy as carbohydrate or MUFA for SAFA for a period of 6 weeks each. Fasting and postprandial blood samples in response to corresponding SAFA, carbohydrate, or MUFA-enriched meal-challenges were collected after 6 weeks on each diet treatment for the assessment of outcomes.


As expected, postprandial non-esterified fatty acid suppression and elevation of C-peptide, insulin and glucose secretion were the greatest with high-carbohydrate (CARB) meal. Interestingly, CARB meal attenuated postprandial insulin secretion corrected for glucose response; however, the insulin sensitivity and disposition index were not affected. SAFA and MUFA had similar effects on all markers except for fasting glucose-dependent insulin tropic peptide concentrations, which increased after MUFA but not SAFA when compared with CARB.


In conclusion, a 6-week lower-fat/higher-carbohydrate (increased by 7% refined carbohydrate) diet may have greater adverse effect on insulin secretion corrected for glucose compared with isocaloric higher-fat diets. In contrast, exchanging MUFA for SAFA at 7% energy had no appreciable adverse impact on insulin secretion.

Carboholics and Diabetics; This is your warning to steer clear of carbs, if you want to control your diabetes. There is no literature that can  definitively prove that you must eat carbs to survive.

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 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.

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 on 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 you 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.

  • Advancedglycation 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 about 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 amount 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 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.





Is Your Cancer Curable or Just Treatable

Can Your Type of Cancer 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. For all forms of cancer, I’ll reserve this notice for that purpose only. All reports Of CVDs and other heart disorders will be located on the Atherosclerosis page.  Dementias will be on a separate post as well with all other diseases and disorders inflammation is responsible for.

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

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 you 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.

This report is dated Aug 9, 2016 and details AGEs role in lung cancer;

Hsia TC1,2, Yin MC3,4, Mong MC5.

Author information


Effects of carboxymethyllysine (CML) and pentosidine, two advanced glycation end-products (AGEs), upon invasion and migration in A549 and Calu-6 cells, two non-small cell lung cancer (NSCLC) cell lines were examined. CML or pentosidine at 1, 2, 4, 8 or 16 μmol/L were added into cells. Proliferation, invasion and migration were measured. CML or pentosidine at 4-16 μmol/L promoted invasion and migration in both cell lines, and increased the production of reactive oxygen species, tumor necrosis factor-α, interleukin-6 and transforming growth factor-β1. CML or pentosidine at 2-16 μmol/L up-regulated the protein expression of AGE receptor, p47(phox), intercellular adhesion molecule-1 and fibronectin in test NSCLC cells. Matrix metalloproteinase-2 protein expression in A549 and Calu-6 cells was increased by CML or pentosidine at 4-16 μmol/L. These two AGEs at 2-16 μmol/L enhanced nuclear factor κ-B (NF-κ B) p65 protein expression and p38 phosphorylation in A549 cells. However, CML or pentosidine at 4-16 μmol/L up-regulated NF-κB p65 and p-p38 protein expression in Calu-6 cells. These findings suggest that CML and pentosidine, by promoting the invasion, migration and production of associated factors, benefit NSCLC metastasis.

KEYWORDS:  CML; invasion; migration; non-small cell lung cancer; pentosidine

PMID: 27517907

PMCID: PMC5000686 DOI: 10.3390/ijms17081289 [PubMed – in process]  Free PMC Article

The following report submitted Sept 1, 2008 was concerned about RAGEs their correlation with cervical cancer;

  • Induction ofreceptor for advanced glycation end products by EBV latent membrane protein 1 and its correlation with angiogenesis and cervical lymph node metastasis in nasopharyngeal carcinoma.



The EBV oncoprotein, latent membrane protein 1 (LMP1), contributes to the metastasis of nasopharyngeal carcinoma (NPC) by inducing factors to promote tumor invasion and angiogenesis. The receptor for advanced glycation end products (RAGE) is associated with abnormal angiogenesis in diabetic microangiopathies. Moreover, some papers have suggested the association of RAGE overexpression with tumor metastasis; thus, the associations of RAGE with LMP1 and angiogenesis in NPC were examined.


Forty-two patients with NPC were evaluated for expressions of LMP1, RAGE, and S100 proteins and for microvessel counts by immunohistochemistry. Then, the RAGE induction by LMP1 was examined with Western blotting and luciferase reporter assay.


The microvessel counts were significantly higher in patients with high LMP1 expression or high RAGE expression compared with cases with low expressions (P=0.0049 and P<0.0001), respectively. Patients with advanced N classification were also significantly increased in these groups (P=0.0484 and P=0.0005). The expressions of LMP1 and RAGE proteins were clearly correlated in NPC tissues (P=0.0093). Transient transfection with LMP1 expression plasmid induced RAGE protein in Ad-AH cells. The expression of LMP1 transactivated the RAGE promoter as shown by luciferase reporter assay. Mutation of the reporter at nuclear factor-kappaB binding site (-671 to -663) abolished transactivation of the RAGE promoter by LMP1.


These results suggest that LMP1-induced RAGE enhances lymph node metastasis through the induction of angiogenesis in NPC. Nuclear factor-kappaB binding site (-671 to -663) is essential for transactivation of the RAGE promoter by LMP1.

As of today January 10, 2017 this news still has not been publicized, yet! No warnings about what causes glycation, only warnings against what doesn’t cause it.

One wouldn’t think that brain cancer would be affected by glycation, yet with clear evidence of it in the following report, dated Mar 2008;

  • HMGB1 as an autocrine stimulus in human T98G glioblastoma cells: role in cell growth and migration.


HMGB1 (high mobility group box 1 protein) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation and migration, mainly through RAGE (the receptor for advanced glycation end products); HMGB1-RAGE interactions have been found to be important in a number of cancers. We investigated whether HMGB1 is an autocrine factor in human glioma cells. Western blots showed HMGB1 and RAGE expression in human malignant glioma cell lines. HMGB1 induced a dose-dependent increase in cell proliferation, which was found to be RAGE-mediated and involved the MAPK/ERK pathway. Moreover, in a wounding model, it induced a significant increase in cell migration, and RAGE-dependent activation of Rac1 was crucial in giving the tumour cells a motile phenotype. The fact that blocking DNA replication with anti-mitotic agents did not reduce the distance migrated suggests the independence of the proliferative and migratory effects. We also found that glioma cells contain HMGB1 predominantly in the nucleus, and cannot secrete it constitutively or upon stimulation; however, necrotic glioma cells can release HMGB1 after it has translocated from the nucleus to cytosol. These findings provide the first evidence supporting the existence of HMGB1/RAGE signalling pathways in human glioblastoma cells, and suggest that HMGB1 may play an important role in the relationship between necrosis and malignancy in glioma tumours by acting as an autocrine factor that is capable of promoting the growth and migration of tumour cells.

Even brain cancer is susceptible to glycation and its destructive effects. I can’t seem to find a cancer that isn’t affected by glycation.

The following study done in Sep 2013, and was concerned with the role of insulin and Insulin Growth Factor (IGF-1) signaling in cancer;


Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors in aging. GH/Insulin/insulin-like growth factor 1 (IGF-1) signaling molecules that have been linked to longevity include daf-2 and InR and their homologues in mammals, and inactivation of the corresponding genes increases lifespan in nematodes, fruit flies and mice. The life-prolonging effects of caloric restriction are likely related to decreasing IGF-1 levels. Evidence has emerged that antidiabetic drugs are promising candidates for both lifespan extension and prevention of cancer. Thus, antidiabetic drugs postpone spontaneous carcinogenesis in mice and rats, as well as chemical and radiation carcinogenesis in mice, rats and hamsters. Furthermore, metformin seems to decrease the risk for cancer in diabetic patients…

Research conducted during the last 15-20 years firmly established insulin, insulin-like and homologous signaling as key regulators of aging and longevity in organisms ranging from yeast to mammals.…disregulation of insulin signaling and carbohydrate homeostasis in diabetes produces numerous aging-like symptoms including increased risk of cancer and other age-related disease.

Three years after that study was completed and no word has reached the media to tell the public about this finding.

Published Oct 12, 2016, the following report acknowledges that diet plays a large role in the formation of AGEs the single most important factor in cancer, as AGEs are at the root of all cancers;


While the socioeconomic and environmental factors associated with cancer disparity have been well documented, the contribution of biological factors is an emerging field of research. Established disparity factors such as low income, poor diet, drinking alcohol, smoking, and a sedentary lifestyle may have molecular effects on the inherent biological makeup of the tumor itself, possibly altering cell signaling events and gene expression profiles to profoundly alter tumor development and progression. Our understanding of the molecular and biological consequences of poor lifestyle is lacking, but such information may significantly change how we approach goals to reduce cancer incidence and mortality rates within minority populations. In this review, we will summarize the biological, socioeconomic, and environmental associations between a group of reactive metabolites known as advanced glycation end-products (AGEs) and cancer health disparity. Due to their links with lifestyle and the activation of disease-associated pathways, AGEs may represent both a biological consequence and a bio-behavioral indicator of poor lifestyle which may be targeted within specific populations to reduce disparities in cancer incidence and mortality.

Published at the end of last year was this report on the effects of HMGB1 on most all lung diseases;


Lung diseases remain a serious problem for public health. The immune status of the body is considered to be the main influencing factor for the progression of lung diseases. HMGB1 (high-mobility group box 1) emerges as an important molecule of the body immune network. Accumulating data have demonstrated that HMGB1 is crucially implicated in lung diseases and acts as independent biomarker and therapeutic target for related lung diseases. This review provides an overview of updated understanding of HMGB1 structure, release styles, receptors and function. Furthermore, we discuss the potential role of HMGB1 in a variety of lung diseases. Further exploration of molecular mechanisms underlying the function of HMGB1 in lung diseases will provide novel preventive and therapeutic strategies for lung diseases.

The following report details the overexpression of glycation in ovarian cancer. It was submitted Oct 28, 2016;



Ovarian cancer is one of the important challenges in the field of gynecologic oncology because of some problems in understanding its etiology and pathogenesis. Receptor for advanced glycation end products (RAGE) is a multiligand trans-membranous receptor which is upregulated in some human cancers. Mechanisms of RAGE involvement in carcinogenesis of ovarian cancer are unknown.


This study aimed to investigate the expression of RAGE in ovarian cancers and its association with clinicopathological characteristics.


The RAGE expression level in ovarian cancer and corresponding noncancerous tissues were analyzed by real time quantitative RT-PCR and immunohistochemistry techniques.


Results indicated that RAGE gene was overexpressed in ovarian cancer tissue compared with adjacent noncancerous tissue (p < 0.001). A significant association between RAGE expression and tumor size (p = 0.04), depth of stromal invasion (p = 0.031), lymphovascular invasion (p = 0.041) and stage of cancer (p = 0.041) was observed. The receiver operating characteristic (ROC) analyses yielded the area under the curve (AUC) values of 0.86 for RAGE in discriminating ovarian cancer samples from non-cancer controls.


In conclusion overexpression of RAGE in ovarian cancer may be a useful biomarker to predict tumor progression.

What interests me is that nothing is said about what creates these RAGEs. For thirty years they’ve been examining the nature of glycation but have said nothing about what is responsible for the major portion of glycation, glucose consumption in the form of sugar and grains. I guess that’s not profitable.

What is profitable is finding more drugs to make people need more and more drugs. Evidenced here in this report dated Oct 23, 2014, yet nothing has been announced about this report, Did you hear about it?


A hypoxic tumor microenvironment is characteristic of many cancer types, including one of the most lethal, pancreatic cancer. We recently demonstrated that the receptor for advanced glycation end products (RAGE) has an important role in promoting the development of pancreatic cancer and attenuating the response to chemotherapy. We now demonstrate that binding of RAGE to oncogenic KRAS facilitates hypoxia-inducible factor 1 (HIF1)α activation and promotes pancreatic tumor growth under hypoxic conditions. Hypoxia induces NF-κB-dependent and HIF1α-independent RAGE expression in pancreatic tumor cells. Moreover, the interaction between RAGE and mutant KRAS increases under hypoxia, which in turn sustains KRAS signaling pathways (RAF-MEK-ERK and PI3K-AKT), facilitating stabilization and transcriptional activity of HIF1α. Knock down of RAGE in vitro inhibits KRAS signaling, promotes HIF1α degradation, and increases hypoxia-induced pancreatic tumor cell death. RAGE-deficient mice have impaired oncogenic KRAS-driven pancreatic tumor growth with significant downregulation of the HIF1α signaling pathway. Our results provide a novel mechanistic link between NF-κB, KRAS, and HIF1α, three potent molecular pathways in the cellular response to hypoxia during pancreatic tumor development and suggest alternatives for preventive and therapeutic strategies.

Obviously the continuing need to examine the damage instead of warning about the glycating substance proves to be more lucrative than realizing the actual cure, removing the glycating substances from the diet. Too be removal involves conquering an addiction. That wouldn’t be too bad if this addiction wasn’t inflicted on us. But it was, making this addiction damn near impossible to conquer.

This is evidenced by this study dated July 18, 2016 and shows the influence of HMGB1 and M2 like macrophages;


Hypoxia is a hallmark of cancer that is strongly associated with invasion, metastasis, resistance to therapy and poor clinical outcome. Tumour hypoxia affects immune responses and promotes the accumulation of macrophages in the tumour microenvironment. However, the signals linking tumour hypoxia to tumour-associated macrophage recruitment and tumour promotion are incompletely understood. Here we show that the damage-associated molecular pattern High-Mobility Group Box 1 protein (HMGB1) is released by melanoma tumour cells as a consequence of hypoxia and promotes M2-like tumour-associated macrophage accumulation and an IL-10 rich milieu within the tumour. Furthermore, we demonstrate that HMGB1 drives IL-10 production in M2-like macrophages by selectively signalling through the Receptor for Advanced Glycation End products (RAGE). Finally, we show that HMGB1 has an important role in murine B16 melanoma growth and metastasis, whereas in humans its serum concentration is significantly increased in metastatic melanoma. Collectively, our findings identify a mechanism by which hypoxia affects tumour growth and metastasis in melanoma and depict HMGB1 as a potential therapeutic target.

Stomach cancer is influenced as well by glycation as explained in this report submitted Oct 1, 2015;


Micrometastasis is the major cause of treatment failure in gastric cancer (GC). Because epithelial-to-mesenchymal transition (EMT) is considered to develop prior to macroscopic metastasis, EMT-promoting factors may affect micrometastasis. This study aimed to evaluate the role of extracellular high-mobility group box-1 (HMGB1) in EMT and the treatment effect of combined targeting of HMGB1 and interleukin-8 (IL-8) at early-stage GC progression through interrupting EMT promotion. Extracellular HMGB1 was induced by human recombinant HMGB1 and pCMV-SPORT6-HMGB1 plasmid transfection. EMT activation was evaluated by immunoblotting, immunofluorescence and immunohistochemistry. Increased migration/invasion activities were evaluated by in vitro transwell migration/invasion assay using all histological types of human GC cell lines (N87, MKN28 SNU-1 and KATOIII), N87-xenograft BALB/c nude mice and human paired serum-tissue GC samples. HMGB1-induced soluble factors were measured by chemiluminescent immunoassay. Inhibition effects of tumor growth and EMT activation by combined targeting of HMGB1 and IL-8 were evaluated in N87-xenograft nude mice. Serum HMGB1 increases along the GC carcinogenesis and reaches maximum before macroscopic metastasis. Overexpressed extracellular HMGB1 promoted EMT activation and increased cell motility/invasiveness through ligation to receptor for advanced glycation end products. HMGB1-induced IL-8 overexpression contributed the HMGB1-induced EMT in GC in vitro and in vivo. Blocking HMGB1 caused significant reduction of tumor growth, and addition of human recombinant IL-8 rescues this antitumor effects. Our results imply the role of HMGB1 in EMT through IL-8 mediation, and a potential mechanism of GC micrometastasis. Our observations suggest combination strategy of HMGB1 and IL-8 as a promising diagnostic and therapeutic target to control GC micrometastasis.

More evidence of Glycation in Breast cancer is in this report from Dec 23, 2016;

Nass N1, Ignatov A2, Andreas L3, Weißenborn C2, Kalinski T3, Sel S4.

Author information


Advanced glycation end products (AGEs) accumulate as a result of high concentrations of reactive aldehydes, oxidative stress, and insufficient degradation of glycated proteins. AGEs are therefore accepted biomarkers for aging, diabetes, and several degenerative diseases. Due to the Warburg effect and increased oxidative stress, cancer cells frequently accumulate significant amounts of AGEs. As the accumulation of AGEs may reflect the metabolic state and receptor signaling, we evaluated the potential prognostic and predictive value of this biomarker. We used immunohistochemistry to determine the AGE Nε-carboxymethyl lysine (CML) in 213 mammary carcinoma samples and Western blotting to detect AGEs in cell cultures. Whereas no significant correlation between hormone receptor status and CML was observed in cell lines, CML accumulation in tumors was positively correlated with the presence of estrogen receptor alpha, the postmenopausal state, and age. A negative correlation was found for grade III carcinomas and triple-negative cases.

Again, this form of cancer can be curable if you remove the glycating factor. I have yet to find a cancer that can’t be cured by taking away the glycating factor, glucose. Why then is glucose still a recommended food, as in carbohydrates such as “whole grains”?

It amazes me how many studies they find to say the same thing over and over again. Yet they keep doing it, day after day after day, in an unending cycle dependence. This report on the effects of RAGEs on esophageal and lung cancers;


The receptor for advanced glycation end products (RAGE) interacts with several ligands and is involved in various human diseases. Several splicing forms of the RAGE gene have been characterized, and two general mechanisms are usually responsible for the generation of soluble receptors. However, variants distribution and respective roles in different tumors are not clear. We analyzed RAGE and hRAGEsec mRNA expression in esophageal and lung cancer by RT-polymerase chain reaction. The Agilent clipper 1000 Bioanalyzer using lab-on-a-chip technology was applied to size and quantify the polymerase chain reaction products. Western blotting was performed to measure total soluble RAGE protein levels. The results showed that RAGE and its splice variants increased in esophageal cancers and decreased in lung cancers. We conclude that RAGE presents as a major isoform; soluble RAGE may also play certain roles in esophageal cancer and lung cancer.

How many reports does the FDA or the USDA need to tell them that what they’re recommending for everyone to eat, is doing them more harm than good, far more.

This report dated June 15, 2007 shows the effects if AGEs on chondrosarcoma, a bone cancer;



Chondrosarcoma, the second most frequent primary malignant bone tumor, is classified into 3 grades according to histologic criteria of malignancy. However, a low-grade lesion can be difficult to distinguish from a benign enchondroma, whereas some histologically low-grade lesions may carry a poor prognosis. The receptor for advanced glycation endproducts (RAGE) and its ligand, high-mobility group box-1 (HMGB1), was quantified in enchondromas and chondrosarcomas to determine whether these markers were associated with histological malignancy and prognosis.


Enchondromas (n = 20) and typical chondrosarcomas (n = 39) were evaluated for RAGE, endogenous secretory RAGE (esRAGE, a splice variant form), and HMGB1 protein expression by immunohistochemistry including laser confocal microscopy. The content of esRAGE in resected specimens was measured with an enzyme-linked immunosorbent assay. Associations of these molecules with histology and clinical behavior of tumors were analyzed.


Expression of esRAGE and HMGB1 was observed in all specimens. The numbers of cells positive for esRAGE and HMGB1 expression were positively associated with histologic grade. Expression of esRAGE was significantly higher in chondrosarcomas than in enchondromas (P < .001). Tissue esRAGE content was also significantly higher in grade 1 and 2 chondrosarcomas than enchondromas (P = .0255 and P = .008, respectively). High expression of esRAGE in grade 1 chondrosarcoma was associated with subsequent recurrence (P = .0013), lung metastasis (P = .0071), and poor survival (P < .001).


Assessment of esRAGE expression should aid in diagnostic and prognostic determinations in chondrosarcoma.

This report dated Nov 23, 2016 shows the effects that glycation and  AGEs have on ovarian cancer, prostate cancer,

  1. Introduction

Reactive oxygen species (ROS), generated as consequence of oxidative metabolism, activate signal transduction pathways, which contribute to cellular homeostasis [1]. Metabolically active cells, neutrophils, and macrophages from the immune system produce high levels of ROS.

  1. The Function of HMGB Proteins and Other Redox Sensors during Oxidative Stress in Ovarian Cancer

OS has been proposed as a cause of ovarian cancer. HMGB1 is considered a biomarker for ovarian cancer [3839] and increased levels of interleukin-8 protein (IL-8) and HMGB1 correlate with poor prognosis in prostate and ovarian cancer cells [125].

  1. Oxidative Stress in Prostate Cancer and the Function of HMGB Proteins and Other Redox Sensors

The human prostate anatomy displays a zonal architecture, corresponding to central, periurethral transition, peripheral zone, and anterior fibromuscular stroma. The majority of prostate carcinomas are derived from the peripheral zone, while benign prostatic hyperplasia arises from the transition zone [129].

Finally, several research lines outline the direct importance of HMGB proteins in prostate cancer and their implications in therapy. Increased HMGB2 expression [177], HMGB1 expression [41], or coexpression of RAGE and HMGB1 [178179] has been associated with prostate cancer progression and has been correlated to poor patient outcome.

  1. Conclusions and Perspectives

ROS overproduction and imbalance are a primary cause of malignancy in the onset of cancer. Cells have evolved multiple strategies in response to ROS production and HMGB proteins play a major role in many molecular mechanisms participating in these responses. In the nucleus, HMGB proteins affect DNA repair, transcription, and chromosomal stability; in cytoplasm they determine key decisions that finally lead towards autophagy or apoptosis; as extracellular signals they produce changes that affect the microenvironment of the tumour and attract cells from the immune system. In turn, the inflammatory onset can increase ROS production and therefore enhances the response. HMGB1 and HMGB2 are expressed at the highest levels in immune cells and, besides, they have been related to cancers, which are hormone-responsive, such as ovarian and prostate cancers. Since HMGB proteins have many different functions and are necessary in healthy cells, an improved strategy to modulate their role in cancer progression could be to act through other proteins interacting specifically with them. The identification of HMGB partners, which could be univocally associated with specific cancerous processes or with mechanism of cisplatin resistance, is a field of interest for ongoing translational cancer research. Interactome strategies are outstanding for the development of these research lines.

A search for cervical cancer and glycation returned 602 studies in the PMC index and started with this study;

We investigated the significance of high- mobility group box1 (HMGB1) and T-cell-mediated immunity and prognostic value in cervical cancer… HMGB1 expression may activate Tregs or facilitate Th2 polarization to promote immune evasion of cervical cancer. Elevated HMGB1 protein in cervical carcinoma samples was associated with a high recurrence of HPV infection in univariate analysis… Data collected here demonstrated that the expression of HMGB1 in cervical lesions increased with tumor progression.

I wanted to see the relationship between glycation and bladder cancer. My search returned 616 studies, with the first one dated Feb 25, 2015;

Bladder cancer is the 4th most common cancer among men in the U.S. and more than half of patients experience recurrences within 5 years after initial diagnosis.

Oct 29, 1993;

  • Expression of receptors foradvanced glycosylation end products on renal cell carcinoma cells in vitro.


Proteins that have been modified by long-term expose to glucose accumulate advanced glycosylation end products (AGEs) as a function of protein age. In these studies, we have examined the interaction of AGE-protein with renal cell carcinoma cells (RCC) in vitro, using AGE-modified bovine serum albumin (AGE-BSA) as a probe. AGE-BSA showed tendency to induce in vitro cell growth of RCC cells and promoted the production of interleukin-6 (IL-6), an in vitro autocrine growth factor. Reverse transcriptase-polymerase chain reaction analysis revealed that RCC cells used here express mRNA for a receptor for AGEs (RAGE). These results suggested that AGEs taken up through RAGE on RCC cells might play a role in promoting the growth of RCC cells.

This was discovered in the summer of 1993 or prior, yet nothing was ever announced by the FDA or the USDA that there might be a preventative diet to protect against cancer. Did you hear anything about sugar or carbohydrates causing this kind of damage? I didn’t. Yet the evidence is clear as day from a study done over 20 years ago. Still, nobody announced these revelations as they were being discovered. This report submitted Dec 2012;

  • Functional amyloid formation byStreptococcus mutans

In summary, there is a growing realization that amyloid formation is a directed, widespread, functional process that contributes to the biology of numerous micro-organisms, with particular relevance for adhesion and biofilm formation. We have now demonstrated amyloid formation by the cariogenic pathogen S. mutans, which is not surprising considering its biofilm niche. In addition to the contribution of amyloids to virulence by facilitating the adhesion, biofilm formation and invasion of pathogens, microbial amyloids have been postulated to contribute to systemic diseases, including Alzheimer’s and Parkinson’s, possibly by seeding amyloid formation in the brain (Broxmeyer, 2002Díaz-Corrales et al., 2004MacDonald, 2006Miklossy et al., 2006).

Copied from PMC on Liver cancer;

According to the database from GLOBOCAN 2012, liver cancer has the fifth highest incidence rate and is the second most life-threatening cancer in the world. There were an estimated 14.1 million new cases and 8.2 million cancer deaths worldwide in 2012, among which there were 782,500 new patients and 745,500 deaths caused by liver cancer [1].

HMGB1 has been demonstrated as a critical role in a number of cancers, including colorectal [10], breast [11,12], lung [13,14,15,16], prostate [17], cervical [18], skin [19], kidney [20,21], gastric [22,23,24,25,26], pancreatic [27,28,29], osteosarcoma [30] and leukemia [31].

Recently, HMGB1 has been recognized as a pro-angiogenesis factor leading to the generation of vascular endothelial growth factor (VEGF) in colon cancer [54,55], while RAGE was identified as the requirement for cell angiogenesis in HCC [56].

Autophagy and apoptosis are recognized as both the programmed cell deaths. In HCC, the release of HMGB1 from nuclei to cytoplasm was reported as an inducer for cell autophagic cell death, which may be associated with ROS and/or Beclin-1.

In summary, HMGB1 plays a pivotal role in oncogenesis and progression in HCC which may be a potential target for therapies and is worthy of further study.

This free report appeared in PubMed 3/1/2016, it expresses the role AGEs and RAGE play in Colorectal  cancer;



Advanced glycation end products (AGEs) and their receptor RAGE emerge as important pathogenic contributors in colorectal carcinogenesis. However, their relationship to the detoxification enzyme Glyoxalase (GLO)-I and Adiponectin receptors (AdipoR1, AdipoR2) in colorectal carcinoma (CRC) is currently understudied. In the present study, we investigated the expression levels of the above molecules in CRC compared to adjacent non-tumoral tissue and their potential correlation with clinicopathological characteristics and patients’ survival.


We analyzed the immunohistochemical expression of AGE, RAGE, GLO-1, AdipoR1 and AdipoR2 in 133 primary CRC cases, focusing on GLO-I. The tumour MSI status was further assessed in mucinous carcinomas. Western immunoblotting was employed for validation of immunohistochemical data in normal and tumoral tissues as well in three CRC cell lines. An independent set of 55 patients was also used to validate the results of univariate survival analysis regarding GLO-I.


CRC tissue showed higher intensity of both AGE and RAGE expression compared with normal colonic mucosa which was negative for GLO-I in most cases (78 %). Western immunoblotting confirmed AGE, RAGE and GLO-I overexpression in tumoral tissue. GLO-I expression was directly related to RAGE and inversely related to AGE immunolabeling. There was a trend towards higher expression of all markers (except for RAGE) in the subgroup of mucinous carcinomas which, although of borderline significance, seemed to be more prominent for AdipoR1 and AGE. Additionally, AGE, AdipoR1 and Adipo R2 expression was related to tumor grade, whereas GLO-1 and AdipoR1 to T-category. In survival analysis, AdipoR2 and GLO-I overexpression predicted shortened survival in the entire cohort and in early stage cases, an effect which for GLO-I was reproduced in the validation cohort. Moreover, GLO-I emerged as an independent prognosticator of adverse significance in the patients’ cohort.


We herein provide novel evidence regarding the possible interactions between the components of AGE-RAGE axis, GLO-I and adiponectin receptors in CRC. AGE and AdipoR1 are possibly involved in colorectal carcinogenesis, whereas AdipoR2 and GLO-I emerged as novel independent prognostic biomarkers of adverse significance for patients with early disease stage. Further studies are warranted to extend our observations and investigate their potential therapeutic significance.

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 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.

Is Your Dementia Curable or Just Treatable?

Can Your Dementia or Alzheimer’s, Osteoarthritis, IBS/ IBD, or Other Disease of Inflammation be Cured or Just Treated?

This poses an interesting question osteoarthritis and dementia have something in common? Yes they do. They are diseases of inflammation and inflammation is caused by glycation. It’s these glycative cytokines and plaques that are responsible for all the damage that is responsible for all diseases of inflammation. They are also related to IBS, IBD, Lupus, Psoriasis, COPD, and every other disease that is influenced by inflammation, which would include most heart diseases and cancer. I posted those entries on different pages because of the extent of each one. That alone tells me to stay clear of anything that creates glycation.

Unfortunately, like arthritis, much of the damage has already been done and can’t be undone.  However you can stop the decline immediately and start some recovery. Just realize that the recovery will take twice as long as it took for you to create this quagmire in the first place. That only means that you must stop the glycation as soon as possible. (I suggest immediately, with a 3 day water only fast.) This will give your body more time to repair the damage.

Since the body needs proteins and cholesterol to operate, and doesn’t need the sugar, that leaves only one type of food to be responsible for glycation, carbs. I’ve learned through my research that the body can create all the glucose it needs with a process called gluconeogenesis. Gluconeogenesis is a process your body goes through whenever is needs glucose and has none readily available.

I produces this glucose with your own glycogen. That’s what your body turns glucose into when you eat it. That is what makes me question our need to eat glucose. If you body can create what it needs, why eat it? You can live perfectly well without it because your body can make it.

Why then, were we fed the line, for 50 years that we had to make grains (the foundation of glucose in the body) the largest part of our diet? Could it be because these studies started about 60 years ago? They intensified 30 years ago when Monsanto took over GD Searle pharmaceuticals. This was also about the time when the whole grain ruse started, convincing the public to consume massive amounts of this carcinogenic, atherosclerotic, inflammatory food. Do you wonder now, why all the disease exists?

When you cure a disease, you have nothing to treat. Where’s the money flow in our medical industry? It flows through the treatment process. Every hospital proves this, every weight loss clinic proves this, every orthopedic clinic proves this. Actually, every clinic proves this. If a cure was found for all modern disease, what would it do to the health and medical industries? Reduce it to treating emergencies only?  In several other posts, I show you how reducing carb consumption will reduce emergencies as well. (That’s where this really gets good.) It has something to do with its effect on your emotions.

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. For all forms of dementia, I’ll reserve this notice for that purpose only. All reports Of CVDs and other heart disorders will be located on the Atherosclerosis page.  Cancers will be on 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 you 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.

Probably the first condition to hit you will be IBS of IBD, Irritable Bowel Syndrome or Inflammatory Bowel Disease. It was just submitted in this year;

Prevalence and Impact of Inflammatory Bowel Disease-Irritable Bowel Syndrome on Patient-reported Outcomes in CCFA Partners.



Inflammatory bowel disease (IBD) patients with persistent symptoms despite no or minimal inflammation are frequently described as having an overlap of IBD and irritable bowel syndrome (IBD-IBS). Limited data are available on how IBS impacts the individual patient with IBD. In this study, we aimed to evaluate the prevalence of IBD-IBS and investigate its impact on patient-reported outcomes.


We performed a cross-sectional analysis within the CCFA Partners Study. Bivariate analyses and logistic regression models were used to investigate associations between IBD-IBS and various demographic, disease factors, and patient-reported outcomes including anxiety, depression, sleep disturbances, pain interference, and social satisfaction.


Of the 6309 participants included, a total of 1279 (20%) reported a coexisting IBS diagnosis. The prevalence of IBD-IBS in this cohort was similar within disease subtypes. A diagnosis of IBD-IBS was associated with higher narcotic use compared with those with no IBS diagnosis for both Crohn’s disease, 17% versus 11% (P < 0.001) and ulcerative colitis/indeterminate colitis, 9% versus 5% (P < 0.001). Quality of life, as measured by Short Inflammatory Bowel Disease Questionnaire (SIBDQ) was lower in patients with IBD-IBS compared with those without. IBD-IBS diagnosis was associated with anxiety, depression, fatigue, sleep disturbances, pain interference, and decreased social satisfaction.


In this sample of patients with IBD, high prevalence of concomitant IBS diagnosis was observed. IBD-IBS diagnosis was associated with increased narcotic use and adverse patient-reported outcome. Appropriate diagnosis, treatment, and counseling may help improve the functional status of IBD-IBS patients and decrease narcotic use.

My appropriate treatment for this disorder isn’t a treatment. Those always lead to more treatments. I propose a cure. All the inflammation involved in these disorders can be controlled by your intake of carbs, meaning, by going keto you can avoid all inflammation. How fat would that go to providing relief?

IBS and IBD aren’t the only inflammatory disorders, there are several others such as Lupus;


Early diagnosis is important for the outcome of lupus nephritis (LN). However, the pathological type of lupus nephritis closely related to the clinical manifestations; therefore, the treatment of lupus nephritis depends on the different pathological types.


To assess the level of monocyte chemotactic protein (MCP-1), fractalkine (Fkn), and receptor for advanced glycation end product (RAGE) in different pathological types of lupus nephritis and to explore the value of these biomarkers for predicting the prognosis of lupus nephritis.


Patients included in this study were assessed using renal biopsy. Class III and class IV were defined as the proliferative group, class V as non-proliferative group, and class V+III and class V+IV as the mixed group. During the follow-up, 40 of 178 enrolled patients had a poor response to the standard immunosuppressant therapy. The level of markers in the different response groups was tested.


The levels of urine and serum MCP-1, urine and serum fractalkine, and serum RAGE were higher in the proliferative group, and lower in the non-proliferative group, and this difference was significant. The levels of urine and serum MCP-1 and serum RAGE were lower in the poor response group, and these differences were also significant. The relationship between urine MCP-1 and urine and serum fractalkine with the systemic lupus erythematosus disease activity index was evaluated.


The concentration of cytokines MCP-1, fractalkine, and RAGE may be correlated with different pathology type of lupus nephtitis. Urine and serum MCP-1 and serum RAGE may help in predicting the prognosis prior to standard immunosuppressant therapy.

Do you have Lupus? Were you told not to eat your bagels for breakfast? If you weren’t, then it’s probably because someone needed you back for treatment.

This following report dated

Background/Purpose: HMGB1, which may act as a proinflammatory mediator, has been proposed to contribute to the pathogenesis of multiple chronic inflammatory and autoimmune diseases including systemic lupus erythematosus (SLE); however, the precise mechanism of HMGB1 in the pathogenic process of SLE remains obscure.

Method: The expression of HMGB1 was measured by ELISA and western blot. The ELISA was also applied to detect proinflammatory cytokines levels. Furthermore, nephritic pathology was evaluated by H&E staining of renal tissues. Results: In this study, we found that HMGB1 levels were significantly increased and correlated with SLE disease activity in both clinical patients and murine model. Furthermore, gain- and loss-of-function analysis showed that HMGB1 exacerbated the severity of SLE. Of note, the HMGB1 levels were found to be associated with the levels of proinflammatory cytokines such as TNF-α and IL-6 in SLE patients. Further study demonstrated that increased HMGB1 expression deteriorated the severity of SLE via enhancing macrophage inflammatory response. Moreover, we found that receptor of advanced glycation end products played a critical role in HMGB1-mediated macrophage inflammatory response.

Conclusion: These findings suggested that HMGB1 might be a risk factor for SLE, and manipulation of HMGB1 signaling might provide a therapeutic strategy for SLE.

Listed below from PubMed or PMC or the FDA are reports of studies done on the effects of glycation and its influence in osteoporosis or any disease influenced by inflammation.


Only three decades ago adipose tissue was considered inert with little relationship to insulin resistance. Similarly bone has long been thought purely in its structural context. In the last decade, emerging evidence has revealed important endocrine roles for both bone and adipose tissue. The interaction between these two tissues is remarkable. Bone marrow mesenchymal stem cells give rise to both osteoblasts and adipocytes. Leptin and adiponectin, two adipokines secreted by fat tissue, control energy homeostasis, but also have complex actions on the skeleton. In turn, the activities of bone cells are not limited to their bone remodeling activities, but also to modulation of adipose sensitivity and insulin secretion. This review will discuss these new insights linking bone remodeling to the control of fat metabolism and the association between diabetes mellitus and osteoporosis.


Chronic hyperglycemica profoundly affects multiple tissues and directly affects the frequency of complications in diabetes mellitus. Hypoinsulinemia is the primary hormonal disturbance leading to T1DM, whereas insulin resistance causing hyperglycemia is the principal event in T2DM. As discussed, bone mineral density is a relatively poor surrogate for defining bone structure during long standing hyperglycemia. Low bone mass is often detected in T1DM although the pathogenesis is likely to be multifactorial. On the other hand, BMD can be low, normal or increased in T2DM. Yet both forms of diabetes are associated with an increased risk of fracture. In part, higher rates of fracture can be related to neuropathic, nephropathic and retinopathic changes that lead to a greater risk of falling. In addition, low body weight, hypoinsulinemia, low serum levels of IGF-I and altered gonadal steroids favor a catabolic state in the skeleton of Type I diabetics. The presence of obesity and T2DM, although associated with increased cortical bone mass, does not translate to a lower fracture risk, and paradoxically may enhance risk. Hyperglycemia can lead to degenerative changes in bone quality through advanced end product glycation, which particularly affects collagen cross-linking. Not surprisingly, one of the classic late clinical features of diabetes mellitus, i.e. vascular calcification, is associated with lower bone mass and impaired bone strength. Those two processes may be linked to reduced renal function and aberrant deposition of calcium in blood vessels rather than in the appropriate collagen matrix. Notwithstanding the potential numerous insults associated with sustained hyperglycemia, several recent developments suggest there is now a greater awareness of the skeleton as both a target of diabetic complications, and a potential pathogenetic factor in the disease itself.

The following study looked at the brains of Alzheimer’s disease patients. It’s dated Jan 3 2017. Theyu officially label Alzheimer’s disease as type 3 diabetes;


The brain of patients with Alzheimer disease (AD) showed the evidence of reduced expression of insulin and neuronal insulin receptors, as compared with those of age-matched controls. This event gradually and certainly leads to a breakdown of the entire insulin-signaling pathway, which manifests insulin resistance. This in turn affects brain metabolism and cognitive functions, which are the best-documented abnormalities in AD. These observations led Dr. de la Monte and her colleagues to suggest that AD is actually a neuroendocrine disorder that resembles type 2 diabetes mellitus. The truth would be more complex with understanding the role of Aβ derived diffusible ligands, advanced glycation end products, and low-density lipoprotein receptor-related protein 1. However, now it’s known as “brain diabetes” and is called type 3 diabetes mellitus (T3DM). This review provides an overview of “brain diabetes” focusing on the reason why the phenomenon is called T3DM.

Evidence of inflammation’s role in myasthenia gravis, dated Jan 3, 2017; I used to have a granddaughter with myasthenia gravis, as I recall at that time, there was no cause. I guess the cause wasn’t known then. It’s a nice thing that it is now, but who suggesting that we remove the instigating factor from this equation, the glucose that is responsible for the glycation? I can’t believe that there are only a few of us;


This study describes specific patterns of elevated inflammatory proteins in clinical subtypes of myasthenia gravis (MG) patients. MG is a chronic, autoimmune neuromuscular disease with antibodies most commonly targeting the acetylcholine receptors (AChRab), which causes fluctuating skeletal muscle fatigue. MG pathophysiology includes a strong component of inflammation and a large proportion of patients with early onset MG additionally present thymus hyperplasia. Due to the fluctuating nature and heterogeneity of the disease, there is a great need for objective biomarkers as well as novel potential inflammatory targets. We examined the sera of 45 MG patients (40 AChRab seropositive and 5 AChRab seronegative), investigating 92 proteins associated with inflammation. Eleven of the analysed proteins were significantly elevated compared to healthy controls, out of which the three most significant were: matrix metalloproteinase 10 (MMP-10; p = 0.0004), transforming growth factor alpha (TGF-α; p = 0.0017) and extracellular newly identified receptor for advanced glycation end-products binding protein (EN-RAGE) (also known as protein S100-A12; p = 0.0054). Further, levels of MMP-10, C-X-C motif ligand 1 (CXCL1) and brain derived neurotrophic factor (BDNF) differed between early and late onset MG. These novel targets provide valuable additional insight into the systemic inflammatory response in MG.

The following report was submitted Dec 29 2016 and explains the damage that oxidative stress, apoptosis, autophagy and inflammation play in kidney disease;

Diabetic kidney disease (DKD) can occur in approximately 30-40% of both type 1 and type 2 diabetic patients. The well-established features of DKD include increased serum glucose levels along with chronic low-grade inflammation, OxS, increased advanced glycation end products, sorbitol accumulation, increased hexosamine, and protein kinase C pathway activation. On the other hand, accumulating evidence suggests that novel pathways including apoptosis and autophagy might also play important roles in the pathogenesis and progression of DKD. In this review, the integrated mechanisms of inflammation, oxidative stress, apoptosis, and autophagy are discussed in the pathogenesis as well as progression of DM and DKD.

This following report dated Feb 2017 shows the importance of sRAGE involved in lung infections and other inflammatory precursors to lung cancer;



The membrane-bound isoform of the receptor for advanced glycation end products (FL-RAGE) is primarily expressed by alveolar epithelial cells and undergoes shedding by the protease ADAM10, giving rise to soluble cleaved RAGE (cRAGE). RAGE has been associated with the pathogenesis of several acute and chronic lung disorders. Whether the proteolysis of FL-RAGE is altered by a given inflammatory stimulus is unknown. Pseudomonas aeruginosa causes nosocomial infections in hospitalized patients and is the major pathogen associated with chronic lung diseases.


These data are the first to suggest that inhibition of FL-RAGE shedding, by affecting the FL-RAGE/cRAGE levels, is a novel mechanism for controlling inflammation to acute P. aeruginosa pneumonia. sRAGE in the alveolar space sustains inflammation in this setting.

Below is evidence that the destruction of glycation starts before you were ever born, thank to your mother’s glucose ingestion. This is where your addiction began. Do you think if she knew how much harm she was inflicting, she would do it again? That would depend on her addiction;


Ectopic calcifications in intervertebral discs (IVDs) are known characteristics of IVD degeneration that are not commonly reported but may be implicated in structural failure and dysfunctional IVD cell metabolic responses. This study investigated the novel hypothesis that ectopic calcifications in the IVD are associated with advanced glycation end products (AGEs) via hypertrophy and osteogenic differentiation. Histological analyses of human IVDs from several degeneration stages revealed areas of ectopic calcification within the nucleus pulposus and at the cartilage endplate. These ectopic calcifications were associated with cells positive for the AGE methylglyoxal-hydroimidazolone-1 (MG-H1). MG-H1 was also co-localised with Collagen 10 (COL10) and Osteopontin (OPN) suggesting osteogenic differentiation. Bovine nucleus pulposus and cartilaginous endplate cells in cell culture demonstrated that 200 mg/mL AGEs in low-glucose media increased ectopic calcifications after 4 d in culture and significantly increased COL10 and OPN expression. The receptor for AGE (RAGE) was involved in this differentiation process since its inhibition reduced COL10 and OPN expression. We conclude that AGE accumulation is associated with endochondral ossification in IVDs and likely acts via the AGE/RAGE axis to induce hypertrophy and osteogenic differentiation in IVD cells. We postulate that this ectopic calcification may play an important role in accelerated IVD degeneration including the initiation of structural defects. Since orally administered AGE and RAGE inhibitors are available, future investigations on AGE/RAGE and endochondral ossification may be a promising direction for developing non-invasive treatment against progression of IVD degeneration.

From the study report itself, dated Nov 2016;

Ectopic calcifications were present in human IVDs of various degeneration stages and often co-localised with MG-H1… dochondral ossification. There is a need for non-invasive therapies to prevent or reverse early degenerative IVD changes. Currently there is a phase 3 clinical trial using the orally bioavailable RAGE inhibitor Azeliragon (TTP488; trial for Mild Alzheimer’s disease), suggesting additional anti-AGE drugs are available. A clinical study further reported that restriction of oral AGE intake reduced systemic AGE levels and improved insulin resistance in humans with type 2 diabetes (Uribarri et al., 2011), suggesting that effects of AGEs might be reversible. Importantly, we observed indications for endochondral ossifications in human IVDs already in grade II IVDs, a stage at which preventative treatment could still inhibit further degeneration. In conclusion, accumulation of the AGE MG-H1 was associated with endochondral ossifications, hypertrophy and osteogenic differentiation in human IVDs and mechanistic investigations on IVD cells showed a direct relationship involving RAGE, suggesting that AGE/RAGE could be a potential therapeutic target. Further investigations in animal experiments are warranted to assess whether targeting AGEs via the AGE/RAGE axis can potentially provide a non-invasive treatment option for preventing progression of IDD

This report makes me wonder, how long will it take until the FDA or the USDA to wake up and realize that what they’re recommending everyone eat is actually what’s making everyone sick. Then I think about who controls the FDA and the USDA, it somehow nullifies my curiosity, I know who is responsible. A multinational chemical company intent on bolstering their profits at whatever cost may be brought about their actions.

It’s when those actions bolster the profits of another related industry that I get bothered. When I see people conned into consuming foods that make them sicker every day, I get a little upset. When I see this, I see my mother dying because she bought into this ruse herself. This makes this ruse the most danger con game ever to hit mankind.

The following report submitted Mar 2 2009 details the beginning of glycation from the fundamental elements of glucose, glyoxal and methylglyoxal, and their roles in aging and disease;

  • Protein and nucleotide damage by glyoxal and methylglyoxal in physiological systems – role in ageing and disease

Glyoxal and methylglyoxal are potent glycating agents. Glycation of proteins is a complex series of parallel and sequential reactions collectively called the Maillard reaction. It occurs in all tissues and body fluids. Early stage reactions in glycation of protein by glucose lead to the formation of fructosyl-lysine (FL) and N-terminal amino acid residue-derived fructosamines. Later stage reactions form stable end-stage adducts called advanced glycation endproducts (AGEs). FL degrades slowly to form AGEs – and also glyoxal and methylglyoxal. In contrast, glyoxal and methylglyoxal react with proteins to form AGE residues directly and relatively rapidly. 

Glycation by glyoxal and methylglyoxal, and the related influence of Glo1, are now emerging as playing a critical role in ageing and disease processes – vascular complications associated with diabetes renal failure, Alzheimer’s disease, and tumourigenesis and multidrug resistance in cancer chemotherapy. They may also have roles in pathologic anxiety, autism, obesity and other disorders. 

Again, this is just one of 804 return reports from a search of Lymphoma and glycation. To think that one has nothing to do with the other is what the FDA and the USDA seem to be doing in the continued recommendations to eat the food that does the glycating. If you were to tell me that the influence of Monsanto’s execs in the offices and agencies had nothing to do with these decisions to alert the public about the dangers in what they’re eating, I’d have to tell you that you are completely misinformed. Can I sell you some ocean front property in Kansas?

Does this mean that you’re stupid? Absolutely not. It just means that you’ve been duped like everyone else. It’s really easy to do. All you have to do is taste the food. One taste and you’re hooked. Since it doesn’t kill you immediately, it’s assumed safe. This assumption is what’s killing America and the rest of the world. This is the most deadly assumption to make, bread is safe to eat. Bread nowadays is deadly.

The next report I looked at was from Nov 10, 2016 and it displays the extent this industry will go to, to simply allow this addiction to kill as many people as it possibly can, by it to continue. Its purpose is to show the benefits of Bazedoxifene, a new drug being tested for reducing apoptosis and oxidative stress, when all they have to do is to recommend the cessation of the consumption of grains and sugar that leads to the glycation that is responsible for all these diseases. They’re not interested in arresting it or abating it. Their sole interest is to expand its influence, to addict more and more people. This appears to be done solely to increase the profits of the pharmaceutical industry. It explains the benefits of a new drug that the industry wants to impose upon the people, probably in the guise of helping the people;

  • Bazedoxifene Ameliorates Homocysteine-Induced Apoptosis and Accumulation ofAdvanced Glycation End Products by Reducing Oxidative Stress in MC3T3-E1 Cells.


Elevated plasma homocysteine (Hcy) level increases the risk of osteoporotic fracture by deteriorating bone quality. However, little is known about the effects of Hcy on osteoblast and collagen cross-links. This study aimed to investigate whether Hcy induces apoptosis of osteoblastic MC3T3-E1 cells as well as affects enzymatic and nonenzymatic collagen cross-links and to determine the effects of bazedoxifene, a selective estrogen receptor modulator, on the Hcy-induced apoptosis and deterioration of collagen cross-links in the cells. Hcy treatments (300 μM, 3 mM, and 10 mM) increased intracellular reactive oxygen species (ROS) production in a dose-dependent manner. Propidium iodide staining showed that 3 and 10 mM Hcy induced apoptosis of MC3T3-E1 cells. Moreover, the activities of caspases-8, 9, and 3 were increased by 3 mM Hcy. The detrimental effects of 3 mM Hcy on apoptosis and ROS production were partly reversed by bazedoxifene and 17β estradiol. In addition, real-time PCR, immunostaining and Western blot showed that 300 μM Hcy decreased the expression of lysyl oxidase (Lox). Furthermore, 300 μM Hcy increased extracellular accumulation of pentosidine, an advanced glycation end product. Treatment with bazedoxifene ameliorated Hcy-induced suppression of Lox expression and increase in pentosidine accumulation. These findings suggest that high-dose Hcy induces apoptosis of osteoblasts by increasing oxidative stress, and low-dose Hcy decreases enzymatic collagen cross-links and increases pentosidine accumulation, resulting in the deterioration of bone quality. Bazedoxifene treatment effectively prevents the Hcy-induced detrimental reactions of osteoblasts. Thus, bazedoxifene may be a potent therapeutic drug for preventing Hcy-induced bone fragility.

Even though we’ve had an idea of the damage of glycation and what causes it for over 30 years, This industry is still concentrating on making new drugs. Drugs always have side effects that lead to more drugs, yet this is this industry’s modus operandi. They don’t know how to operate otherwise. It’s the ties to the grains industry that I object to and the power we’ve given to these industries, simply to allow the public to continue to feed their addiction. You might as well tell us to stand in front of a racing bus or semi. You’re basically selling us the same thing, future time in the hospital;


Elevated plasma homocysteine (Hcy) level increases the risk of osteoporotic fracture by deteriorating bone quality. However, little is known about the effects of Hcy on osteoblast and collagen cross-links. This study aimed to investigate whether Hcy induces apoptosis of osteoblastic MC3T3-E1 cells as well as affects enzymatic and nonenzymatic collagen cross-links and to determine the effects of bazedoxifene, a selective estrogen receptor modulator, on the Hcy-induced apoptosis and deterioration of collagen cross-links in the cells. Hcy treatments (300 μM, 3 mM, and 10 mM) increased intracellular reactive oxygen species (ROS) production in a dose-dependent manner. Propidium iodide staining showed that 3 and 10 mM Hcy induced apoptosis of MC3T3-E1 cells. Moreover, the activities of caspases-8, 9, and 3 were increased by 3 mM Hcy. The detrimental effects of 3 mM Hcy on apoptosis and ROS production were partly reversed by bazedoxifene and 17β estradiol. In addition, real-time PCR, immunostaining and Western blot showed that 300 μM Hcy decreased the expression of lysyl oxidase (Lox). Furthermore, 300 μM Hcy increased extracellular accumulation of pentosidine, an advanced glycation end product. Treatment with bazedoxifene ameliorated Hcy-induced suppression of Lox expression and increase in pentosidine accumulation. These findings suggest that high-dose Hcy induces apoptosis of osteoblasts by increasing oxidative stress, and low-dose Hcy decreases enzymatic collagen cross-links and increases pentosidine accumulation, resulting in the deterioration of bone quality. Bazedoxifene treatment effectively prevents the Hcy-induced detrimental reactions of osteoblasts. Thus, bazedoxifene may be a potent therapeutic drug for preventing Hcy-induced bone fragility.

This displays the true despair of this problem, an industry more intent on driving profits than healing the people they affect. Their only interest is in making more drugs to allow the continuation of an addiction that’s putting more people in the hospital than any other one thing. To me, that is the definition of criminal behavior. This is a clear indication of legal extortion….and we allow it to continue, to feed our addiction.

This next report dated Oct 18, 2016, shows the influence of Metformin on the AGE population in our blood. It turns out to be another way to get you to take more drugs, as this drug encourages increased levels of CML (another AGE).


Metabolic syndrome (MetS) is considered one of the most important public health problems. Several and controversial studies showed that the role of advanced glycation end products (AGEs) and their receptor in the development of metabolic syndrome and therapeutic pathways is still unsolved. We have investigated whether plasma pentosidine, carboxymethyl-lysine (CML), and soluble receptor for advanced glycation end products (sRAGE) levels were increased in patients with MetS and the effect of metformin in plasma levels of pentosidine, CML, and sRAGE. 80 control subjects and 86 patients were included in this study. Pentosidine, CML, and sRAGE were measured in plasma by enzyme-linked immunosorbent assay (ELISA). Plasma pentosidine, CML, and sRAGE levels were significantly increased in patients compared to control subjects (P < 0.001, P < 0.001, and P = 0.014, resp.). Plasma levels of pentosidine were significantly decreased in patients who received metformin compared to untreated patients (P = 0.01). However, there was no significant difference between patients treated with metformin and untreated patients in plasma CML levels. Plasma levels of sRAGE were significantly increased in patients who received metformin and ACE inhibitors (P < 0.001 and P = 0.002, resp.). However, in a multiple stepwise regression analysis, pentosidine, sRAGE, and drugs treatments were not independently associated. Patients with metabolic syndrome showed increased levels of AGEs such as pentosidine and CML. Metformin treatment showed a decreased level of pentosidine but not of CML. Therapeutic pathways of AGEs development should be taken into account and further experimental and in vitro studies merit for advanced research.

The purpose of this study was to look at Metformin’s effect on two different AGEs, pentosidine and CML. Again the emphasis is on finding ways to keep the glycating substances in the diet and offering treatment only, not in finding a cure. That would involve removing the glycating substances from the diet and that would hurt the grain industry. Their treatment though, involves the continuation of their prescribed drug regimen. This is why they pay the prettiest reps to sell their drugs to all the doctors who prescribe them.

Dated May 2016 is this report on the role of DAMP in inflammation, cancer and tissue repair;



This review aimed to take stock of the current status of research on damage-associated molecular pattern (DAMP) protein. We discuss the Janus-faced role of DAMP molecules in inflammation, cancer, and tissue repair. The high-mobility group box (HMGB)-1 and adenosine triphosphate proteins are well-known DAMP molecules and have been primarily associated with inflammation. However, as we shall see, recent data have linked these molecules to tissue repair. HMGB1 is associated with cancer-related inflammation. It activates nuclear factor kB, which is involved in cancer regulation via its receptor for advanced glycation end-products (RAGE), Toll-like receptors 2 and 4. Proinflammatory activity and tissue repair may lead to pharmacologic intervention, by blocking DAMP RAGE and Toll like receptor 2 and 4 role in inflammation and by increasing their concentration in tissue repair, respectively.


We conducted a MEDLINE search for articles pertaining to the various issues related to DAMP, and we discuss the most relevant articles especially (ie, not only those published in journals with a higher impact factor).


A cluster of remarkable articles on DAMP have appeared in the literature in recent years. Regarding inflammation, several strategies have been proposed to target HMGB1, from antibodies to recombinant box A, which interacts with RAGE, competing with the full molecule. In tissue repair, it was reported that the overexpression of HMGB1 or the administration of exogenous HMGB1 significantly increased the number of vessels and promoted recovery in skin-wound, ischemic injury.


Due to the bivalent nature of DAMP, it is often difficult to explain the relative role of DAMP in inflammation versus its role in tissue repair. However, this point is crucial as DAMP-related treatments move into clinical practice.

Another study proving the role of glycation in the pathogenesis of arthritis proves once again how inflammation is the result of glycation, something you have control over:

  • The potential role of advancedglycation end products (AGEs) and soluble receptors for AGEs (sRAGE) in the pathogenesis of adult-onset still’s disease.


Accumulating evidence has demonstrated a pathogenic role of advanced glycation end products (AGEs) and receptors for AGEs (RAGE) in inflammation. Soluble RAGE (sRAGE), with the same ligands-binding capacity as full-length RAGE, acts as a “decoy” receptor. However, there has been scanty data regarding AGEs and sRAGE in adult-onset Still’s disease (AOSD). This study aimed to investigate AGEs and sRAGE levels in AOSD patients and examine their association with clinical characteristics.


Using ELISA, plasma levels of AGEs and sRAGE were determined in 52 AOSD patients, 36 systemic lupus erythematosus(SLE) patients and 16 healthy controls(HC). Their associations with activity parameters and disease courses were evaluated.


Significantly higher median levels of AGEs were observed in active AOSD patients (16.75 pg/ml) and active SLE patients (14.80 pg/ml) than those in HC (9.80 pg/ml, both p < 0.001). AGEs levels were positively correlated with activity scores (r = 0.836, p < 0.001), ferritin levels (r = 0.372, p < 0.05) and CRP levels (r = 0.396, p < 0.005) in AOSD patients. Conversely, significantly lower median levels of sRAGE were observed in active AOSD patients (632.2 pg/ml) and active SLE patients (771.6 pg/ml) compared with HC (1051.7 pg/ml, both p < 0.001). Plasma sRAGE levels were negatively correlated with AOSD activity scores (r = -0.320, p < 0.05). In comparison to AOSD patients with monocyclic pattern, significantly higher AGEs levels were observed in those with polycyclic or chronic articular pattern. With treatment, AGEs levels declined while sRAGE levels increased in parallel with the decrease in disease activity.


The elevation of AGEs levels with concomitant decreased sRAGE levels in active AOSD patients, suggests their pathogenic role in AOSD.

Juvenile arthritis is shown in this study to be the product of glycation, again something you have control over by what goes in your body for food. If you or your child suffers from this, your only cure is to stop the glycation. The older you are the less you can reverse. But if you’re young enough, you may be able to reverse a majority of it.


The involvement of high mobility group box-1 (HMGB1) in various inflammatory and autoimmune diseases has been documented but clinical trials on the contribution of this pro-inflammatory alarmin in children with juvenile idiopathic arthritis (JIA) and systemic lupus erythematosus (SLE) are basically absent. To address the presence of HMGB1 and a soluble receptor for advanced glycation end products (sRAGE) in different subtypes of JIA and additionally in children with SLE, we enrolled a consecutive sample of children harvested peripheral blood as well as synovial fluids (SF) at diagnosis and correlated it with ordinary acute-phase reactants and clinical markers.


Serum and synovial fluids levels of HMGB1 and sRAGE in total of 144 children (97 with JIA, 19 with SLE and 27 healthy controls) were determined by ELISA.


The children with JIA and those with SLE were characterised by significantly higher serum levels of HMGB1 and significantly lower sRAGE levels compared to the healthy controls. A positive correlation between serum HMGB1 and ESR, CRP, α2 globulin was found while serum sRAGE levels were inversely correlated with the same inflammatory markers in children with JIA. Additionally, high level of serum HMGB1 was related to hepatosplenomegaly or serositis in systemic onset JIA.


The inverse relationship of the HMGB1 and its soluble receptor RAGE in the blood and SF indicates that inflammation triggered by alarmins may play a role in pathogenesis of JIA as well as SLE. HMGB1 may serve as an inflammatory marker and a potential target of biological therapy in these patients. Further studies need to show whether the determination of HMGB1 levels in patients with JIA can be a useful guideline for detecting disease activity.

What’s important is that you stop the glycation as soon as possible to arrest to glycation. The secret to this cure is an end to all glycation. The magic of this cure is the end of the hunger cycle.

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 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 100’s 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.


For 2500 years, physicians have used fasting as a means to find the way back to health, by a simple and inexpensive manner in which one could actually heal themselves from virtually any of the modern diseases that have plagued man, since the dawn of civilization. For me, it’s easy to see the correlation of the emergence of modern diseases with the gradual increase of consumption of einkorn wheat, the precursor to our modern strains of wheat. From Emmer (one of the first domesticated strains) and Durum Semolina which is little higher in gluten yet it’s still considered a weak wheat. (The wheat doesn’t rise as well as it holds the dough together to hold the pasta shape.) Winter Red, spelt and other bread wheats or common wheats that’re higher in gluten have been used for bread for thousands of years, because it rises better. Today’s forms of highly modified wheat act nothing like the strains from thousands of years ago as today’s  highly domesticated strains of wheat cannot survive in the wild. That’s according to Wikipedia and that’s due to their inability to disperse their seeds. Monsanto has made certain of that through their genetic modifying to create ender seeds that won’t pollinate so a farmer has no seed for next year’s crop forcing them to buy GMO seed from Monsanto. (GMO by itself is not dangerous. It’s what the modifying allows the farmer to do that makes it dangerous and that’s to spray it with Roundup. Their seed is genetically modified to handle applications of the glyphosate herbicide.) This is the wheat that Monsanto is forcing their farmers to grow for your cereal, bread and snacks. The same exists in the corn fields as well, contaminating every corn chip that you eat. (When was the last time you ate Mexican food?)

But we’re talking about wheat right now which was originally cultivated in the Fertile Crescent 10,000 years ago, approximately the same time that modern disease started showing up in the bones of the remains of the people. This is a clear indication of the glycation that wheat was responsible for even then, even as slow as the einkorn wheat is to digest (which slows the progression of glycation). The glycation existed then as it does now, only it took it much longer to manifest. Today, it manifests itself immediately (as soon as it touches your tongue) and this is due to the fast dissolving gluten flour that’s used for bread and pastries as well as pasta and cereal. It just glycates more now as the grain has changed immensely in the last 10,000 years. As these foods increased in prevalence in our diet, the rates of disease increased, as it’s these grains that have always generated disease. They generate it so slowly that it’s never noticed until it’s too late or you stop eating it. This is the value of fasting and why fasting is so important to the health of anyone on this type of carbohydrate diet.

This is why fasting has always cured disease. 98% of all disease is a direct result of our diet. With that being said, it’s easy to see why removing everything damaging from our diet is going to heal the damage caused by keeping those foods in the diet. Fasting produces such good results it’s been the subject of over 20,000 studies on PMC in the NLM at the NIH. (PMC has reports from across the world. Pubmed has 590 reports from studies done in the US alone.) It’s that important, yet what has your doctor shared with you about this life saving course of intervention? Your doctor comes into your appointed meeting with his/her prescription tablet in hand ready to prescribe pharmaceuticals. (Now it’s a laptop that affords them more latitude in their diagnosis. I sometimes see a primary care physician who still carries a prescription pad with him everywhere he goes, but then he has drug reps going in and out of his office all the time, so to speak.) Their whole intent is to prescribe drugs for your ailments, which are more than likely caused by the ingestion of grain foods. Prescribing drugs is the way they’re trained to treat patients, not with recommendations of diet. (Monsanto wouldn’t allow that to take place as they have far more control over your life than what you could ever believe.)

That’s exactly why fasting is so healthy. It removes the worst of the toxins in our bodies that’s built up from the diets of bread, wheat and grain based products, and doesn’t put more toxins back in with the prescribed drugs. Those grain products also happen to be the most addictive, which is what makes them the hardest to give up. The addictive nature of sugar, at its worst, is displayed in this manner (when it drives pharmaceuticals). When one fasts, they give up the sugars that are doing all the glycating and it’s this glycation that is at the root of all disease and this is why going without food is so healthy.

It also sets your body up for future health by resetting the hormonal structure in your body. This is mostly the result of your hormones transitioning to a starvation mode of survival, where the Ghrelin your stomach releases, sends this growth hormone throughout your body allowing them to do their magic in repairing damage and extending cell life where cell death took place before. (This is directly due to the carbohydrate influence in the diet, creating glycation.) It’s the elimination of glycation that initially brings back a resemblance of health but that’s not what brings future health. It’s the breaking of an addiction. This addiction is built into our society so much, It starts in our prenatal body and continues through the first year of life and then on. (This is due to the prevalence of sugar and high fructose corn syrup in baby foods, formula and infant medicines.) The prenatal starts with mama diet before you’re born, if your mother ate carbs, you got them before your were born. But that only explains why you’re dependent. It doesn’t explain how to break the dependence. That’s with fasting and the keto diet, or ketogenic diet (the diet our ancestors were on ever since our existence). The keto involves fasting as part of the diet, making it much easier to maintain. (There’s no hunger.) Fasting does that by sending your body into ketosis.

According to Wikipedia; in the early 20th century around 1911; Bernarr Macfadden, an American exponent of physical culture, popularized the use of fasting to restore health. His disciple, the osteopathic physician Hugh Conklin, of Battle Creek, Michigan, began to treat his epilepsy patients by recommending fasting.  Conklin conjectured that epileptic seizures were caused when a toxin, secreted from the Peyer’s patches in the intestines, was discharged into the bloodstream. Conklin’s fasting therapy was adopted by neurologists in mainstream practice. In 1916, a Dr McMurray wrote to the New York Medical Journal claiming to have successfully treated epilepsy patients with a fast, followed by a starch- and sugar-free diet, since 1912. In 1921, prominent endocrinologist H. Rawle Geyelin reported his experiences to the American Medical Association convention. He had seen Conklin’s success first-hand and had attempted to reproduce the results in 36 of his own patients. He achieved similar results despite only having studied the patients for a short time. He reported that three water-soluble compounds, β-hydroxybutyrateacetoacetate and acetone (known collectively as ketone bodies), were produced by the liver in otherwise healthy people when they were starved or if they consumed a very low-carbohydrate high-fat diet.

With fasting being able to eliminate so many disorders, a path was sought to bring this form of healing to the mainstream by creating a diet to encourage fasting. Thus the ketogenic diet was born in 1921 through the efforts of Russel Wilder. According to Wikipedia, Russel Wilder, at the Mayo Clinic, built on this research and coined the term ketogenic diet to describe a diet that produced a high level of ketone bodies in the blood (ketonemia) through an excess of fat and lack of carbohydrate.

Fasting is the quickest manner in which to allow your body to go into ketosis, yet it may not be the easiest. Although on second thought, being the quickest way may make it the easiest. I went through two weeks of withdrawal because I couldn’t give up all foods I loved to eat all at once, to allow my body to go into ketosis in a few days. I could have avoided 10 days of want by fasting and only want something to eat for a few days, as what happens when you fast for a minimum of 3 days. A longer fast is more beneficial but the three days allows your body to respond by going into ketosis which is a fat burning mode. It’s this fat burning mode that forces your body to make its own glucose, which is a much cleaner glucose than you get from the sugar you eat, as it’s a clean glucose made from your own glycogen or fat storage. Getting into ketosis quicker could allow you to start your fat burning diet, but continuing some carbs will only make the withdrawal more difficult as it may drop your body back out of ketosis. This was my problem and why my transition took so long. (Thankfully, they’ll be no next time.)

Ketosis refers to acids in the body that are derived and used while in a state of low glucose in the blood. Because my body has been in a state of ketosis for the last 3 years, I feel qualified to speak about this lifestyle. I call it a lifestyle because it really is. It’s a lifestyle completely different from the lifestyle of a carboholic. Carboholics require food every other hour or so, it’s the law of glucose consumption, appetite follows glucose levels in the blood. It’s that simple, blood sugar levels raise and satiety sets in, releasing hormones controlling feel-good emotions influencing behavior, sometimes unrecognizable behavior. But, that usually happens when the blood sugars fall again after a couple hours releasing hormones of hunger, need and want. These hormones are completely different than the satiety hormones and have much different affects on the body.

This is where carboholics do not have the advantage that ketonemiacs have. Ketonemiacs (those who have allowed their bodies to go into a state of ketosis) aren’t controlled by their hormones, so they don’t have to follow any hunger cycle. They’re in full control of their hormones. This also means that they’re in more control of their emotions because of that. I know that it doesn’t sound like it’s that big of a deal, but it’s more important than you ever could imagine.

First, let’s look at the state of ketosis, as explained in Wikipedia;

Ketosis is a metabolic state in which most of the body’s energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis in which blood glucose provides most of the energy. Ketosis is similar to a condition called ketoacidosis, in that both cause a side effect known to laypeople as acetone breath.”

“Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet, and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes.[6] In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed.[5][7] For this reason, ketosis is sometimes referred to as the body’s “fat burning” mode.”

Even body builders have recognized ketonemia as being to most beneficial state to keep their body in as it’s in this state where they produce more growth hormones because of the amount of Ghrelin their stomachs release to enable them to grow their muscles bigger without the carbs.

It used to be one of the biggest problems, being in a state of ketosis is often confused with ketoacidosis, which has nothing to do with being in a state of nutritional ketosis. Ketoacidosis is a state of extreme ketosis that can only happen to type 1 diabetics because their pancreas is incapable of secreting enough insulin to handle even a large amount of glucose in the system. Because of this the liver of type 1 diabetics secretes more ketones than what the body needs to operate.  Again Wikipedia says on the subject of ketosis;

“Ketosis is deliberately induced by use of a ketogenic diet as a medical intervention in cases of intractable epilepsy. Other uses of low-carbohydrate diets remain controversial.[15][16] Induced ketosis or low-carbohydrate diet terms have very wide interpretation. Therefore, Stephen S. Phinney and Jeff S. Volek coined the term “nutritional ketosis” to avoid the confusion.[17]Although I appreciate ketosis as being a “fat burning mode”, it’s the other benefits that I appreciate more. Benefits like less pain, no headaches, no stomachaches, far more energy than what I’ve ever had, ability to get more work done, as I don’t have to stop all the time to eat and although I do eat at my desk, I’m usually at my desk 16-18 hours out of the day, except on therapy days. I take 3 hours, 3 days a week for therapy. My therapy is exercise. My brain needs it, but my body benefits.”

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. “

“In diabetic ketoacidosis, a high concentration of ketone bodies is usually accompanied by insulin deficiency, hyperglycemia, and dehydration. Particularly in type 1 diabetics the lack of insulin in the bloodstream prevents glucose absorption, thereby inhibiting the production of oxaloacetate (a crucial precursor to the β-oxidation of fatty acids) through reduced levels of pyruvate (a byproduct of glycolysis), and can cause unchecked ketone body production (through fatty acid metabolism) potentially leading to dangerous glucose and ketone levels in the blood. Hyperglycemia results in glucose overloading the kidneys and spilling into the urine (transport maximum for glucose is exceeded). Dehydration results following the osmotic movement of water into urine. (Osmotic diuresis), exacerbates the acidosis.”

“I bring this up to make the point that nutritional ketosis is not ketoacidosis. It’s far from it. According to Wikipedia again, “Normal serum reference ranges for ketone bodies are 0.5–3.0 mg/dL, equivalent to 0.05–0.29 mmol/L.[23]” In ketosis, the levels range from 3 – 6 mg/dL. Ketoacidosis requires a level of 15 – 25 mg/dL, more the three times needed for ketosis, making it virtually impossible for anyone to into ketoacidosis if you’re not a type 1 diabetic. Type 1 diabetics are required to make sure their bodies don’t produce many ketones because of the risk of ketoacidosis”.

According to PMC’s report on Calorie Restriction (CR) or fasting, submitted; July 2010; Nevertheless, ongoing research continues to draw a more complete picture of CR at the molecular level, which may ultimately allow for the development of therapeutics that might be able to confer at least some of the health benefits of this dietary regimen.

Remaining in a state of ketosis, on the other hand, has allowed my body to regain that which was lost 31 years ago in a car accident that left me severely disabled because of a severe closed head injury, (It was the two strokes that were the most devastating.)

It’s become evident to me since I’ve been carb free and in a state of ketonemia or ketosis, how much our society is addicted to this drug (sugar/glucose/fructose) that does little more than to lead those who eat it to further drug use. Our food industrial complex sees to that by their advertising . I’m convinced it’s because they’re associated with the pharmaceutical industry. They used to be merged into one corporation that controlled the seed supply for the farmers as well as the pharmaceuticals that treated to pain and discomfort brought on by the products grown by the crop seed sold to the farmer to supply the grains for the snack foods everyone everywhere love to eat.

The unfortunate result of this love affair with those snack and comfort foods is what this diet brings, as its cost of this pleasure. The price to be paid is in the discomfort that this food brings to all those who eat it, regardless of how much they eat. The food industry (Monsanto in particular) has a fortune invested in keeping you eating this deadly food. They’ve built an industry just to treat diabetes, with all the glucose meters and pumps out there, just so addicts can get their next fix. The trouble this industry goes to just to keep their addicts happy. I know now. I didn’t 4 years ago when I was an addict.

The less an addict consumes at each, sitting dictates how much damage it’s going to do, but it’s going to do damage. There is no way to avoid it. That’s the way our digestion and metabolism works. That’s why this addiction is by far, the worst addiction our society has to deal with. This addiction leads to every other addiction that we’re actively fighting, including alcoholism, heroin and tobacco and even gambling. Yes, even gambling, as gambling is driven by the hunger cycle which is one of the biggest underlying influences of a carbohydrate diet. Hunger in this diet drives absolutely everything, even breathing, and because of that, eventually drugs.

This is a cycle that I don’t need. As a matter of fact, it’s the last thing I need. The biggest reason I refuse to take any of these drugs anymore is because all of them carry side effects, some major, some minor. Whether the side effects are major or minor, I don’t want to experience any of them, anymore. I’ve had my fill of side effects, especially the ones that make my health worse, which is where most of these side effects should be classified. After living for twenty years needing to take massive amounts of opioids for my chronic severe pain, diuretics for my high blood pressure, anti-depressants for the pain, and living with the side effects of not only the opioids, but every other drug they had me on, all twelve of them, I got fed up with it. I wasn’t going to take it anymore as I just couldn’t afford it. And I was only up to twelve medications. I have a friend who’s on this diet, who’s lowered his needs to thirteen daily medications from twenty-three. How many meds do you take every day? How many would you like to do without, if your health would allow? This is where fasting needs to replace doping. A change in diet will go much further than any drug and the cure lasts longer than any treatment.

I live by the theory that if the meds aren’t needed in the first place, my health is going to be that much better. That is why I removed everything from my diet that I could, that is responsible for these horrendous diseases, requiring the need for these medications. By fasting, one can reach this healing state much quicker than I did, just by cutting my bread. Where it took me two weeks to get into full ketosis, by fasting I could have jump started the state by starving my body, then gone on from there with my ketogenic diet to keep my body in this healing state. This is the advantage of fasting, it not only starts the healing from the beginning by putting your body in a starvation mode, it allows you to stay in that mode for the rest of your life. That one little option in itself is what’s going to extent your life beyond 100 years. I can see where ultimately man will be able to extend it lifespan to over 150 years old. !00 years from now, when all mankind is on a ketogenic or paleo diet again, I can see the oldest people in the world living into their 180’s, doubling today’s average lifespan.

This can be easily obtained simply by allowing our bodies to heal themselves and not keep depending on drugs for the perception of healing, which ultimately brings nothing but more drug use, which ultimately is what ruins the liver and kidneys leading to all the cancers and disorders of the hepatic and renal systems. It’s this drug dependence that driven by another dependence that we’ve all been born into. I hope that you’re beginning to see how our drug addictions are driven by one thread that drives all modern diseases along with it.  That one thread is what ties 100% of all cancers, 98% of all heart diseases, and 99.9 % of all dementia, all arthritis, all headaches, and almost all stomachaches together is one substance that can be removed from the diet without any severe side effects. I shouldn’t need to tell you what that substance is by now. You should know. You eat it every day. You live with the effects of addiction. Pain always comes with addiction. (That’s what makes breaking the addiction rewarding, limiting the pain cycle. Oh what sweet bliss!)

The idea then is to limit to miniscule amounts, the foods that make up these addictive substances. You should know by now what these foods are, you eat them every morning, either in your coffee as creamer, in the toast you have, or the cereal you consume. You have it every lunch with your sandwich or burrito and with every dinner with your rolls. I have known several families that would just put a plate of bread on the table every evening. This is the display of addiction, a full out need to satisfy the taste buds by dumping more and more sugar in the body, usually in the form of starchy carbs. I’ve also noticed that in those houses that served bread there was always beer cans in the garbage indicating another addiction. If you remove one addiction from our society, you remove all addictions, as this addiction to sugar and carbs is the foundation of all other addictions as they are all based on a hunger cycle which is the result of an addiction to sugar. Does that make it the root of all evil?

I hope that you can see now that it’s this addiction to sugar and carbs that’s driving the pharmaceutical industry, and that both industries are driven by the same people who have a major influence in the offices of the agencies that are supposed to regulate this industry, the FDA and the USDA. With that kind of influence, there’s only one way to fight it and that’s to not buy into it. To not buy into it does require a diet of grain abstinence, though. That requires breaking the addiction and moving to as, ketogenic of a diet, as possible. The easiest manner to do this is to do a strict three day, water only fast. The longer you can do it the better, but it must be at least 3 days with absolutely no food. (That’s why it’s important to check with your doctor first).

All of the consumption of the grain industry’s products is what’s driving the pharmaceutical industry today, tomorrow, next year, and for the next 500 and beyond. If we don’t put and end to this now, our society is doomed to suffer the consequences of a carbohydrate addiction that no one is responsible for. The greed of the grain industry combined with the ambition of the pharmaceutical industry, has made us all carboholic slaves to the desires these industries. It’s these industries that are rewarding from the most, from this arrangement. For me, it’s scary, how much power we’ve given these industries, simply because we listen to their advertising. We’ve also let them take over the regulating agency that’s supposed to control this industry. Because our health depends on it, we can’t allow Monsanto to dictate how there are going to poison our food, so they can bolster the profits of the pharmaceutical industry.

Not knowing what you put in your body can cost you your life. It is costing you your life if you eat carbs. Those who listen to the advertising and are influenced by it, fall prey to that influence, and become their slaves for life or until they quit consuming the grains. There’s very little difference than that of alcoholism except that it’s pretty much forced upon us, in our baby food. Feed your babies on your own milk, if you want them to be healthy.

I know what you’re thinking right now, what are all the foods involved in this addiction? The list is enormous and that’s why this is such a dangerous addiction. This industry has virtually forced us to celebrate this addiction. It involves every one of our holidays, with the holiday season being the worst. Every celebration involves some form of sugar. From the Sugar Bowl to the Tostido’s Fiesta Bowl, our celebration is never-ending. Just after the “holiday season” comes Valentine’s Day barely a month later. Then, comes Easter and spring break. Are you beginning to understand why this addiction is our worst? With all the celebrating we need to keep this addiction, how do you change tradition without changing the world? The quickest way that I know is to organize an international health weekend, for 3 days, where everyone goes keto to heal their diseases and give their bodies a chance to go into ketosis, the ever healing state of metabolism.

The nicest advantage of this diet is the amount of control it gives you over your own emotions. You may think that you control your emotions right now, but I can tell you with full confidence, if you’re on a carb diet, you have no control over your emotions. They’re completely controlled by what you eat because what you eat controls your hunger cycle and it’s your hunger cycle that drives every other cycle your body goes through. Since your hunger cycle is controlled by your hormones (mostly leptin and ghrelin), it’s these hormones that are controlling your emotions. You know this every time you crave that bagel or biscotti. Once you bite into it, your saliva starts digesting that instantly gratifying food to give you that aww feeling, that instantly hits you brain, even before you can swallow it. This is your first sign of addiction and dependence that only gives you the perception that you have control of your own emotions. It’s this cycle that is in full control of your emotions. As much as you try to control them, too often they have a tendency to slip out of your control and back into theirs.

Anyone who can’t control their emotions entirely by themselves is a slave to their own hormones. This makes every carboholic a slave to their emotions and therefore a slave to these industries. This displays the dependence of the hunger cycle and the carb diet that drives that hunger cycle. You may not classify these as emotions, but I submit that they actually are. Satiety is defined as the state of being satisfied. If that is not an emotion, as it expresses feelings of calmness and security, I don’t know what is. Hunger, on the other hand, is defined as a strong desire. Is not that an emotion? These emotions are controlled by both leptin and ghrelin, which ultimately are controlled by the grain industry, more than anything else. This is the ruse I refuse to take part in. I can’t afford this trap anymore. The only way out for our society is to break the hold of this industry, to let them know that we’re not going to stand for this kind of abuse. To go ketogenic in your diet is the best way you can get yourself to everlasting health.

With emotions being controlled by our hormonal balance like this, it’s easy to see how carbs could influence that balance. For this to not have an effect on our behavior is beyond comprehension. It has to. When you combine the drive of an addiction (which is what we’re talking about) with the advertisements promoting that addiction, how can it not have an effect on our health and ultimately our society? That is why I make the statement that this cycle has to change. If it doesn’t cease, our health as a society, will never get better. There’s never been a better time for a cure, and that cure is a ketogenic diet, not only for each and everybody to be as healthy as possible, but also to regain the health of our whole society. Can you imagine a world where everyone not only controls their own emotions but they’re in control of their emotions? (That includes reactions.)

Let’s go back to addiction, though, for you may still not consider this an addiction. I understand, few caught in an addiction can recognize that addiction when they’re feeding it because the addiction has ways of hiding itself. You can ask anyone who has to have at least one beer a day. They’re not addicted to their beer, as far as they’re concerned, yet they have to have it. And often they don’t even drink more than just one. But they still have to have that one. That is what makes it an addiction. The body can and does live much better without beer, so it’s not a substance the body requires to survive. Yet the beer drinker needs that daily beer to satisfy their addiction. To go without, many times causes more problems because of the work your hormones are doing on your emotions and worse yet your actions by controlling how receptors work in your brain. That makes it a natural thing that you need to do, and not an addiction, to appease that desire to drink the beer. This is how addiction works and it happens to carboholics too. I know I am a carboholic. The desire for sweets is still with me. It’s a last refuge of my addiction. It’s something that I get to fight for the rest of my life.

Fact of the matter is, if you were fed baby food, you’ve been fed carbs, on the premise that this food is healthy to eat. Actually, you’ve been sold that this is the only healthy food to eat. Fault has been found in every other type of nutrition except  grains until recent history. For more than 60 years, we’ve been told to eat grains. Thirty years ago, they said whole grains are healthy. They still say, ”whole grains are healthy”, yet according to all the studies I’ve seen out of the hundreds I‘ve looked at, nothing about this food is safe to ingest, leaving me to wonder why do they still recommend it. Then I look at who controls the FDA, the USDA and what interest they have in their industrial farming, and it becomes pretty clear whose influence this is, controlling what we eat.

This simple little act of feeding you baby formula laced with sugars to get you to eat it, has addicted you to a lifetime of dependence. It addicted me. Even though I broke the addiction, I’m still affected by what control it did have over me. That’s exactly why I’m pleading with you, don’t let it control you. I can virtually guarantee that you won’t like the end results. Whether they come late or soon, they always come.

When I think about this, my first response is to get angry, for I never asked for this nor could I ever wish for it, or wish it upon anyone else. Yet, there is an industry that is committed to not only continuing this pattern, they’re goal is to increase its scope. You can see this in all the advertising. This is your grain industry pushing this celebration of this addiction and you’re buying into it every time you feed your carb diet, by buying all your snacks, pasta, cereal, soft drinks and beer, just for starters. I’d go on with the rest but space limits that list in this book. You can find it in both my first and second books, It’s Time for a Cure and Time for the Ultimate Cure. Your best guide is to use the glycemic index as your guide for what foods that are safe to eat or not. It’s the general consensus that you should keep your foods lower than 50 on the glycemic index. My contention is to keep carbs out of your diet completely, and let your body make its own glucose. The reason you want to keep your blood glucose low is to avoid the hunger cycle. The hunger cycle is emotionally the worst manifestation of a carb diet. As it controls your emotions, it controls your actions and reactions. This is an undeniable truth. You know it as well as I do. You feel it every time you taste that divine taste when you bite into it, MMM how good it is.

This is where you need to ask yourself, what is it you crave most? If what you crave has any carbohydrate in it, then that’s your first indication that you’re addicted. What kind of carb you crave, quite often tells how bad your addiction is. One wouldn’t think that a hamburger could be a sign of addiction, when actually when you think about the taste you crave, it’s a combination of everything including the bun, which happens to be the addictive ingredient in the hamburger. Everything else in the hamburger is healthy. It’s just the gluten in the bun that’s so addictive. I wouldn’t doubt that they use extra high gluten bread dough for the buns used for these sandwiches, as it’s more addictive, due to the high gluten content. I know they use high gluten bread dough for making pizza dough because it needs to rise, and the more the gluten the better it rises. That makes it taste better, but it also makes it more addictive. That’s why when you’re at one of these restaurants, most everyone there is overweight. They’re there because they crave that high gluten bread dough. You get it in both pizzas and fast food hamburgers. This is how they make you repeat customers.

If you think my assessment is wrong, just try eating your favorite hamburger between to slices of lettuce. The taste is completely different. Most fast food restaurants offer low carb sandwiches but few order them. The only ones that I know of who order them are those who suffer from celiac disease. I believe that all of us suffer somewhat from celiac disease. I think that there are only a very few that can get through life with showing or suffering the effects of a carb diet….especially an excessive carb diet as is the case with most people worldwide today. The reason you crave the taste of the hamburger is because of the high gluten bread dough the buns are made from because it’s that bun that raises your blood glucose as soon as it hits your tongue. Therein lies the addictive nature of glucose, the constant tug on your hunger cycle. It’s caused by the foods you eat, if you’re on a carb diet. When you stop to think about it, you know it, as well as I. You just need to do something about it, as I did, three years ago, and then again one year ago when I went complete keto. It took me three years to go completely keto. You can do it in one month if you’ve got the guts to do a thirty day fast. I didn’t and I may have suffered because of it. I guess I was still persuaded to eat the carbs even after I gave up the bread. If I had to do it over again, I’d fast, to go keto. The adjustment is a lot quicker. The adjustment is equivalent to breaking the addiction.

What do you think they’re advertising when they show you those commercials for pizza and their soft drinks, fruit drinks, cereals, breads, pastas, pastries, candy, etc, etc? They selling you that mmmm feeling of dependence and addiction. It’s that feeling your get as soon as your favorite food hits your tongue and makes you go “oh, I needed that”. That’s the same feeling a junkie feels when he gets his latest fix.

They’re using your emotions to control your behavior. That’s because they can. They already control your hormones and it’s your hormones that control your emotions. Is it any wonder that so many are addicted? Our food industry has done their absolute best to sell you their goods, and that means playing to your emotions in order to sell you that great taste that’s going to bring you oh so much discomfort, pain and disease. If you had known that this could and would happen to any one of your kids, you’d do everything in your power to change it. You do have the power to change it, every time you go to the store. Read the label of everything you buy. If it contains wheat, corn, soy or grains at all, don’t buy it. If you do, you’ll be buying into a lifetime of pain and discomfort for your family. Choose something else to feed your family. You’ll be much further ahead in the long run. The money it will save you in pharmaceuticals is nothing short of astounding.

In my estimation, this is criminal behavior. It’s criminal behavior being done on an industrial level. Monsanto has politically engineered their control of the FDA and USDA to ensure their compliance in their dominance of our food supply.

That is why I included my third chapter on our celebration of our addiction. Corporate does this on purpose. They do this because they know that we are addicted by our rate of consumption of their wares. They also know that with their lobbying power, they can get away with virtually anything. It’s kind of the same situation as that of the military industrial complex. They support congressmen and senators in every state and district, securing their interests, with this influence. Monsanto has even gone to the extent of contracting every farmer that they can, even to the point of suing farmers, just to corner the market. The last corporations that got away with this kind of behavior were busted up by Teddy Roosevelt in the late 19th century. No industry in our history has had more influence in our health, either as an individual or as a society than this grain and sugar industry has with it addictive food. It’s created a multi-trillion dollar medical and pharmaceutical industry. The thing that scares them the most is the ketogenic diet as it’s the only diet that can save you and the world, from their clutches.

We allow these corporations to addict us, even worse than we’ve been any time in the history on man, for which we should be ashamed. I would be but I didn’t set up the Supreme Court to allow Monsanto to patent life in patenting GMO seeds. This may end up being the bane of mankind, as it is a very deadly path for our food industry to be taking. But then it’s only deadly to those who buy into it. That’s why I won’t.

The Best Way to Fight Hunger Fights Terrorism As Well

The Best Way to Fight Hunger

Fights Terrorism As Well

Hunger pervades our society. Everybody experiences hunger every day. Some people experience hunger all day all night long. At least it’s thought so. Actually those who go without food don’t often experience hunger except for the ones who haven’t broken the cycle of hunger. This is a cycle that controls hunger a few hours at a time at a time. This is also addiction. This is your addiction to glucose. It works by playing with your hormones every your blood glucose levels change. When you eat carbs your glucose levels are altered, it’s this alteration of your blood glucose levels that alters the reaction of your hormones. It’s those changes in your hormones that affect your behavior, and makes you act in the manner you do. It’s those changes in hormones that also affect your hunger cycles.

This is a simple one. At least, to me, it’s simple. Actually, this may be the easiest and simplest cure for hunger that exists today. If you think it’s time for a cure for hunger, I’ve got the solution; to best fight hunger, you need to stop the hunger cycle. You need to do this not by feeding the starving people bags of flour and corn to eat, but by giving them education about nutrition and diet to get them off of the flour and corn diet. That is what makes them hungry and dependent on the grains for their diet. They will remain dependent until they either quit eating the grains, or die. The death part always comes prematurely, always. This is the addiction part of the cycle.

Since you can live better without carbs (I’m proving that), your body does not need them. That is the definition of addiction, the body requiring something it doesn’t need and manifesting discomfort when it’s not available for the affected to use. This is the same as what an alcoholic goes though when they can’t get a drink. It’s what cigarette smokers feel when they need a smoke. It’s a need that has to be satisfied, but it can only be satisfied in your mind, where your hormones affect your emotions. They affect your emotions in your mind, more than anywhere else. This is your instruction center for the body, for what happens in the body and how you react to whatever stimuli affect the body.

How Glucose Creates Terrorism

Your emotions should remain in your control, not in the control of what you eat. When you allow that to happen, you’re allowing the industry that controls what you eat, to control how you feel and what you do, by controlling your emotions. This is a cycle. It’s a cycle of dependence. It’s a cycle of dependence on the grain industry. Not the beef industry or dairy industry, simply the grain industry and its manufacturers and processors. It’s this industry that’s responsible for all glycation that occurs in your blood. It’s this industry that’s responsible for your hunger cycles and that put’s responsibility on them for your changes in emotions and behavior. It can also give them some responsibility for the terrorism that exists in the world today as it’s controlled by the amount of anger and hate that’s expressed which in turn is controlled by what controls the hate and anger and that’s a glucose diet. A diet that’s responsible for emotional changes by changing your hormones. This diet creates this hunger cycle that all who are living on a glucose diet can expect to live with. It’s the cost of a diet of carbs.

It’s not only a cycle of hunger, it’s a cycle of addiction. Every addict has to feed their addiction. When you feel hungry, what do you hunger for? What is the first thing you want to eat or drink? That tells you where your addiction lies. I know what you’re thinking right now, how can hunger to eat be an addiction? That’s the first question I’m asked, whenever I call this an addiction. This is how addictions work, they force your body to want something that it really doesn’t need. It creates discomfort in the body until that need is met. When that need is met, comfort takes place and damage internally begins. While your emotions are being controlled by your glucose infusion and making you feel comfortable, the glucose from the sugar and carbs is busy, very busy glycating whatever cholesterol or protein the glucose can find.

Those grains not only increase hunger, but they’re the prime agent behind all modern diseases caused by the creation of glycation in the blood. That’s exactly what these foods do. How they do it, right now, isn’t important. What’s important is that these foods, in the manner in which they are digested, not only create the glycation but they create hunger as well. It’s this hunger they create that makes them addictive and dangerous to the point of deadly.

It has to do with the fluctuation of your hormones due to your diet of grains. Once grains are ground, they lose their fiber. This is important because it’s the fiber that slows down the breakdown of the sugars in the grains that influence your blood glucose. The slower those sugars are introduced into your system, the slower they raise your blood glucose. Most diabetics know this, as it’s the quick rise in blood glucose that is responsible for the glycation and the release of hormones that disrupt the normal functions of the body. This is what drives the hunger cycle. This is what makes everyone hungry. My theory is to eliminate this cycle, and to eliminate the cycle, means changing the equation, the equation of digestion. The best way to change that equation is to changes the factors of the equation, in this case one factor. All you have to do to cure hunger and glycation is to remove carbohydrates from the equation and thus the diet. The solution is that simple. Maybe not easy, but simple.

When one considers the fact that the primary driver of hunger is a carbohydrate diet, it’s easy to see that the solution for hunger is to eliminate the hunger of hunger by changing the diet. Taking carbohydrates out of the diet removes the hunger factor and thus the hunger cycle. Anyone doubting this can go on the diet that I’ve been on for three years and they’ll know. Three years on the diet that I’ve been on will not only convince anyone of this concept, it will also improve their health in unimaginable ways. The last time I got hungry was 3 yrs 2 weeks ago. That was when I broke my addiction to glucose. Others who are on this diet will tell you the same thing, they don’t get hungry and the reason they don’t get hungry is that they don’t have the glucose going through their systems to create the hunger cycle.

Because this is an addiction, those who still eat carbs, can’t see. You have to break the addiction to know this. That’s the way it is with any addiction, you can’t see it while you’re in it. Yet, almost everyone knows that sugar is addictive. I think because nobody wants to equate that sugar with carbs, they don’t want to fully grasp that the carbs they were told they need, is sugar. Carbs,something your were told you have to have, breaks down to the exact same thing as sugar, and that’s glucose. Yet, they’re still telling everyone to eat whole grains. Maybe it’s always been spoken of in that manner because it seemed to justify our need for it. That, my friends, is the definition of co-dependent and I think you know what that deals with, when co-dependency deals with a substance,  Well here’s your news flash; sugar including carbs, is addictive. That means that carbs are an addictive food to eat. It’s also deadly, deadlier than alcohol, deadlier than heroin, than cigarettes and drug addiction. Sugar addiction is responsible for ECC, Excessive Carbohydrate Consumption. ECC is the deadliest addiction a person can have. It’s responsible for over 2000 deaths every day in the US alone. That number jumps to over 50,000 worldwide (daily). I can guarantee a manifestation of disease causing AGEs to anyone who consumes a diet of grains. How much they consume will dictate how much glycation they get to deal with, but they will deal with it, guaranteed. The manner in which you cure the glycation will also cure the hunger. What it does is to wipe out the hunger cycle (and it does it altogether), it also does to the glycation cycle. That is how you cure hunger. That is also how you conquer and cure all modern diseases. You can do it in one fell swoop. This is exciting.

To me, the cure for hunger is the same cure for all the modern diseases that are responsible for over 2000 deaths every day. If you cure one, you cure the other. That will go miles to cure the problem of hunger around the world. We need to stop supplying the world with our killing field grains. It’s the hunger that proves the addictive nature of carbs. Once you break the addiction, you lose the hunger cycle and without a cycle to create your hunger, the hunger can’t exist. Hunger is then cured. You just have to solve the problem of too many people going without nutritious food and being subjected to a diet of non-nutritious food, which includes the category of grains.

It’s the cycle of hunger that’s responsible not only for growth, but also for all harm done in the name of growth  or progress, as well as advancement, or security, or improvement Those are all desires driven by the cycle of hunger. It’s this cycle of hunger that drives these emotions. Deep down inside, you know this to be true. After you eat, when you blood sugars are at their highest, you are at one of your most relaxed attitudes of the day. The only other times you feel this secure is right after you eat any meal or snack (unless you’re consciously cheating on a diet and are dealing with guilt issues). This is the high side of the cycle, this is when you feel that everything is OK, “my stomach is full and I don’t feel like I need anything except to sit here and relax for a minute. This is how you feel at the end of Thanksgiving Dinner, Christmas Dinner, New Years Day dinner, Easter Dinner, etc, etc, etc. This is also the end of every meal you eat, to some extent. This is the glucose hitting your blood stream, waiting to give you fuel for energy. This is also the start of glycation and the hunger cycle.

It’s the start of glycation because all that glucose you just put into your blood by eating your starchy grains, is now floating all through your blood after being broken down to glucose, starting with the saliva in your mouth. That means that before it hits your stomach, your blood glucose levels are reacting. This is the start of the hunger cycle to which there is no end, until you stop feeding it. When your blood glucose levels fall and your stomach starts to shrink just a little bit after the digestion of your meal, that triggers your stomach to release Ghrelin, your hunger hormone. That’s the hormone that nobody on a carbohydrate diet can resist. That’s because many of those on a carb diet, must satisfy that Ghrelin hormone. Once they get hungry they feel the need to satisfy their hunger usually with some form of carbohydrate more than anything else. This is the low side of the cycle that drives people to abhorrent behavior because of their need. This hunger and satiety cycle influences almost every other cycle our bodies go through. It’s what drives all human behavior, of those that are on a carbohydrate diet. This is the cycle that drives people into the use and abuse, of social media to slander, attack, and accuse without evidence, others they disagree with. As the Late Gwen Ifill said, “we have to guard against how we treat each other”. I noticed it was cancer that took Gwen from us.

This manner in how we treat each other is one of the reasons why I’m writing this post about what this food source that Monsanto has given us to eat is doing to everyone who eats it. Up until I watched Food, inc, (Monsanto only played a small part in my equation. I didn’t realize they were behind this to the extent that they actually are. I now see that they are a much larger part of it than I expected.)

What their grains do with their glycating destruction starts with premature aging. It does that by driving fat production and the glycation factor that influences all modern disorders. That figures into everything glycation plays a factor in. Glycation is another name for inflammation. I know this. I’ve experienced the release from the addiction. The evidence in my books prove this. I know why we behave like the society that we do. It has to do with what we eat.

Nobody will believe me until they heed my advice and kick their own addiction. Only then, can they see the true light. I can guarantee the light you’ll see is a light of freedom, true freedom. Freedom from the  cycle of hunger that drives virtually every other cycle. If you can eliminate this cycle, you can eliminate everything this cycle creates and drives, starting with obesity and diabetes and moving on to glycation. That will go far to improve not only health, but mental attitudes, and hence better emotional outcomes and less strife. That is true freedom, freedom from the cycle of hunger, freedom from the cycle of addiction. Freedom from the wild roller coaster ride of emotional swings. The freedom I experience is true freedom as this cycle does not affect anybody on a purely ketogenic diet. We’re not subject to the hunger cycle that the carb diet requires. By the same token, we’re not subject to the glycation cycle of destruction either. This cycle is also at the root of all violence and terrorism, as it subject to the same hormone changes that control your emotions, as explained above. These emotions are just slightly altered because of their influence from the glucose fluctuations in your blood.

To control the glucose fluctuations, the easiest way is to control what feeds the cycle. That means to control the cycle you need to control the introduction of glucose into your body. Controlling the flow of sugars (carbs and fructose) is the only way you can control the blood glucose fluctuations. As easy as this may sound, that may be furthest from the truth. Controlling the inflow of carbs into your body is as difficult as fighting any addiction, because that’s exactly what you’re doing, fighting an addiction. That’s also why you must break the addiction, addictions kill prematurely and you can live without this addictive food.

This brings me to the conclusion that a ketogenic diet is the optimal diet for a society to be following for the best health of the society. The ketogenic diet not only removes the hormonal control out of the equation, it removes glycation out of the equation. That makes it a truly win, win diet for everyone to follow.

The problem here is sticking to a ketogenic diet. We’ll cover that here because it’s not only important, it’s vital to convert to the ketogenic diet to save yourself and our society as a whole. This is also how curing hunger can also cure terrorism by curing abhorrent behavior by removing your emotions from the hunger cycle. This removal of your emotions from the hunger cycle has multiple other benefits for your emotional behavior. It puts those emotions back in your control and not the control of the industry that promotes them. It also return other emotional control you’d thought you’d lost years ago. The control you lost was a relinquish of control to the industry that has addicted you. This isn’t your fault. You’ve always eaten carbs and sugar. They were considered healthy at one time. That again is because of their addictive nature.

In order to be able to stick to a ketogenic diet does that does mean breaking the addiction. Once it’s broke, you’ll know it and you’ll know it firmly, distinctly. It’s a feeling I still remember clearly, three years later. It’s a feeling of freedom. It’s a feeling of freedom from dependence on a substance that is as satisfying as it as dangerous. That is what makes it so dangerous, the fact that is so satisfying, so satiating, so hormonal fluctuating. That makes it also emotionally fluctuating. That makes it prone to emotional outbursts and terrorism. If you control your emotions and not let what you eat control them, that gives you more control over your emotional reactions and the consequences of those emotional reactions. This is a small synopsis of the control that glucose has on your actions and reactions. I being on a ketogenic diet do not experience this control of my emotions or actions or reactions due to glucose influence. I’ve learned how to live without that influence. I learned that three years, two weeks ago. It may have been the best day in my life. But I have to admit that sticking to a ketogenic diet is difficult to get into. It took me over two years to transform to the diet I’ve been on since I started writing my books. One thing I know, is that I could have never accomplished this without being on this diet. It’s not only overcome severe chronic pain, but it’s also over come pre-diabetic conditions as well as high blood pressure, chronic constipation from the drugs that were prescribed, near obesity, and brain drain, more than anything else. Being on my ketogenic diet has sharpened my brain to a point I wish it could have been when I was in school.  Boy, would my life have been different.

This is why I want to help you succeed at your attempt to convert, it’s that important for our society, if we’re to end hunger and terrorism. In order to do that I recommend to stop buying everything that raises your blood glucose more than 50 pts on the glycemic index. This will keep your blood glucose levels from reaching glycating or hunger cycling proportions. This is the starting point that I used when I started three years ago. I cut out bread first. That was the hardest because that included everything that flour is used in. To do otherwise is not giving up the bread. After the magic came from giving up the bread, I switched those calories to calories from higher fiber carbs like vegetables and fresh fruit. I was still reluctant to put dairy in my diet then, as I still have some Almond Milk in my fridge, I didn’t realize it then because my knowledge hadn’t grown to the point to where I decided to go completely ketogenic, so I was still putting more sugar in my body than what I am now, where I’m experiencing the improvements in my mental functions as well as my physical abilities.  I’m actually healing my paralysis, little by little. My fight side is actually getting more functional every day that I remain on this diet,

That is why I decided to convert to a completely keto diet after two years of simply a low carb diet. That may have got me to my weight goal, but it wasn’t getting me my brain back. Quitting bread prompted me to quit all grains and starchy carbohydrates like potatoes and beans. That felt so great, I decided to go completely keto approximately one year ago. That’s when I started my website and started writing all the information that I’m packing into three books. If anyone else were doing this I would think it phenomenal. But because it’s myself doing this, I’m just driven to get this information our there where the public can see it. Killing my mother has become my driving force to get this known. My ability to accomplish this working in a state of paralysis, to me is phenomenal. for that I have to thank Dr Perlmutter, Thank you Dr Perlmutter, I couldn’t have done this without your book or advice.

For those who want something to kill? I’ve got something for you to kill. Kill your hunger cycle. Kill it before it kills you first. Monsanto may have different ideas, though. Their profits depend on your hunger cycle. Their drug industry depends on your hunger cycle. Your hunger cycle drives you to eat more and more carbs to satisfy that hunger cycle. If you want to kill something worth killing, kill your hunger cycle and do it as quick as you can. The following report from Wikipedia shows why;

The influence of funding on research and the management of conflicts of interests as explained from The New England Journal of Medicine (Aug 19, 1993)

“Conflict of interest” in the field of medical research has been defined as “a set of conditions in which professional judgment concerning a primary interest (such as a patients welfare or the validity of research) tends to be unduly influenced by a secondary interest (such as financial gain).”]

In the early 1900s private companies such as the Carbolic Smoke Ball Company,[15] Mrs. Winlow’s Soothing Syrup[16]among other snake medicine remedies were solicited around the world and were the cause of many deaths due to misinformation. Information was not readily available to consumers nor was it required of the pharmaceutical producers to inform their customers of the ingredients that they were consuming. Samuel Hopkins Adams was an investigator to uncover the wide corruption and falsehoods that existed within the American pharmaceutical industry. He is quoted saying: “Gullible America will spend this year some seventy-five millions of dollars in the purchase of patent medicines. In consideration of this sum it will swallow huge quantities of alcohol, an appalling amount of opiates and narcotics, a wide assortment of varied drugs ranging from powerful and dangerous heart depressants to insidious liver stimulants; and far in excess of all other ingredients, undiluted fraud.”[15]

Regulation on industry funded biomedical research has seen great changes since Samuel Hopkins Adams declaration. In 1906 congress passed the Pure Food and Drugs Act of 1906.[16] In 1912 Congress passed the Shirley Amendment to prohibit the wide dissemination of false information on pharmaceuticals.[16] The Food and Drug Administration was formally created in 1930 under the McNarey Mapes Amendment to oversee the regulation of Food and Drugs in the United States.[16] In 1962 the Kefauver-Harris Amendments to the Food, Drug and Cosmetics Act made it so that before a drug was marketed in the United States the FDA must first approve that the drug was safe.[16] The Kefauver-Harris amendments also mandated that more stringent clinical trials must be performed before a drug is brought to the market.[15]The Kefauver-Harris amendments were met with opposition from industry due to the requirement of lengthier clinical trial periods that would lessen the period of time in which the investor is able to see return on their money. In the pharmaceutical industry patents are typically granted for a 20-year period of time, and most patent applications are submitted during the early stages of the product development.[15]According to Ariel Katz on average after a patent application is submitted it takes an additional 8 years before the FDA approves a drug for marketing.[15] As such this would leave a company with only 12 years to market the drug to see a return on their investments. After a sharp decline of new drugs entering the US market following the 1962 Kefauver-Harris amendments economist Sam Petlzman concluded that cost of loss of innovation was greater than the savings recognized by consumers no longer purchasing ineffective drugs.[15] In 1984 the Hatch-Waxman Act or the Drug Price Competition and Patent Term Restoration Act of 1984 was passed by congress.[16] The Hatch-Waxman Act was passed with the idea that giving brand manufacturers the ability to extend their patent by an additional 5 years would create greater incentives for innovation and private sector funding for investment.[17]

The relationship that exists with industry funded biomedical research is that of which industry is the financier for academic institutions which in turn employ scientific investigators to conduct research. A fear that exists wherein a project is funded by industry is that firms might negate informing the public of negative effects to better promote their product.[15] A list of studies show that public fear of the conflicts of interest that exist when biomedical research is funded by industry can be considered valid after a 2003 publication of “Scope and Impact of Financial Conflicts of Interest in Biomedical Research” in The Journal of American Association of Medicine. This publication included 37 different studies that met specific criteria to determine whether or not an academic institution or scientific investigator funded by industry had engaged in behavior that could be deduced to be a conflict of interest in the field of biomedical research. Survey results from one study concluded that 43% of scientific investigators employed by a participating academic institution had received research related gifts and discretionary funds from industry sponsors.[11]Another participating institution surveyed showed that 7.6% of investigators were financially tied to research sponsors, including paid speaking engagements (34%), consulting arrangements (33%), advisory board positions (32%) and equity (14%).[11] A 1994 study concluded that 58% out of 210 life science companies indicated that investigators were required to withhold information pertaining to their research as to extend the life of the interested companies’ patents.[11] Rules and regulations regarding conflict of interest disclosures are being studied by experts in the biomedical research field to eliminate conflicts of interest that could possibly affect the outcomes of biomedical research.

This is almost a definition of what Monsanto has accomplished in the last 40 years and they seem to be doing their level best to increase their power. It’s their food that glycates your blood. It’s their food that addicts you to eat more and more of their food. It’s their food that creates the hunger cycle that drives your behavior. It’s this company that is forcing farmers to grow their seed to grow the crops to put on your table to eat. That means that it’s this company that is responsible for over 45,000 deaths every day from ECC, Excessive Carbohydrate Consumption. ECC is the deadliest addiction mankind has ever experienced. It’s Monsanto who’s infiltrated their execs into the offices of the USDA and the FDA the government departments that control all the agencies and offices within them.

This has given them unprecedented control over what goes in our mouths to eat. That has given them full control over the diseases and disorders all who eat their food will acquire. That is something I can virtually guarantee. Why? It lies in the science of a glucose diet, the deadliest diet now that a man can use.

Thank you Monsanto :(

Glycation – The Real Poisoning of America

The Real Poisoning of America – Glycation

Of the causes of death below from Wikipedia, Ischaemic heart disease @ 7.4 million ranks right at the top. This is the result of glycation, 5 of the following 8 are also caused by non-enzymatic glycation. Hence my proposal, control the glycation and you control all modern diseases.

According to Wikipedia;

It is estimated that of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes because they have aged prematurely. Glycation is responsible for aging and the more of that, that you allow to happen in your body, the quicker your age. That is why keeping glycation to a minimum is what’s going to help you live longer and healthier. Even though aging may not be able to be reversed completely, it can be slowed dramatically by eating the right diet.  (Deep down you know that to be true. It’s just so hard to stick to when you have to.)

Leading causes of preventable death worldwide as of the year 2001, according to researchers working with the Disease Control Priorities Network (DCPN) and the World Health Organization (WHO). (The WHO’s 2008 statistics show very similar trends.) Imagine what they are right now, 8 years later and what they will be eight years from now, if nothing is done about it. Think it might be time for a cure?

The top 10 causes of preventable death, ones influenced by glycation are in red. Although it may me difficult to stop all glycation in the body, due to its commonality, you can control a major portion of it. Excessive Carbohydrate Consumption, the primary cause of glycation is controllable. Failure to control your consumption leads directly to any of the following disorders in red ;

  1. Ischaemic heart disease @ 7.4 mil
  2. Stroke@ 6.7 mil
  3. COPD @ 3.1 mil
  4. Lower Respiratory infection @ 3.1mil
  5. Trachea bronchus, lung infection@1.6 mil
  6. HIV/AIDS@1.5 mil
  7. Diarrheal diseases@1.5 mil
  8. Diabetes mellitus@1.5 mil
  9. Road injury@1.3 mil
  10. Hypertension@1.1 mil

40% of these deaths or 16.7 million are directly linked to ECC, Excessive Carbohydrate Consumption, making them the most preventable causes of death. 16.7 million deaths each and every year amounts to over 45,750 people each and every day. That includes approximately 1830 Americans each and every day. We have full control of this. All it would take is to say no to the sugar and grain industries. This one response would allow over 1830 more Americans to stay alive, every day. The cessation of carb consumption could add an additional 10-20 years to their lives, simply by eliminating the primary cause of inflammation, glucose. The continuation of carb consumption will, by contrast, prove the destructive power of sugar, by eventually killing its hosts.

Glycation is a common everyday experience that you accelerate with a carbohydrate diet. The more carbs you eat, the more glycation you’ll get to deal with. Glycation is controllable by controlling what you put in your mouth to eat. Although not totally responsible for some of these cancers, they would not exist if the glycation didn’t exist. This is the basis of my contention that if you eliminate the reason for the glycation, you eliminate the reason for inflammation, which in turn will eliminate the reason for these diseases, thereby eliminating the disease. It’s really not hard to see, once you take a good look at it; carb consumption is responsible for the inflammation that builds in the blood that is responsible for 90% of all modern diseases. Remove the inflammation by removing the sugar, which means removing the carbs. A simpler solution doesn’t exist and this cure can be yours.

These Are the Smoking Gun Articles Of

Evidence That The FDA Are Ignoring.

They’re Putting Your Health and Life at Risk.

48 of the 11667 studies done on glycation are below. These research studies were chosen from 231 studies that I examined for evidence of what glycation does to the body. By going through only 7% of these studies, I was able to find enough damning evidence to condemn this food 31 times over. By this ratio, I’ll end up finding at the least 850 more studies showing damage that glycation does.

I chose to search glycation because I know that it’s at the root of all modern diseases from cancer to CVDs to arthritis to dementia including Alzheimer disease. The following studies are the proof of what glycation does, and with sugar being the primary instigator of glycation, removal of sugar from the diet will eliminate everything it’s responsible for. These AGEs are responsible for all modern diseases and thus, are the reason for this book. When you eat carbs, you need to know what those carbs do to your body.

Foundation of Glycation

The study that piqued my interest initially was the report on RAGEs,

This report can be found on PubMed at Receptor for advanced glycation endproductsmediated inflammation and diabetic vascular complications. It explains how glycation turns your body’s fuel (cholesterol) and proteins (hemoglobin) into AGEs before they can be used for fuel and body repair.

“Exposure of amino residue of proteins to reducing sugars, such as glucose, glucose 6‐phosphate, fructose, ribose and intermediate aldehydes, results in non‐enzymatic glycation, which forms reversible Schiff bases and Amadori compounds. A series of further complex molecular rearrangements then yield irreversible advanced glycation end‐products (AGE). The aldehydes, highly reactive AGE precursors, are produced by both enzymatic and non‐enzymatic pathways. The enzymatic pathways include a route of myeloperoxidase in inflammatory cells, such as activated macrophages, which produces hypochlorite, then reacting with serine to generate glycolaldehyde.” Study Link

Arthritis is a Result of Glycation From Inflammation

The following report is the evidence of glucose’s involvement in arthritis. By being responsible for glycation, the glucose from broken carbs, again, is directly responsible for arthritis, just like if was in the 4,000 yr old ice mummy recovered from a receding glacier.

 “Glycated, oxidized and nitrated proteins and amino acids were detected in synovial fluid and plasma of arthritic patients with characteristic patterns found in early and advanced OA and RA, and non-RA, with respect to healthy controls. In early-stage disease, two algorithms for consecutive use in diagnosis were developed: (1) disease versus healthy control, and (2) classification as OA, RA and non-RA. “  Study Link

Alzheimer’s and Parkinson’s – a Result of Glycation

The following report shows the effects that AGEs have on the body in the diseases it promotes.

“Vast evidence supports the view that glycation of proteins is one of the main factors contributing to aging and is an important element of etiopathology of age-related diseases, especially type 2 diabetes mellitus, cataract and neurodegenerative diseases. Counteracting glycation  can therefore be a means of increasing both the lifespan and health span. In this review, accumulation of glycation products during aging is presented, pathophysiological effects of glycation are discussed and ways of attenuation of the effects of glycation are described, concentrating on prevention of glycation. The effects of glycation and glycation inhibitors on the course of selected age-related diseases, such as Alzheimer’s disease, Parkinson’s disease and cataract are also reviewed.”   Study Link

This study looks at the damaging effects of glycation along with the protective effects of certain phytochemicals (anti-oxidant producing agents).

“Reducing sugars can react non-enzymatically with amino groups of proteins and lipids to form irreversibly cross-linked macroprotein derivatives called as advanced glycation end products (AGEs). Cross-linking modification of extracellular matrix proteins by AGEs deteriorate their tertiary structural integrity and function, contributing to aging-related organ damage and diabetes-associated complications, such as cardiovascular disease (CVD). Moreover, engagement of receptor for AGEs, RAGE with the ligands evoke oxidative stress generation and inflammatory, thrombotic and fibrotic reactions in various kinds of tissues, further exacerbating the deleterious effects of AGEs on multiple organ systems. So the AGE-RAGE axis is a novel therapeutic target for numerous devastating disorders. Several observational studies have shown the association of dietary consumption of fruits and vegetables with the reduced risk of CVD in a general population. Although beneficial effects of fruits and vegetables against CVD could mainly be ascribed to its anti-oxidative properties, blockade of the AGE-RAGE axis by phytochemicals may also contribute to cardiovascular event protection. Therefore, in this review, we focus on 4 phytochemicals (quercetin, sulforaphane, iridoids, and curcumin) and summarize their effects on AGE formation as well as RAGE-mediated signaling pathway in various cell types and organs, including endothelial cells, vessels, and heart.”

Glycation, Amyloid Plaque and Neurodegenerative Disorders

This report examines the nature of amyloid plaque and glyoxal (Glyoxal is an inflammatory compound formed when cooking oils and fats are heated to high temperatures). It’s also made in your body when you body breaks down glucose.

“Glyoxal, a highly reactive α-oxoaldehyde, increases in diabetic condition and reacts with proteins to form advanced glycation end products (AGEs). In the present study, we have investigated the effect of glyoxal on experimental rat hemoglobin in vivo after external administration of the α-dicarbonyl compound in animals. Gel electrophoretic profile of hemolysate collected from glyoxal-treated rats (32mg/kg body wt. dose) after one week exhibited the presence of some high molecular weight protein bands that were found to be absent for control, untreated rats. Mass spectrometric and absorption studies indicated that the bands represented hemoglobin. Further studies revealed that the fraction exhibited the presence of intermolecular cross β-sheet structure. Thus glyoxal administration induces formation of high molecular weight aggregates of hemoglobin with amyloid characteristics in rats. Aggregated hemoglobin fraction was found to exhibit higher stability compared to glyoxal-untreated hemoglobin. As evident from mass spectrometric studies, glyoxal was found to modify Arg-30β and Arg-31α of rat hemoglobin to hydroimidazolone adducts. The modifications thus appear to induce amyloid-like aggregation of hemoglobin in rats. Considering the increased level of glyoxal in diabetes mellitus as well as its high reactivity, the above findings may be physiologically significant.

In view of its inflammatory function in innate immunity and its ability to detect a class of ligands through a common structural motif, rage is often referred to as a pattern recognition receptor.”     Study link

This report examines the relationship of high mobility group box 1 (HMGB1) and the effects it has on the body. HMGB1 is one of the most prevalent RAGE’s, as near as I can tell. It comes up in more studies…

RAGE and Inflammation
·        HMGB1 Activates Proinflammatory Signaling via TLR5 Leading to Allodynia.

Infectious and sterile inflammatory diseases are correlated with increased levels of high mobility group box 1 (HMGB1) in tissues and serum. Extracellular HMGB1 is known to activate Toll-like receptors (TLRs) 2 and 4 and RAGE (receptor for advanced glycation end products) in inflammatory conditions. Here, we find that TLR5 is also an HMGB1 receptor that was previously overlooked due to lack of functional expression in the cell lines usually used for studying TLR signaling. HMGB1 binding to TLR5 initiates the activation of NF-κB signaling pathway in a MyD88-dependent manner, resulting in pro-inflammatory cytokine production and pain enhancement in vivo. Biophysical and in vitro results highlight an essential role for the C-terminal tail region of HMGB1 in facilitating interactions with TLR5. These results suggest that HMGB1-modulated TLR5 signaling is responsible for pain hypersensitivity.” Study Link

I see HMGB1 come up in almost all modern diseases. This must be the most popular RAGEs.

COPD, Lung Cancer and RAGE

The proof that carb consumption also contributes to lung cancer is in the following report. The underlying cause is inflammation.

·        The Ser82 RAGE Variant Affects Lung Function and Serum RAGE in Smokers and sRAGE Production In Vitro.”



Genome-Wide Association Studies have identified associations between lung function measures and Chronic Obstructive Pulmonary Disease (COPD) and chromosome region 6p21 containing the gene for the Advanced Glycation End Product Receptor (AGER, encoding RAGE). We aimed to (i) characterize RAGE expression in the lung, (ii) identify AGER transcripts, (iii) ascertain if SNP rs2070600 (Gly82Ser C/T) is associated with lung function and serum sRAGE levels and (iv) identify whether the Gly82Ser variant is functionally important in altering sRAGE levels in an airway epithelial cell model.


Immunohistochemistry was used to identify RAGE protein expression in 26 human tissues and qPCR was used to quantify AGER mRNA in lung cells. Gene expression array data was used to identify AGER expression during lung development in 38 fetal lung samples. RNA-Seq was used to identify AGER transcripts in lung cells. sRAGE levels were assessed in cells and patient serum by ELISA. BEAS2B-R1 cells were transfected to over express RAGE protein with either the Gly82 or Ser82 variant and sRAGE levels identified.


Immunohistochemical assessment of 6 adult lung samples identified high RAGE expression in the alveoli of healthy adults and individuals with COPD. AGER/RAGE expression increased across developmental stages in human fetal lung at both the mRNA (38 samples) and protein levels (20 samples). Extensive AGER splicing was identified. The rs2070600T (Ser82) allele is associated with higher FEV1, FEV1/FVC and lower serum sRAGE levels in UK smokers. Using an airway epithelium model overexpressing the Gly82 or Ser82 variants we found that HMGB1 activation of the RAGE-Ser82 receptor results in lower sRAGE production.


This study provides new information regarding the expression profile and potential role of RAGE in the human lung and shows a functional role of the Gly82Ser variant. These findings advance our understanding of the potential mechanisms underlying COPD particularly for carriers of this AGER polymorphism.  Study Link

I wonder if the ACS, American Cancer Society will take this information and realize what foods are responsible for this report showing how RAGEs have a role in COPD and ultimately lung cancer? Will it provoke a response from the ACS on the consumption of the foods responsible for this RAGE? Will they issue a warning or are they more concerned with an industry that depends on this disorder, the pharmaceutical industry, or maybe an industry that provokes this disorder, the grain industry?

You may ask though, shouldn’t smoking play a larger role in this equation? I submit that if the glycation never existed in the first place, the smoking wouldn’t play as large of a role as it does with the inflammation in the body. It takes the glycation to create the RAGE responsible for lung cancer, yet no one knows of glycation or its effects from the FDA, the USDA or the CDC. Who are they trying to protect? Why isn’t glycation considered a disease?

Skin Cancer and Glycation

In the following study the emergence of the HMGB1 RAGE in head and the skin cancer, neck squamous cell carcinoma;

·        “Clinical Value of High Mobility Group Box 1 and the Receptor for Advanced Glycation End-products in Head and Neck Cancer: A Systematic Review.”

Introduction High mobility group box 1 is a versatile protein involved in gene transcription, extracellular signaling, and response to inflammation. Extracellularly, high mobility group box 1 binds to several receptors, notably the receptor for advanced glycation end-products. Expression of high mobility group box 1 and the receptor for advanced glycation end-products has been described in many cancers. 

Objectives To systematically review the available literature using PubMed and Web of Science to evaluate the clinical value of high mobility group box 1 and the receptor for advanced glycation end-products in head and neck squamous cell carcinomas. 

Data synthesis A total of eleven studies were included in this review. High mobility group box 1 overexpression is associated with poor prognosis and many clinical and pathological characteristics of head and neck squamous cell carcinomas patients. Additionally, the receptor for advanced glycation end-products demonstrates potential value as a clinical indicator of tumor angiogenesis and advanced staging. In diagnosis, high mobility group box 1 demonstrates low sensitivity. 

Conclusion High mobility group box 1 and the receptor for advanced glycation end-products are associated with clinical and pathological characteristics of head and neck squamous cell carcinomas. Further investigation of the prognostic and diagnostic value of these molecules is warranted.” Study Link

Cataracts and Glycation

Although the study above was published in Oct 2016, this kind of evidence has been around for over 20 years. These reports started showing up in 1984;

We have examined the nonenzymatic glycation of human lens crystallin, an extremely long-lived protein, from 16 normal human ocular lenses 0.2-99 yr of age, and from 11 diabetic lenses 52-82-yr-old…the nonenzymatic glycation of nondiabetic lens crystallin may be regarded as a biological clock…The glucitol-lysine (Glc-Lys) content of soluble and insoluble crystallin was determined after reduction with H-borohydride followed by acid hydrolysis, boronic acid affinity chromatography, and high pressure cation exchange chromatography…Over an age range comparable to that of the control samples, the diabetic crystallin samples contained about twice as much Glc-Lys.

Cardiovascular Disease and RAGE

This study shows glycations implication in cardiovascular disease;

·        Therapeutic interventions for Advanced Glycation-End Products and its Receptor-Mediated Cardiovascular Disease.

“Advanced glycation end products (AGEs) are heterogeneous group of molecules formed from non-enzymatic reaction of reducing sugars with amino group of proteins, lipids, and nucleic acid. Interaction of AGEs with its cell-bound receptor (RAGE) results in generation of oxygen radicals, nuclear factor kappa-β, pro-inflammatory cytokines and cell adhesion molecules, and is involved in the pathophysiology of cardiovascular diseases (CVD). Circulating soluble forms of RAGE (sRAGE) and endo-secretory RAGE (esRAGE) compete with RAGE for ligand binding and function as a decoy. This paper describes the endogenous and exogenous (high dietary AGEs, cooking food under high dry heat, elevated pH, and long period) sources of AGEs. AGE-RAGE-mediated CVD includes atherosclerosis, coronary artery disease, carotid artery disease, hypertension, peripheral vascular diseases, heart failure, cardiomyopathy, and microangiopathy. The therapeutic intervention with reduction in AGEs and RAGE, and elevation in sRAGE has been reported for the treatment of AGE-RAGE-mediated CVD. Reduction in levels of AGEs can be achieved by reduction in consumption of food containing or creating low amount of AGEs, cooking food at low temperature, moist heat, and shorter duration. AGE formation can be reduced with drugs, vitamins and stoppage of cigarette smoking. Statins, telmisartan, and curcumin have been used for suppression of RAGE. Statins, ACE-inhibitors, Rosiglitazone and vitamin D have been used to increase levels of sRAGE. Finally exogenous administration of sRAGE can be helpful in amelioration of CVD. In conclusion, AGE-RAGE-mediated CVD could be attenuated with reduction in consumption of AGEs, suppression of RAGE and elevation of sRAGE.”

Dangers of Statins

Statins are the most dangerous in the above equation as they unbalance your cholesterol which puts everything in your body out of balance. It’s your cholesterol that regulates a good portion of your hormones. You should already know how much your hormones affect your emotions, energy, intelligence, aging, and basic proper functioning of your body, right down to digesting carbs (insulin). Granted insulin is made in the pancreas, although other more influential hormones are made in your fat which is what statins reduce. Side effects of statins include; Common statin-related side effects (headaches, stomach upset, abnormal liver function tests and muscle cramps) were similar to other statins. Side effects of statins include muscle pain, increased risk of diabetes mellitus, and abnormalities in liver enzyme tests. Additionally, they have rare but severe adverse effects, particularly muscle damage. As of 2010, a number of statins are on the market: atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin and simvastatin. Several combination preparations of a statin and another agent, such as ezetimibe/simvastatin, are also available. In 2005 sales were estimated at $18.7 billion in the United States.

Side effects ultimately lead to other drugs down the road. It’s inevitable. This is how the pharmaceutical corporations make as much money as they do. And you gladly give it to them, simply to keep up your addiction and later to fight your CVD or cancer. How much sense this make to you?

What concerns me more than anything else is the fact the atorvastatin in the best selling pharmaceutical in history, with sales of $12.4 billion in 2008. With all of the side effects listed above, how many patients taking these drugs will not ever have to use any more pharmaceuticals. This is the way they guarantee a return consumer. I know. (I was one of them. I won’t be any more due to my keto diet.)

The best-selling statin is atorvastatin, which in 2003 became the best-selling pharmaceutical in history. The manufacturer Pfizer reported sales of US$12.4 billion in 2008. Pfizer and Monsanto were under one roof at in 2003. That was the year Pfizer started their divesture of Monsanto. (Maybe it was the lawsuits that were starting to pile up, that they didn’t appreciate.) I wonder how many law suits Pfizer has against itself for its pharmaceutical statins. Below are the contraindications for atorvastatin (Lipitor);


The side effects of Lipitor are even longer and include diarrhea, dyspepsia, myalgia and nausea. Are you on statins? Did you read over your drug disclosure? Were you told that you could cure this without drugs? Were you ever told that this disorder started in your diet of carbs? The earliest report in the PMC I found was dated Jan, 1974 and simply stated that weight reduction was important to controlling hyperlipoproteinemia, a fancy word for high amounts of apolipoproteins in the body which indicate levels of cholesterol.

According to a study completed in 1995;

Population studies linking low cholesterol to noncoronary mortalities do not demonstrate cause-and-effect relations. In fact, based on current studies, the opposite is more likely to be the case. Drug intervention, however, should be used conservatively, particularly in young adults and the elderly. Drugs should be used only after diet and lifestyle interventions have failed. The evidence linking high blood cholesterol to coronary atherosclerosis and cholesterol lowering to its prevention is broad-based and definitive. Concerns about cholesterol lowering and spontaneously low cholesterols should be pursued but should not interfere with the implementation of current public policies to reduce the still heavy burden of atherosclerosis in Western society.

Another study from 1994 showed the rethinking of the low-fat hi-carb diet that has been pushed for over 40 years (probably at the insistence of Monsanto). Since they owned GD Searle at the time it makes me wonder, was their intent to hook us on more drugs? Even as recent Dec 31, 2016 the dept of research at Kaiser Permanente Southern California, Pasadena came to the conclusion; Statin use rather than cholesterol level was associated with lower mortality risk in patients with pancreatic cancer. Statins appear to improve survival through a lipid-independent mechanism. Apparently they’re rethinking their strategies. I have a strategy, don’t eat carbs. I go keto and let the fasting take care of the illnesses. If it can work for me it can work for you.

Our medical industry has had research for over 20 years on the benefits of cholesterol and the dangers of lowering it, yet because of our dependence on grains and sugar and Monsanto’s influence in the FDA and USDA, the recommendations from the USDA’s agency for food labeling to food safety to Myplate, the CCNP and at least 3 other agencies in the USDA alone, the CDC, the ADA, the ACS still recommend that you keep whole grains in your diet, regardless of the studies completed that show their danger. Why? Monsanto is in the crop seed industry owning over 15 crop seed companies, all wanting to sell GMO seed ready to handle Roundup herbicide to farmers contracted by Monsanto waiting to plant their next crop. They’ll spray their crops according to their contract with Monsanto. It then goes on your table.

This article appeared 22 years ago in PubMed in Aug, 1994. Even then low cholesterol was being questioned, yet in some corners, it’s still promoted today;

Although hypercholesterolemia is associated with increased liability to death from heart disease, it is as frequently associated with increased overall life expectancy as with decreased life expectancy. These findings are incompatible with labeling hypercholesterolemia an overall health hazard. Moreover, it is questionable if the cardiovascular liability associated with hypercholesterolemia is either causal or reversible. The complex relationships between diet, serum cholesterol, atherosclerosis and mortality and their interactions with genetic and environmental factors suggest that the effects of simple dietary prescriptions are unlikely to be predictable, let alone beneficial. These cautions are borne out by numerous studies which have shown that multifactorial primary intervention to lower cholesterol levels is as likely to increase death from cardiovascular causes as to decrease it. Importantly, the only significant overall effect of cholesterol-lowering intervention that has ever been shown is increased mortality.

With Monsanto’s influence in the FDA, the USDA, the EPA and who knows what else, who’s to protect our food supply? You have to protect yourself. Monsanto has proven they can’t self regulate their industry and keep us safe. The best way to start being safe is to not eat their food, which happens to include all grains. If you don’t buy them, that may send the message.

Direct Influence of Glycation in Cancer

More evidence of its influence in cancer is when this HMGB1 RAGE rears its ugly head again, influencing cancer;

·        Blockade of High Mobility Group Box 1 (HMGB1) augments anti-tumor T-cell response induced by peptide vaccination as a co-adjuvant.

“High Mobility Group Box 1 (HMGB1) is a member of the damage-associated molecular patterns (DAMPs), which cause inflammation and trigger innate immunity through Toll-like receptors (TLRs) 2/4 and the receptor for advanced glycation end products (RAGE). We examined the effect of glycyrrhizin, a selective inhibitor of HMGB1, on the induction of cytotoxic T-lymphocytes (CTLs) in mice. B6 mice, either OT-1 spleen cell-transferred or untransferred, were immunized with an s.c. injection of OVA257-264 peptide with topical imiquimod, and glycyrrhizin was mixed with the antigen peptide. Proliferation of OT-1 cells after immunization was enhanced by glycyrrhizin. The effect of glycyrrhizin was confirmed in other adjuvant systems, such as CpG oligonucleotide and monophosphoryl lipid A (MPL), but glycyrrhizin was not effective in Freund’s incomplete adjuvant system. The augmenting effects of glycyrrhizin were also observed in other synthetic HMGB1 inhibitors, i.e., gabexate mesilate, nafamostat, and sivelstat. Thus the effects are common to the HMGB1 inhibitors. Induction of CTLs detected by IFN-γ ELISPOT assay was similarly augmented by glycyrrhizin. In a therapeutic vaccine model, glycyrrhizin inhibited the growth of s.c. transplanted EG.7 tumors. Expression of inflammatory cytokines in the skin inoculation site was downregulated by glycyrrhizin. These results suggest that HMGB1 inhibitors might be useful as a co-adjuvant for peptide vaccination with an innate immunity receptor-related adjuvant. This article is protected by copyright. All rights reserved.” Study Link

Were you ever told that this could happen if you continued your diet of bread, corn, soy and other carbs? (Neither was I.)

This is evidence of glycation’s effect on the kidneys:

·        AGEs/sRAGE, a novel risk factor in the pathogenesis of end-stage renal disease.

“Interaction of advanced glycation end products (AGEs) with its cell-bound receptor (RAGE) results in cell dysfunction through activation of nuclear factor kappa-B, increase in expression and release of inflammatory cytokines, and generation of oxygen radicals. Circulating soluble receptors, soluble receptor (sRAGE), endogenous secretory receptor (esRAGE) and cleaved receptor (cRGAE) act as decoy for RAGE ligands and thus have cytoprotective effects. Low levels of sRAGE and esRAGE have been proposed as biomarkers for many diseases. However sRAGE and esRAGE levels are elevated in diabetes and chronic renal diseases and still tissue injury occurs. It is possible that increases in levels of AGEs are greater than increases in the levels of soluble receptors in these two diseases. Some new parameters have to be used which could be an universal biomarkers for cell dysfunction. It is hypothesized that increases in serum levels of AGEs are greater than the increases in the soluble receptors, and that the levels of AGEs is correlated with soluble receptors and that the ratios of AGEs/sRAGE, AGEs/esRAGE and AGEs/cRAGE are elevated in patients with end-stage renal disease (ESRD) and would serve as an universal risk marker for ESRD. The study subject comprised of 88 patients with ESRD and 20 healthy controls. AGEs, sRAGE and esRAGE were measured using commercially available enzyme linked immune assay kits. cRAGE was calculated by subtracting esRAGE from sRAGE. The data show that the serum levels of AGEs, sRAGE, cRAGE are elevated and that the elevation of AGEs was greater than those of soluble receptors. The ratios of AGEs/sRAGE, AGEs/esRAGE and AGEs/cRAGE were elevated and the elevation was similar in AGEs/sRAGE and AGEs/cRAGE but greater than AGEs/esRAGE. The sensitivity, specificity, accuracy, and positive and negative predictive value of AGEs/sRAGE and AGEs/cRAGE were 86.36 and 84.88 %, 86.36 and 80.95 %, 0.98 and 0.905, 96.2 and 94.8 %, and 61.29 and 56.67 % respectively. There was a positive correlation of sRAGE with esRAGE and cRAGE, and AGEs with esRAGE; and negative correlation between sRAGE and AGEs/sRAGE, esRAGE and AGES/esRAGE, and cRAGE and AGES/cRAGE. In conclusion, AGEs/sRAGE, AGEs/cRAGE and AGEs/esRAGE may serve as universal risk biomarkers for ESRD and that AGEs/sRAGE and AGEs/cRAGE are better risk biomarkers than AGEs/esRAGE.” Study Link

Breast Cancer and RAGE

This is the evidence that breast cancer is influenced by glycation;

·        Increased Expression of the Receptor for AdvancedGlycation End-Products (RAGE) Is Associated with Advanced Breast Cancer Stage.



The receptor for advanced glycation end-products (RAGE) is a multiligand transmembrane receptor that is overexpressed in various pathological conditions including cancers. However, the expression pattern of RAGE in breast cancer tumors is still not completely clear.


In this study, we investigated the expression levels of RAGE in 25 fresh-frozen breast cancer samples and corresponding noncancerous tissue samples collected from breast cancer patients, by real-time polymerase chain reaction (PCR). Additionally, we performed immunohistochemistry on breast cancer specimens.


The results indicate a high expression of the RAGE-encoding gene in the cancerous tissues. RAGE expression at the mRNA and protein levels was statistically significantly up-regulated in advanced-stage and triple-negative breast tumors and node-positive tissues compared with other tissues (p < 0.001). A significant association between RAGE expression and tumor size was observed (p = 0.029).


Overexpression of RAGE in advanced-stage tumors may be a useful biomarker for diagnosis and the prediction of breast cancer progression.” Study Link

I’m only sorry that I could include studies and reports for all forms of cancer, but with they’re being so many of them, that’s a virtually impossible task.

Evidence of bone density decline from glycation;

·        AdvancedGlycationEnd Products, Diabetes, and Bone Strength.

“Diabetic patients have a higher fracture risk than expected by their bone mineral density (BMD). Poor bone quality is the most suitable and explainable cause for the elevated fracture risk in this population. Advanced glycation end products (AGEs), which are diverse compounds generated via a non-enzymatic reaction between reducing sugars and amine residues, physically affect the properties of the bone material, one of a component of bone quality, through their accumulation in the bone collagen fibers. On the other hand, these compounds biologically act as agonists for these receptors for AGEs (RAGE) and suppress bone metabolism. The concentrations of AGEs and endogenous secretory RAGE, which acts as a “decoy receptor” that inhibits the AGEs-RAGE signaling axis, are associated with fracture risk in a BMD-independent manner. AGEs are closely associated with the pathogenesis of this unique clinical manifestation through physical and biological mechanisms in patients with diabetes mellitus.” Study link

Evidence of Alzheimer’s disease from glycation;

Genetic association between RAGE polymorphisms and Alzheimer’s disease and Lewy body dementias in a Japanese cohort: a case-control study.



Interaction of receptor for advanced glycation end products (RAGE) with amyloid-β increases amplification of oxidative stress and plays pathological roles in Alzheimer’s disease (AD). Oxidative stress leads to α-synuclein aggregation and is also a major contributing factor in the pathogenesis of Lewy body dementias (LBDs). Therefore, we aimed to investigate whether RAGE gene polymorphisms were associated with AD and LBDs.


Four single nucleotide polymorphisms (SNPs)-rs1800624, rs1800625, rs184003, and rs2070600-of the gene were analyzed using a case-control study design comprising 288 AD patients, 76 LBDs patients, and 105 age-matched controls.


Linkage disequilibrium (LD) examination showed strong LD from rs1800624 to rs2070600 on the gene (1.1 kb) in our cases in Japan. Rs184003 was associated with an increased risk of AD. Although there were no statistical associations for the other three SNPs, haplotypic analyses detected genetic associations between AD and the RAGE gene. Although relatively few cases were studied, results from the SNPs showed that they did not modify the risk of developing LBDs in the Japanese population.


Our findings suggested that polymorphisms in the RAGE gene are involved in genetic susceptibility to AD. Copyright © 2016 John Wiley & Sons, Ltd.”  Study Link

With the above evidence showing its involvement in brain diseases, how does this information get hidden? Doesn’t anyone of authority examine these reports?  More evidence below of cancer causing agents from glycation leaving me to wonder; is anyone looking out for our benefit?

·        M2 macrophages do not fly into a “RAGE”.

“Tumor-associated macrophages (TAMs) are key elements in orchestrating host responses inside tumor stroma. This population may undergo a polarized activation process, thus rendering a heterogeneous spectrum of phenotypes, where the classically activated type 1 macrophages (M1) and the alternative activated type 2 macrophages (M2) represent two extreme phenotypes. In this commentary, based on very recent research findings, we intend to highlight how complex could be the crosstalk among all components of tumor stroma, where the coexistence of non-natural partners may even skew the canonical responses that we can expect.”  Study Link

This is where your addiction starts with this evidence of glycation causing agents in baby food. This is indicative of the glucose in the formula. Ask yourself why this is done, if glucose is capable of doing this much harm;

·        “Protein breakdown and release of β-casomorphins during in vitro gastro-intestinal digestion of sterilized model systems of liquid infant formula.”

“Protein modifications occurring during sterilization of infant formulas can affect protein digestibility and release of bioactive peptides. The effect of glycation and cross-linking on protein breakdown and release of β-casomorphins was evaluated during in vitro gastro-intestinal digestion (GID) of six sterilized model systems of infant formula. Protein degradation during in vitro GID was evaluated by SDS-PAGE and by measuring the nitrogen content of ultrafiltration (3kDa) permeates before and after in vitro GID of model IFs. Glycation strongly hindered protein breakdown, whereas cross-linking resulting from β-elimination reactions had a negligible effect. Only β-casomorphin 7 (β-CM7) was detected (0.187-0.858mgL(-1)) at the end of the intestinal digestion in all untreated IF model systems. The level of β-CM7 in the sterilized model systems prepared without addition of sugars ranged from 0.256 to 0.655mgL(-1). The release of this peptide during GID was hindered by protein glycation.” Study Link

This study explains that it’s the glycative results are what drives inflammation and  in type 1 diabetics, this was just released Oct15, 2016. Watch to see if you’ll hear anything about it. If you don’t, it’s probably because Big Pharma has something to say about it;

·        The Receptor for AdvancedGlycationEndproducts Drives T Cell Survival and Inflammation in Type 1 Diabetes Mellitus.

“The ways in which environmental factors participate in the progression of autoimmune diseases are not known. After initiation, it takes years before hyperglycemia develops in patients at risk for type 1 diabetes (T1D). The receptor for advanced glycation endproducts (RAGE) is a scavenger receptor of the Ig family that binds damage-associated molecular patterns and advanced glycated endproducts and can trigger cell activation. We previously found constitutive intracellular RAGE expression in lymphocytes from patients with T1D. In this article, we show that there is increased RAGE expression in T cells from at-risk euglycemic relatives who progress to T1D compared with healthy control subjects, and in the CD8+ T cells in the at-risk relatives who do versus those who do not progress to T1D. Detectable levels of the RAGE ligand high mobility group box 1 were present in serum from at-risk subjects and patients with T1D. Transcriptome analysis of RAGE+ versus RAGE T cells from patients with T1D showed differences in signaling pathways associated with increased cell activation and survival. Additional markers for effector memory cells and inflammatory function were elevated in the RAGE+ CD8+ cells of T1D patients and at-risk relatives of patients before disease onset. These studies suggest that expression of RAGE in T cells of subjects progressing to disease predates dysglycemia. These findings imply that RAGE expression enhances the inflammatory function of T cells, and its increased levels observed in T1D patients may account for the chronic autoimmune response when damage-associated molecular patterns are released after cell injury and killing.”

Study Link

Evidence of the role of AGEs in the process of neurodegenerative diseases;

·        “Impact of Non-Enzymatic Glycation in Neurodegenerative Diseases: Role of Natural Products in Prevention.”

“Non-enzymatic protein glycosylation is the addition of free carbonyls to the free amino groups of proteins, amino acids, lipoproteins and nucleic acids resulting in the formation of early glycation products. The early glycation products are also known as Maillard reaction which undergoes dehydration, cyclization and rearrangement to form advanced glycation end-products (AGEs). By and large the researchers in the past have also established that glycation and the AGEs are responsible for most type of metabolic disorders, including diabetes mellitus, cancer, neurological disorders and aging. The amassing of AGEs in the tissues of neurodegenerative diseases shows its involvement in diseases. Therefore, it is likely that inhibition of glycation reaction may extend the lifespan of an individual. The hunt for inhibitors of glycation, mainly using in vitro models, has identified natural compounds able to prevent glycation, especially polyphenols and other natural antioxidants. Extrapolation of results of in vitro studies on the in vivo situation is not straightforward due to differences in the conditions and mechanism of glycation, and bioavailability problems. Nevertheless, existing data allow postulating that enrichment of diet in natural anti-glycating agents may attenuate glycation and, in consequence may halt the aging and neurological problems.” Study Link

The following is evidence of glycations role in cardiovascular disease;

·        “Advanced Glycation End-Products Induce Apoptosis of Vascular Smooth Muscle Cells: A Mechanism for Vascular Calcification.”

“Vascular calcification, especially medial artery calcification, is associated with cardiovascular death in patients with diabetes mellitus and chronic kidney disease (CKD). To determine the underlying mechanism of vascular calcification, we have demonstrated in our previous report that advanced glycation end-products (AGEs) stimulated calcium deposition in vascular smooth muscle cells (VSMCs) through excessive oxidative stress and phenotypic transition into osteoblastic cells. Since AGEs can induce apoptosis, in this study we investigated its role on VSMC apoptosis, focusing mainly on the underlying mechanisms. A rat VSMC line (A7r5) was cultured, and treated with glycolaldehyde-derived AGE-bovine serum albumin (AGE3-BSA). Apoptotic cells were identified by Terminal deoxynucleotidyl transferased UTP nick end labeling (TUNEL) staining. To quantify apoptosis, an enzyme-linked immunosorbent assay (ELISA) for histone-complexed DNA fragments was employed. Real-time PCR was performed to determine the mRNA levels. Treatment of A7r5 cells with AGE3-BSA from 100 µg/mL concentration markedly increased apoptosis, which was suppressed by Nox inhibitors. AGE3-BSA significantly increased the mRNA expression of NAD (P)H oxidase components including Nox4 and p22(phox), and these findings were confirmed by protein levels using immunofluorescence. Dihydroethidisum assay showed that compared with cBSA, AGE3-BSA increased reactive oxygen species level in A7r5 cells. Furthermore, AGE3-induced apoptosis was significantly inhibited by siRNA-mediated knockdown of Nox4 or p22 (phox). Double knockdown of Nox4 and p22 (phox) showed a similar inhibitory effect on apoptosis as single gene silencing. Thus, our results demonstrated that NAD (P)H oxidase-derived oxidative stress are involved in AGEs-induced apoptosis of VSMCs. These findings might be important to understand the pathogenesis of vascular calcification in diabetes and CKD.”

Evidence of glycation in mental disorders like schizophrenia;

·        “The regulation of soluble receptor for AGEs contributes to carbonyl stress in schizophrenia.

“Our previous study showed that enhanced carbonyl stress is closely related to schizophrenia. The endogenous secretory receptor for advanced glycation end-products (esRAGE) is a splice variant of the AGER gene and is one of the soluble forms of RAGE. esRAGE is considered to be a key molecule for alleviating the burden of carbonyl stress by entrapping advanced glycation end-products (AGEs). In the current study, we conducted genetic association analyses focusing on AGER, in which we compared 212 schizophrenic patients to 214 control subjects. We also compared esRAGE levels among a subgroup of 104 patients and 89 controls and further carried out measurements of total circulating soluble RAGE (sRAGE) in 25 patients and 49 healthy subjects. Although the genetic association study yielded inconclusive results, multiple regression analysis indicated that a specific haplotype composed of rs17846798, rs2071288, and a 63 bp deletion, which were in perfect linkage disequilibrium (r2 = 1), and rs2070600 (Gly82Ser) were significantly associated with a marked decrease in serum esRAGE levels. Furthermore, compared to healthy subjects, schizophrenia showed significantly lower esRAGE (p = 0.007) and sRAGE (p = 0.03) levels, respectively. This is the first study to show that serum esRAGE levels are regulated by a newly identified specific haplotype in AGER and that a subpopulation of schizophrenic patients are more vulnerable to carbonyl stress. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.” Study Link

Evidence of glycation in renal disease and kidney cancer;

·        Growth arrest specific 2-like protein 1 expression is upregulated in podocytes through advanced  glycation end-products.


Growth arrest specific 2-like protein 1 (GAS2L1) protein is a member of the GAS2 family of proteins, known to regulate apoptosis and cellular cytoskeleton reorganization in different cells. Recently we identified that Gas2l1 gene expression in podocytes is influenced by advanced glycation end product-bovine serum albumin(AGE-BSA).


The study was performed employing cultured podocytes and diabetic (db/db) mice, a model of type 2 diabetes. Akbuminuria as well as urinary neutrophil gelatinase-associated lipocalin (NGAL) excretion as measured with specific ELISAs. Gene expression was analyzed via semiquantitative and real-time polymerase chain reaction. The protein levels were determined by western blotting and immunostaining.


We found that the Gas2l1α isoform is expressed in podocytes. Treatment with AGE-BSA induced Gas2l1α and Gas2 mRNA levels compared with controls incubated with non-glycated control BSA (Co-BSA). Moreover, application of the recombinant soluble receptor of AGEs (sRAGE), a competitor of cellular RAGE, reversed the AGE-BSA effect. Interestingly, AGE-BSA also increased the protein levels of GAS2L1α in a RAGE-dependent manner, but did not affect the GAS2 expression. Periodic acid-Schiff staining and albuminuria as well as urinary NGAL excretion revealed that db/db mice progressively developed diabetic nephropathy with renal accumulation of Nε-carboxy-methyl-lysine (immunohistochemistry, western blots). Analyses of GAS2L1α and GAS2 proteins in diabetic mice revealed that both were significantly elevated relative to their non-diabetic littermates. In addition, GAS2L1α and GAS2 proteins positively correlated with the accumulation of AGEs in the blood plasma of diabetic mice and the administration of sRAGE in diabetic mice reduced the glomerular expression of both proteins.


We show for the first time that the protein expression of GAS2L1α in vitro and in vivo is regulated by the AGE-RAGE axis. The suppression of AGE ligation with their RAGE in diabetic mice with progressive nephropathy reversed the GAS2L1α expression, thus suggesting a role of GAS2L1α in the development of diabetic disease, which needs to be further elucidated. © The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA.” Study Link

Methylglyoxal is what makes up pyruvic acid which is a foundation for energy expenditure. It comes from glycogen which comes from glucose and can be made into lipids to be used for cholesterol or glucose to be used by your brain when it the ketones aren’t enough to power all lobes in the brain. This the link from glucose to disease through its conversion to AGEs, advanced glycation endproducts as explained by this study published Sep, 2016;

“Glucose and fructose metabolism originates the highly reactive by product methylglyoxal (MG), which is a strong precursor of advanced glycation end products (AGE). The MG has been implicated in classical diabetic complications such as retinopathy, nephropathy, and neuropathy, but has also been recently associated with cardiovascular diseases and central nervous system disorders such as cerebrovascular diseases and dementia. Recent studies even suggested its involvement in insulin resistance and beta-cell dysfunction, contributing to the early development of type 2 diabetes and creating a vicious circle between glycation and hyperglycemia. Despite several drugs and natural compounds have been identified in the last years in order to scavenge MG and inhibit AGE formation, we are still far from having an effective strategy to prevent MG-induced mechanisms. This review summarizes the endogenous and exogenous sources of MG, also addressing the current controversy about the importance of exogenous MG sources. The mechanisms by which MG changes cell behavior and its involvement in type 2 diabetes development and complications and the pathophysiological implication are also summarized. Particular emphasis will be given to pathophysiological relevance of studies using higher MG doses, which may have produced biased results. Finally, we also overview the current knowledge about detoxification strategies, including modulation of endogenous enzymatic systems and exogenous compounds able to inhibit MG effects on biological systems.”  Study Link

Evidence of glycations influence in pancreatic cancer;

·        AdvancedGlycationEnd Products Impair Glucose-Stimulated Insulin Secretion of a Pancreatic β-Cell Line INS-1-3 by Disturbance of Microtubule Cytoskeleton via p38/MAPK Activation.

Advanced glycation end products (AGEs) are believed to be involved in diverse complications of diabetes mellitus. Overexposure to AGEs of pancreatic β-cells leads to decreased insulin secretion and cell apoptosis. Here, to understand the cytotoxicity of AGEs to pancreatic β-cells, we used INS-1-3 cells as a β-cell model to address this question, which was a subclone of INS-1 cells and exhibited high level of insulin expression and high sensitivity to glucose stimulation. Exposed to large dose of AGEs, even though more insulin was synthesized, its secretion was significantly reduced from INS-1-3 cells. Further, AGEs treatment led to a time-dependent increase of depolymerized microtubules, which was accompanied by an increase of activated p38/MAPK in INS-1-3 cells. Pharmacological inhibition of p38/MAPK by SB202190 reversed microtubule depolymerization to a stabilized polymerization status but could not rescue the reduction of insulin release caused by AGEs. Taken together, these results suggest a novel role of AGEs-induced impairment of insulin secretion, which is partially due to a disturbance of microtubule dynamics that resulted from an activation of the p38/MAPK pathway.” Study Link

In my estimation this is the worst manifestation of bread in the diet. Amyloid plaque is at the root of most modern diseases, ranging from cancer to heart disease to arthritis to Alzheimer’s disease and Parkinson’s disease;

·        Glycationinduced generation of amyloid fibril structures by glucose metabolites.

“The non-enzymatic reaction (glycation) of reducing sugars with proteins has received increased interest in dietary and therapeutic research lately. In the present work, the impact of glycation on structural alterations of camel serum albumin (CSA) by different glucose metabolites was studied. Glycation of CSA was evaluated by specific fluorescence of advanced glycation end-products (AGEs) and determination of available amino groups. Further, conformational changes in CSA during glycation were also studied using 8-analino 1-nephthlene sulfonic acid (ANS) binding assay, circular dichroism (CD) and thermal analysis. Intrinsic fluorescence measurement of CSA showed a 22 nm red shift after methylglyoxal treatment, suggesting glycation induced denaturation of CSA. Rayleigh scattering analysis showed glycation induced turbidity and aggregation in CSA. Furthermore, ANS binding to native and glycated-CSA reflected perturbation in the environment of hydrophobic residues. However, CD spectra did not reveal any significant modifications in the secondary structure of the glycated-CSA. Thioflavin T (ThT) fluorescence of CSA increased after glycation, illustrated cross β-structure and amyloid formation. Transmission electron microscopy (TEM) analysis further reaffirms the formation of aggregate and amyloid. In summary, glucose metabolites induced conformational changes in CSA and produced aggregate and amyloid structures.”

This is more evidence of glycation’s involvement in Alzheimer’s disease. This report was submitted on Aug 24 2016, have you heard anything about this yet? Who doesn’t want you to know? Who has interests in selling your medication for memory loss? How would you learn this information if you didn’t see it here? Do you know where to look for it? Do you even know to look for it? Am I fishing or can this be a conspiracy?

·        HMGB1 and thrombin mediate the blood-brain barrier dysfunction acting as biomarkers of neuroinflammation and progression to neurodegeneration in Alzheimer’s disease.


The blood-brain barrier (BBB) dysfunction represents an early feature of Alzheimer’s disease (AD) that precedes the hallmarks of amyloid beta (amyloid β) plaque deposition and neuronal neurofibrillary tangle (NFT) formation. A damaged BBB correlates directly with neuroinflammation involving microglial activation and reactive astrogliosis, which is associated with increased expression and/or release of high-mobility group box protein 1 (HMGB1) and thrombin. However, the link between the presence of these molecules, BBB damage, and progression to neurodegeneration in AD is still elusive. Therefore, we aimed to profile and validate non-invasive clinical biomarkers of BBB dysfunction and neuroinflammation to assess the progression to neurodegeneration in mild cognitive impairment (MCI) and AD patients.


We determined the serum levels of various proinflammatory damage-associated molecules in aged control subjects and patients with MCI or AD using validated ELISA kits. We then assessed the specific and direct effects of such molecules on BBB integrity in vitro using human primary brain microvascular endothelial cells or a cell line.


We observed a significant increase in serum HMGB1 and soluble receptor for advanced glycation end products (sRAGE) that correlated well with amyloid beta levels in AD patients (vs. control subjects). Interestingly, serum HMGB1 levels were significantly elevated in MCI patients compared to controls or AD patients. In addition, as a marker of BBB damage, soluble thrombomodulin (sTM) antigen, and activity were significantly (and distinctly) increased in MCI and AD patients. Direct in vitro BBB integrity assessment further revealed a significant and concentration-dependent increase in paracellular permeability to dextrans by HMGB1 or α-thrombin, possibly through disruption of zona occludins-1 bands. Pre-treatment with anti-HMGB1 monoclonal antibody blocked HMGB1 effects and leaving BBB integrity intact.


Our current studies indicate that thrombin and HMGB1 are causal proximate proinflammatory mediators of BBB dysfunction, while sTM levels may indicate BBB endothelial damage; HMGB1 and sRAGE might serve as clinical biomarkers for progression and/or therapeutic efficacy along the AD spectrum.” Study Link

More evidence of the damaging effects of glycation was submitted July15, 2016. Have you heard anything about this report yet?

“The incidence of food allergy has increased dramatically in the last few decades in westernized developed countries. We propose that the Western lifestyle and diet promote innate danger signals and immune responses through production of “alarmins. Alarmins are endogenous molecules secreted from cells undergoing nonprogrammed cell death that signal tissue and cell damage. High molecular group S (HMGB1) is a major alarmin that binds to the receptor for advanced glycation end-products (RAGE). Advanced glycation end-products (AGEs) are also present in foods. We propose the “false alarm” hypothesis, in which AGEs that are present in or formed from the food in our diet are predisposing to food allergy. The Western diet is high in AGEs, which are derived from cooked meat, oils, and cheese. AGEs are also formed in the presence of a high concentration of sugars. We propose that a diet high in AGEs and AGE-forming sugars results in misinterpretation of a threat from dietary allergens, promoting the development of food allergy. AGEs and other alarmins inadvertently prime innate signaling through multiple mechanisms, resulting in the development of allergic phenotypes. Current hypotheses and models of food allergy do not adequately explain the dramatic increase in food allergy in Western countries. Dietary AGEs and AGE-forming sugars might be the missing link, a hypothesis supported by a number of convincing epidemiologic and experimental observations, as discussed in this article.” Study Link

The author  of this report isn’t fully aware of what causes glycation. He still thinks that protein and fat are important as they are what gets glycated, but they’re not the important factor in this equation. It’s the glucose that’s important, as it’s the glucose that does the glycating. If one were to remove the glucose, they’d remove the glycation.

Again no alert about this evidence of the influence of glycation in dementia submitted in Aug 2016 from the Oxford Journal of Gerontology;

·        Inflammatory Biomarkers Predict Domain-Specific Cognitive Decline in Older Adults.


Vascular risk factors, including inflammation, may contribute to dementia development. We investigated the associations between peripheral inflammatory biomarkers and cognitive decline in five domains (memory, construction, language, psychomotor speed, and executive function).


Community-dwelling older adults from the Ginkgo Evaluation of Memory Study (n = 1,159, aged 75 or older) free of dementia at baseline were included and followed for up to 7 years. Ten biomarkers were measured at baseline representing different sources of inflammation: vascular inflammation (pentraxin 3 and serum amyloid P), endothelial function (endothelin-1), metabolic function (adiponectin, resistin, and plasminogen activating inhibitor-1), oxidative stress (receptor for advanced glycation end products), and general inflammation (interleukin-6, interleukin-2, and interleukin-10). A combined z-score was created from these biomarkers to represent total inflammation across these sources. We utilized generalized estimating equations that included an interaction term between z-scores and time to assess effect of inflammation on cognitive decline, adjusting for demographics (such as age, race/ethnicity, and sex), cardiovascular risk factors, and apolipoprotein E ε4 carrier status. A Bonferroni-adjusted significance level of .01 was used. We explored associations between individual biomarkers and cognitive decline without adjustment for multiplicity.


The combined inflammation z-score was significantly associated with memory and psychomotor speed (p < .01). Pentraxin 3, serum amyloid P, endothelin-1, and interleukin-2 were associated with change in at least one cognitive domain (p < .05).


Our results suggest that total inflammation is associated with memory and psychomotor speed. In particular, systemic inflammation, vascular inflammation, and altered endothelial function may play roles in domain-specific cognitive decline of nondemented individuals. © The Author 2016. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved.”        Study Link

Are you beginning to wonder why we’ve never been informed of these dangers? Evidence below of glycation in lung cancer was submitted on Aug9, 2016. I’ve not heard anything about this. Doesn’t the ACS care? They’re still recommending carbs in the diet, so they must not;

“Effects of carboxymethyllysine (CML) and pentosidine, two advanced glycation end-products (AGEs), upon invasion and migration in A549 and Calu-6 cells, two non-small cell lung cancer (NSCLC) cell lines were examined. CML or pentosidine at 1, 2, 4, 8 or 16 μmol/L were added into cells. Proliferation, invasion and migration were measured. CML or pentosidine at 4-16 μmol/L promoted invasion and migration in both cell lines, and increased the production of reactive oxygen species, tumor necrosis factor-α, interleukin-6 and transforming growth factor-β1. CML or pentosidine at 2-16 μmol/L up-regulated the protein expression of AGE receptor, p47(phox), intercellular adhesion molecule-1 and fibronectin in test NSCLC cells. Matrix metalloproteinase-2 protein expression in A549 and Calu-6 cells was increased by CML or pentosidine at 4-16 μmol/L. These two AGEs at 2-16 μmol/L enhanced nuclear factor κ-B (NF-κ B) p65 protein expression and p38 phosphorylation in A549 cells. However, CML or pentosidine at 4-16 μmol/L up-regulated NF-κB p65 and p-p38 protein expression in Calu-6 cells. These findings suggest that CML and pentosidine, by promoting the invasion, migration and production of associated factors, benefit NSCLC metastasis.” Study Link

This is the evidence of your back problems being caused by glycation. This study shows how the inflammatory responses to glycation causing vertebral disk degeneration;

“Inflammation and cytokines have been recognized to correlate with intervertebral disc (IVD) degeneration (IDD), via mediating the development of clinical signs and symptoms. However, the regulation mechanism remains unclear. We aimed at investigating the regulatory role of interleukin (IL)β and high mobility group box 1 (HMGB1) in the inflammatory response in human IVD cells, and then explored the signaling pathways mediating such regulatory effect. Firstly, the promotion to inflammatory cytokines in IVD cells was examined with ELISA method. And then western blot and real time quantitative PCR were performed to analyze the expression of toll-like receptors (TLRs), receptors for advanced glycation endproducts (RAGE) and NF-κB signaling markers in the IL-1β- or (and) HMGB1-treated IVD cells. Results demonstrated that either IL-1β or HMGB1 promoted the release of the inflammatory cytokines such as prostaglandin E2 (PGE2), TNF-α, IL-6 and IL-8 in human IVD cells. And the expression of matrix metalloproteinases (MMPs) such as MMP-1, -3 and -9 was also additively up-regulated by IL-1β and HMGB1. We also found such additive promotion to the expression of TLR-2, TLR-4 and RAGE, and the NF-κB signaling in intervertebral disc cells. In summary, our study demonstrated that IL-1β and HMGB1 additively promotes the release of inflammatory cytokines and the expression of MMPs in human IVD cells. The TLRs and RAGE and the NF-κB signaling were also additively promoted by IL-1β and HMGB1. Our study implied that the additive promotion by IL-1β and HMGB1 to inflammatory cytokines and MMPs might aggravate the progression of IDD.”  Study Link

Even unborn babies are not immune to the effects if glycation;

·        Accumulation of AdvancedGlycationEnd Products Involved in Inflammation and Contributing to Severe Preeclampsia, in Maternal Blood, Umbilical Blood and Placental Tissues.


Ovarian cancer is a consequence of glycation;

S100B is one of the members of the S100 protein family and is involved in the progression of a variety of cancers. Ovarian cancer is driven by cancer stem-like cells (CSLCs) that are involved in tumor genesis, metastasis, chemo-resistance and relapse. We then hypothesized that S100B might exert pro-tumor effects by regulating ovarian CSLCs stemness, a key characteristic of CSLCs. First, we observed the high expression of S100B in ovarian cancer specimens when compared to that in normal ovary. The S100B upregulation associated with more advanced tumor stages, poorer differentiation and poorer survival. In addition, elevated S100B expression correlated with increased expression of stem cell markers including CD133, Nanog and Oct4. Then, we found that S100B was preferentially expressed in CD133+ ovarian CSLCs derived from both ovarian cancer cell lines and primary tumors of patients. More importantly, we revealed that S100B knockdown suppressed the in vitro self-renewal and in vivo tumorigenicity of ovarian CSLCs and decreased their expression of stem cell markers. S100B ectopic expression endowed non-CSLCs with stemness, which has been demonstrated with both in vitro and in vivo experiments. Mechanically, we demonstrated that the underlying mechanism of S100B-mediated effects on CSLCs stemness was not dependent on its binding with a receptor for advanced glycation end products (RAGE), but might be through intracellular regulation, through the inhibition of p53 expression and phosphorylation. In conclusion, our results elucidate the importance of S100B in maintenance of ovarian CSLCs stemness, which might provide a promising therapeutic target for ovarian cancer. Stem Cells 2016.”  Study Link

This study looks at the AGEs responsible for inflammatory bowel disease and Rheumatoid arthritis;

Neutrophils and monocytes belong to the first line of immune defence cells and are recruited to sites of inflammation during infection or sterile injury. Both cells contain huge amounts of the heterodimeric protein S100A8/A9 in their cytoplasm. S100A8/A9 belongs to the Ca2+ binding S100 protein family and has recently gained a lot of interest as a critical alarmin modulating the inflammatory response after its release (extracellular S100A8/A9) from neutrophils and monocytes. Extracellular S100A8/A9 interacts with the pattern recognition receptors Toll-like receptor 4 (TLR4) and Receptor for Advanced Glycation Endproducts (RAGE) promoting cell activation and recruitment. Besides its biological function, S100A8/A9 (also known as myeloid related protein 8/14, MRP8/14) was identified as interesting biomarker to monitor disease activity in chronic inflammatory disorders including inflammatory bowel disease and rheumatoid arthritis. Furthermore, S100A8/A9 has been tested successfully in pre-clinical imaging studies to localize sites of infection or sterile injury. Finally, recent evidence using small molecule inhibitors for S100A8/A9 also suggests that blocking S100A8/A9 activity exerts beneficial effects on disease activity in animal models of autoimmune diseases including multiple sclerosis, systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease. This review will provide a comprehensive and detailed overview into the structure and biological function of S100A8/A9 and also will give an outlook in terms of diagnostic and therapeutic applications targeting S100A8/A9.        Study Link

HMGB1 is a label that’s been assigned to a type of AGE or RAGE. It’s importance lies in its ability to create pain in your body. This is one of over 4976 warnings and notices of what glycation does to the body that available for your perusal on the effects of glycation on PubMed;

Neuropathic pain (NPP) is intolerable, persistent, and specific type of long-term pain. It is considered to be a direct consequence of pathological changes affecting the somatosensory system and can be debilitating for affected patients. Despite recent progress and growing interest in understanding the pathogenesis of the disease, NPP still presents a major diagnostic and therapeutic challenge. High mobility group box 1 (HMGB1) mediates inflammatory and immune reactions in nervous system and emerging evidence reveals that HMGB1 plays an essential role in neuroinflammation through receptors such as Toll-like receptors (TLR), receptor for advanced glycation end products (RAGE), C-X-X motif chemokines receptor 4 (CXCR4), and N-methyl-D-aspartate (NMDA) receptor. In this review, we present evidence from studies that address the role of HMGB1 in NPP. First, we review studies aimed at determining the role of HMGB1 in NPP and discuss the possible mechanisms underlying HMGB1-mediated NPP progression where receptors for HMGB1 are involved. Then we review studies that address HMGB1 as a potential therapeutic target for NPP.             Study Link

The following study was completed in July 2010, explaining the health benefits of calorie restriction. This is what was being researched over 120 years ago, as ketonuria was noticed in the urine of fasting patients, giving them ketonemia. This is a condition that best serves healing in the body for multiple reasons and has been shown to heal many diseases, simply from fasting. Since 500BC fasting has been used to cure many diseases with astonishing success. This is what’s known as ketosis today and is what your body goes through as a healing, fat burning type of metabolism. It uses your own fat to provide everything from hormones to glucose, through gluconeogenesis, the perfect glucose for the body as it made from your fat, making it a clean glucose source;

The societal impact of obesity, diabetes, and other metabolic disorders continues to rise despite increasing evidence of their negative long-term consequences on health span, longevity, and aging. Unfortunately, dietary management and exercise frequently fail as remedies, underscoring the need for the development of alternative interventions to successfully treat metabolic disorders and enhance life span and health span. Using calorie restriction (CR)—which is well known to improve both health and longevity in controlled studies—as their benchmark, gerontologists are coming closer to identifying dietary and pharmacological therapies that may be applicable to aging humans. This review covers some of the more promising interventions targeted to affect pathways implicated in the aging process as well as variations on classical CR that may be better suited to human adaptation.

Another report submitted Nov, 08 to the Official Journal of the International League Against Epilepsy, basically said the same thing while they were looking for the best way to approach putting the body into ketosis;

The ketogenic diet (KD) is a 90% fat diet that is an effective treatment for intractable epilepsy. Rapid initiation of the KD requires hospital admission because of the complexity of the protocol and frequent mild and moderate adverse events. The purpose of the study was to compare the efficacy of a gradual KD initiation with the standard KD initiation preceded by a 24- to 48-h fast.

Perhaps the most damning report against aging was issued in January of 1984, yet nothing was mentioned about this report; it was one of the first indications of what glycation does to the body and with a major cause of glycation being glucose or sugar, I have to wonder why the FDA didn’t say anything about it then. Why weren’t we, at least, informed about this study? Industry concerns?

·       Collagen aging in vitro by nonenzymatic glycosylation and browning.

Aging and diabetes mellitus are associated with cross-linking and nonenzymatic glycosylation of collagen. Incubation of tendon fibers with reducing sugars results in increased breaking time in urea similar to that seen in aging, and in nonenzymatic glycosylation and browning. Effect of a sugar is proportional to the amount of sugar available in the open chain form. The increase in breaking time correlates with the appearance of chromophores characteristic of crosslinked browning products. Collagen altered by nonenzymatic browning may play a role in some age-like major complications of diabetes.   Study Link

This evidence of glycation’s role in atherosclerosis was in this study submitted in May 1988. Was this publicized? Did you hear about this? Did the FDA know?

Adhesion of bovine endothelial cells on fibronectin and collagen before and after nonenzymatic glycation in vitro has been studied. Nonenzymatic glycation of these proteins reduced their ability to bind endothelial cells. Furthermore, nonenzymatically glycated fibronectin failed to bind to normal and nonenzymatically glycated gelatin and to fibrin. So gelatin and fibrin Sepharoses can be used to separate highly glycated fibronectins from fibronectins with a low degree of nonenzymatic glucose substitution. Sodium dodecylsulfate polyacrylamide gel electrophoresis did not demonstrate a covalent cross-link between nonenzymatically glycated fibronectins. These results present further evidences for the role of nonenzymatic glycation of proteins in the development of vascular complications in long-term diabetes and of atherosclerosis.              Study Link

This shows the damage done by glycation on the blood. I posted this study because I wanted to note what the first sentence states, that this damage, at the time of publication, had been known for 20 years. The date on this study is marked as July 29, 1988. That means that his damage was discovered in 1968, 48 years ago.

The association between elevated levels of glycated haemoglobins and diabetes mellitus has been known for twenty years [92]. Since then the determination of glycated haemoglobins has become a valuable tool for the objective assessment of long-term glycaemia in diabetic patients. The marked clinical interest in reliable measurements of glycated haemoglobins has stimulated the development and perfection of the necessary methodology. Limitations of the techniques have led to investigation of the underlying causes. Some of them led to the recognition of processes that were not known to occur in vivo before, such as glycation at sites other than the amino terminus of the beta-chains, modification of haemoglobin by reactants other than glucose or the existence of labile haemoglobin adducts. With ideal methodology these features would have gone unnoticed. Furthermore, the determination of glycated haemoglobin in large populations of diabetic patients has lead to the discovery of new, clinically silent mutant haemoglobins. Today, the routine determination of glycated haemoglobins in diabetic patients probably represents the broadest screening for mutant haemoglobins. The experience with glycated haemoglobins shows that overcoming difficulties in their determination, and progress in biomedical research, are closely intertwined.

This study shows how proteins exposed to glucose undergoes oxidative stress, the basis of aging;

Studies have shown that glycation in vitro is complicated by the ability of glucose to oxidise, in the presence of trace amounts of transition metal, generating protein-reactive ketoaldehydes, hydrogen peroxide and diverse free radicals. Protein exposed to glucose undergoes fragmentational and conformational alterations, and these, as well as thiol oxidation, appear to be caused by hydroxyl radicals. Glycofluorophore formation is dependent upon ketoaldehyde formation. It is suggested that glucose autoxidation contributes to oxidative stress in pathophysiology associated with diabetes and ageing via this newly described process of “autoxidative glycosylation”.

The following report from Oct 30 1981 shows the effects of glycation on cholesterol, LDL particles particularly and how it leads to atherosclerosis ;

Atherosclerosis occurs at an accelerated rate in patients with diabetes mellitus. Since some proteins undergo nonenzymatic glycosylation in diabetic patients and because certain chemical modifications of low density lipoproteins produced alterations in their interactions with certain cultured cells, a fact that may be relevant to atherogenesis, we investigated the effect of in vitro glycosylation on cell-related properties of low density lipoproteins. Glycosylation was carried out by incubating LDL (1-10 mg LDL-protein/ml) with glucose (0-100 mM) in 0.5 M phosphate buffer, pH 8.0, at 37 degrees C. The amount of glucose incorporated into LDL after 1-2 wk of incubation was estimated to be in the range of 1-10 mol/mol LDL-protein. Amino acid analysis of glycosylated LDL showed that glucose was covalently bound to lysine residues. In studies with cultured human fibroblasts, glycosylated LDL was internalized and degraded significantly less than control LDL, in proportion to the estimated degree of glycosylation (12% of control for the most extensively glycosylated LDL). Glycosylation of LDL also impaired significantly its ability to stimulate cholesteryl ester synthesis by cultured fibroblasts. Glycosylated LDL did not stimulate cholesteryl ester synthesis in rat peritoneal macrophages. If glycosylation of LDL occurs in diabetic patients, some pathophysiologic consequences related to the increased incidence of atherosclerosis in these patients may result.

Study Link

In 1981 this was discovered, yet it’s been 35 years since then and yet few people are aware of this. My question is, why?  Maybe I should ask the sugar industry.

The following study shows the how the adhesive qualities of glucose creates fibrinogen, which becomes a target for glycation;

·        Polymerisation and crosslinking of fibrin monomers in diabetes mellitus

Polymerisation and crosslinking of fibrin monomers was studied in 35 healthy volunteers and in 42 poorly controlled diabetic patients. Polymerisation did not show any difference between control subjects (n = 10) and diabetic patients (n = 11) (p greater than 0.1), although fibrinogen was 35% more glycated in the diabetic patients (p less than 0.001). Alpha chain crosslinking in the diabetic patients, however, was impaired as is shown from an increase in intermediate alpha polymers with a concomitant decrease in alpha monomer disappearance. A significant positive correlation was found between the degree of glycation of fibrinogen and the defective alpha chain polymerisation (r = 0.86, p less than 0.005). These results were consistent with the results of thrombin and reptilase experiments. The reaction rate with reptilase did not show any difference between the two groups (p greater than 0.1), whereas the reaction rate with thrombin was significantly slower in the diabetic group compared to the control subjects (p less than 0.001). Purified fibrin clots obtained from the diabetic patients were more susceptible to plasmin than clots obtained from control subjects. It is concluded that in poorly controlled diabetic patients polymerisation of fibrin monomers is normal, but crosslinking of the alpha chains is impaired, leading to a higher susceptibility of the clots to plasmin degradation.

From Wikipedia on Fibrinogen;

Fibrinogen (factor I) is a glycoprotein in vertebrates that helps in the formation of blood clots. It consists of a linear array of three nodules held together by a very thin thread which is estimated to have a diameter between 8 and 15 Angstrom (Å). The two end nodules are alike but the center one is slightly smaller. Measurements of shadow lengths indicate that nodule diameters are in the range 50 to 70 Å. The length of the dried molecule is 475 ± 25 Å.[2]

·        Effect of  of low-density lipoprotein on the immunological determination glycation of apolipoprotein B.

Non-enzymatic glycation of low-density lipoprotein (LDL) may contribute to the premature atherogenesis of patients with diabetes mellitus. To assess whether  glycation of apolipoprotein B, the predominant protein of LDL, interferes with the ability to immunologically quantify this protein, we prepared and purified glycated LDL by incubating normal plasma samples with high concentrations of glucose. Although both the plasma and the LDL specimens incubated with glucose contained significantly more glycated protein than control specimens, the quantitative interaction of an apolipoprotein B-specific antibody with glycated vs nonglycated LDL was not significantly different. We conclude that apolipoprotein B can be accurately quantified immunologically despite the presence of clinically excessive degrees of LDL glycation.

Study Link

I included the following study from November 1989 because of its explanation of how glycation is responsible for inflammation;

·        Changes in concanavalin A-reactive proteins in inflammatory disorders.

Quantitative changes of concanavalin A (Con A)-reactive proteins in serum samples obtained from rats with induced inflammation and from patients with inflammatory and autoimmune diseases were examined by use of lectin blots. Treatment of rats with a single dose of fermented yeast to induce inflammation caused an extensive increase in Con A-reactivity. These changes were time dependent and were similar in both sexes of the animals. When we examined serum samples obtained from patients with various inflammatory disorders for their Con A-reactive proteins as compared with normal donors, we noted that the Con A-reactivity increased in patients with rheumatoid arthritis and systemic lupus erythematosus. Among all the glycoproteins examined by lectin blots with use of Con A, a set of five proteins was selected for detailed analysis by densitometric scanning. These included alpha 2-macroglobulin, P-150, P-95, P-40, and P-35, of Mr 180,000, 150,000, 95,000, 40,000, and 35,000, respectively, by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing conditions. Densitometric scanning analysis of the lectin blots revealed that the Con A-reactivity of these proteins increased during inflammation. Because alpha 2-macroglobulin is not an acute-phase protein in humans, an increase in Con A staining of this protein suggested that altered glycation is associated with autoimmune diseases. Thus, study of changes in Con A-reactive proteins in human sera may facilitate our understanding of the etiology and pathophysiology of autoimmune diseases.                  Study Link

·        Clinical Value of High Mobility Group Box 1 and the Receptor for Advanced Glycation End-products in Head and Neck Cancer: A Systematic Review.

Abstract Introduction High mobility group box 1 is a versatile protein involved in gene transcription, extracellular signaling, and response to inflammation. Extracellularly, high mobility group box 1 binds to several receptors, notably the receptor for advanced glycation end-products. Expression of high mobility group box 1 and the receptor for advanced glycation end-products has been described in many cancers. Objectives To systematically review the available literature using PubMed and Web of Science to evaluate the clinical value of high mobility group box 1 and the receptor for advanced glycation end-products in head and neck squamous cell carcinomas. Data synthesis A total of eleven studies were included in this review. High mobility group box 1 overexpression is associated with poor prognosis and many clinical and pathological characteristics of head and neck squamous cell carcinomas patients. Additionally, the receptor for advanced glycation end-products demonstrates potential value as a clinical indicator of tumor angiogenesis and advanced staging. In diagnosis, high mobility group box 1 demonstrates low sensitivity. Conclusion High mobility group box 1 and the receptor for advanced glycation end-products are associated with clinical and pathological characteristics of head and neck squamous cell carcinomas. Further investigation of the prognostic and diagnostic value of these molecules is warranted.”

“Diabetes is frequently associated with cardiovascular diseases (coronary heart disease, cerebrovascular disease, peripheral vascular disease), and several risk factors have been proposed. Recent studies have strengthened the importance of chronic hyperglycemia because this modifies a variety of circulating substances including lipoproteins, and the glycosylated ones can be involved in the process of accelerating atherosclerosis. In this review, previous studies indicating the significance of glycosylated lipoproteins in the progression of atherosclerosis were overviewed. We also discussed AGE (advanced glycation end products) which may play an important role of atherogenesis in diabetes.”The most recent study, submitted in October 2016 reveals some of the known damage that glycation is responsible for;

·        Relationship between plasma glycation with membrane modification, oxidative stress and expression of glucose trasporter-1 in type 2 diabetes patients with vascular complications.


Enhanced protein glycation in diabetes causes irreversible cellular damage through membrane modifications. Erythrocytes are persistently exposed to plasma glycated proteins; however, little are known about its consequences on membrane. Aim of this study was to examine the relationship between plasma protein glycation with erythrocyte membrane modifications in type 2 diabetes patients with and without vascular complications.


We recruited 60 healthy controls, 85 type 2 diabetic mellitus (DM) and 75 type 2 diabetic patients with complications (DMC). Levels of plasma glycation adduct with antioxidants (fructosamine, protein carbonyl, β-amyloids, thiol groups, total antioxidant status), erythrocyte membrane modifications (protein carbonyls, β-amyloids, free amino groups, erythrocyte fragility), antioxidant profile (GSH, catalase, lipid peroxidation) and Glut-1 expression were quantified.


Compared with controls, DM and DMC patients had significantly higher level of glycation adducts, erythrocyte fragility, lipid peroxidation and Glut-1 expression whereas declined levels of plasma and cellular antioxidants. Correlation studies revealed positive association of membrane modifications with erythrocyte sedimentation rate, fragility, peroxidation whereas negative association with free amino groups, glutathione and catalase.


Our data suggest that plasma glycation is associated with oxidative stress, Glut-1 expression and erythrocyte fragility in DM patients. This may further contribute to progression of vascular complications.

More evidence of the role glucose plays in brain degradation;

Protein glycation is an age-dependent posttranslational modification associated with several neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases. By modifying amino-groups, glycation  interferes with folding of proteins, increasing their aggregation potential. Here, we studied the effect of pharmacological and genetic manipulation of glycation on huntingtin (HTT), the causative protein in Huntington’s disease (HD). We observed that glycation increased the aggregation of mutant HTT exon 1 fragments associated with HD (HTT72Q and HTT103Q) in yeast and mammalian cell models. We found that glycation impairs HTT clearance thereby promoting its intracellular accumulation and aggregation. Interestingly, under these conditions autophagy increased and the levels of mutant HTT released to the culture medium decreased. Furthermore, increased  glycation enhanced HTT toxicity in human cells and neurodegeneration in fruit flies, impairing eclosion and decreasing life span. Overall, our study provides evidence that glycation modulates HTT exon-1 aggregation and toxicity, and suggests it may constitute a novel target for therapeutic intervention in HD.

Evidence of the glycative effects in Cataracts was know in the fall of 1974, yet nothing was said that I can remember, but then I was just getting out of Jr College then;

J Clin Invest. 1984 Nov;74(5):1742-9.

Garlick RLMazer JSChylack LT JrTung WHBunn HF.

We have examined the nonenzymatic glycation of human lens crystallin, an extremely long-lived protein, from 16 normal human ocular lenses 0.2-99 yr of age, and from 11 diabetic lenses 52-82-yr-old. The glucitol-lysine (Glc-Lys) content of soluble and insoluble crystallin was determined after reduction with H-borohydride followed by acid hydrolysis, boronic acid affinity chromatography, and high pressure cation exchange chromatography. Normal lens crystallin, soluble and insoluble, had 0.028 +/- 0.011 nanomoles Glc-Lys per nanomole crystallin monomer. Soluble and insoluble crystallins had equivalent levels of glycation. The content of Glc-Lys in normal lens crystallin increased with age in a linear fashion. Thus, the nonenzymatic glycation of nondiabetic lens crystallin may be regarded as a biological clock. The diabetic lens crystallin samples (n = 11) had a higher content of Glc-Lys (0.070 +/- 0.034 nmol/nmol monomer). Over an age range comparable to that of the control samples, the diabetic crystallin samples contained about twice as much Glc-Lys. The Glc-Lys content of the diabetic lens crystallin samples did not increase with lens age.

This study look at the effects of glycation on your eyes and the cataracts is responsible for. Yes glycation and a glucose diet will buy you cataracts. My mother had two of them. A good who loved to eat her bread had cataracts in both of her eyes as well. What’s interesting, this person was always complaining of headaches and stomach aches, both manifestations of an ECC diet. Again, here is more evidence of the glycative and addictive effects of a grain diet.

The following report provides evidence of glycation’s role in Leukemia.

Extracellular HMGB1 promotes differentiation of nurse-like cells in chronic lymphocytic leukemia.

“Chronic lymphocytic leukemia (CLL) is a disease of an accumulation of mature B cells that are highly dependent on the microenvironment for maintenance and expansion. However, little is known regarding the mechanisms whereby CLL cells create their favorable microenvironment for survival. High-mobility group protein B-1 (HMGB1) is a highly conserved nuclear protein that can be actively secreted by innate immune cells and passively released by injured or dying cells. We found significantly increased HMGB1 levels in the plasma of CLL patients compared with healthy controls, and HMGB1 concentration is associated with absolute lymphocyte count. We therefore sought to determine potential roles of HMGB1 in modulating the CLL microenvironment. CLL cells passively released HMGB1, and the timing and concentrations of HMGB1 in the medium were associated with differentiation of nurse-like cells (NLCs). Higher CD68 expression in CLL lymph nodes, one of the markers for NLCs, was associated with shorter overall survival of CLL patients. HMGB1-mediated NLC differentiation involved internalization of both receptor for advanced  glycation end products (RAGE) and Toll-like receptor-9 (TLR9). Differentiation of NLCs can be prevented by blocking the HMGB1-RAGE-TLR9 pathway. In conclusion, this study demonstrates for the first time that CLL cells might modulate their microenvironment by releasing HMGB1.”         Free PMC Article

J Clin Invest. 1984 Nov;74(5):1742-9.

After searching these last few disorders I got a yen to search any disorder & glycation, and glycation turned up in everything except halitosis. The following report shows its involvement in stomach ulcers. I originally searched just ulcers and got back 30 studies showing involvement. The first few studies in the list were reports on foot ulcers, so I search stomach ulcers and found 3 studies, the following report was the first;

High-mobility group box 1 (HMGB1) was initially discovered as a nuclear protein that interacts with DNA as a chromatin-associated non-histone protein to stabilize nucleosomes and to regulate the transcription of many genes in the nucleus. Once leaked or actively secreted into the extracellular environment, HMGB1 activates inflammatory pathways by stimulating multiple receptors, including Toll-like receptor (TLR) 2, TLR4, and receptor for advanced glycation end products (RAGE), leading to tissue injury. Although HMGB1’s ability to induce inflammation has been well documented, no studies have examined the role of HMGB1 in wound healing in the gastrointestinal field. The aim of this study was to evaluate the role of HMGB1 and its receptors in the healing of gastric ulcers. We also investigated which receptor among TLR2, TLR4, or RAGE mediates HMGB1’s effects on ulcer healing. Gastric ulcers were induced by serosal application of acetic acid in mice, and gastric tissues were processed for further evaluation. The induction of ulcer increased the immunohistochemical staining of cytoplasmic HMGB1 and elevated serum HMGB1 levels. Ulcer size, myeloperoxidase (MPO) activity, and the expression of tumor necrosis factor α (TNFα) mRNA peaked on day 4. Intraperitoneal administration of HMGB1 delayed ulcer healing and elevated MPO activity and TNFα expression. In contrast, administration of anti-HMGB1 antibody promoted ulcer healing and reduced MPO activity and TNFα expression. TLR4 and RAGE deficiency enhanced ulcer healing and reduced the level of TNFα, whereas ulcer healing in TLR2 knockout (KO) mice was similar to that in wild-type mice. In TLR4 KO and RAGE KO mice, exogenous HMGB1 did not affect ulcer healing and TNFα expression. Thus, we showed that HMGB1 is a complicating factor in the gastric ulcer healing process, which acts through TLR4 and RAGE to induce excessive inflammatory responses.                                  Free PMC Article


  • Nonenzymatic glycation of human lens crystallin. Effect of aging and diabetes mellitus.

Garlick RLMazer JSChylack LT JrTung WHBunn HF.

This study looked at the effects of glycation on your eyes and the cataracts it’s responsible for. Yes glycation and a glucose diet will buy you cataracts. My mother had two of them. A good friend who loved to eat her bread had cataracts in both of her eyes as well. What’s interesting, this person was always complaining of headaches and stomach aches. Both of those manifestations are from an ECC diet. Again, here is more evidence of the glycative and addictive effects of a grain diet. In all, there were 3,629 studies on the effects of glucose glycating proteins, hemoglobin, and cholesterol dating back to March, 1984. Incidentally, that was one month after I was released from the hospital after spending a month in a coma and suffering two strokes while comatose. I could have never come back this far without Dr Perlmutter’s help. Again, I have to thank you, Dr Perlmutter.

I found this study done Sep 5, 2014 on autism and environmental factors. The only factor that mirrored the rise in autism was the use of glyphosate herbicides. Note the similarity.  For me, this is enough to shut down the use of Roundup and all generic versions. Will the USDA recommend this? Knowing who runs the USDA, I seriously doubt it. Although it has little to do with glycation, it expresses the danger of the herbicide that’s used on virtually all grains today.

An external file that holds a picture, illustration, etc. Object name is 12940_2014_781_Fig6_HTML.jpg
Temporal trend in autism compared to temporal trend in U.S. application of glyphosate to genetically-modified corn and soy crops, as estimated from US Department of Agriculture data (see Additional file 1 ).
 The author of this last report tries to dance around the issue of the glyphosate herbicide’s relationship to autism, but the evidence is clear.

They’ve had some of this evidence for over 30 years, why hasn’t the public been told about glycation or the AGEs they create? It’s those AGEs that are at the root of all modern diseases. If this was uncovered starting 30+ years ago, why have we just found out about it from the bestselling books from two doctors? Is someone trying to hide something? My guess is yes. This is Monsanto’s path to power and freedom. They’ve politically engineered their freedom to wreak whatever havoc they can on your health by masturbating your taste buds with their glucose laden products, to grant them power by buying into their pharmaceutical cycle in the very near future. By near, I mean, it only takes a couple days before you’re indebted. (That means addicted.) If you want true power and freedom, you can have it in two weeks to two months. That’s how long it takes to break the addiction.

Each and every one of these 11,000+ studies have been vetted and examined by the NIH and PubMed for whom I thank.

You have two choices;

  1. Continue to masturbate your taste buds and collect these diseases and disorders in return.
  2. Cut out as much as possible the starchy carbohydrates, (grains) and live free from dependence.

You need to realize that the comfort in comfort food, brings massive discomfort in the future, starting immediately, with a process called glycation. This is the real poisoning of America and we can correct it. It lies within our power, each and every one of us can correct this. I offer a cure, not a therapy or treatment, My cure simply involves removal of all glycating substances from the diet to eliminate this problem of glycation so that it never affects the body The glycating substances = carbs, sugar, glucose, fructose.

The above reports on the effects of glycation appeared in many cases, over 30 years ago in PubMed. I’ve only showed you 47 reports out of 11,750 studies to date detailing the damaging effects of Excessive Carbohydrate Consumption, the primary cause of glycation, why doesn’t the FDA or the USDA say anything about that? The 42nd   study, submitted in November, 1989 shows how it causes inflammation, and with inflammation a factor in so many diseases, it truly is a wonder that the FDA and USDA never even issued anything so simple as a warning. The FDA’s involvement in this issue is mostly explained by their influence from the one industry, where they get most of their execs from, Monsanto.

From every form of cancer to Alzheimer’s disease to heart disease and cardiovascular disease to arthritis to hypertension to high cholesterol these food sources (sugar and grains) are responsible for each and every one of these disorders. These studies are proof of exactly what sugar does to the body. To cure the glycation factor in these diseases, the best way is to eliminate it as much as possible. To do that you must eliminate its source and to eliminate the source, you have to eliminate the grains and sugar. Thank you Dr Davis and Dr Perlmutter for bringing this to my attention.

In all, there were 3,629 studies in the FDA’s database on the effects of glucose glycating proteins, hemoglobin, and cholesterol dating back to march, 1984. Incidentally, that was one month after i was released from the hospital after spending a month in a coma and suffering two strokes while comatose. I could have never come back this far without Dr Perlmutter’s help. Again, i have to thank you, Dr Perlmutter. The above, reports on the effects of glycation, appeared, in many cases over 30 years ago in PubMed. With 11,667 studies to date detailing the damaging effects of Excessive Carbohydrate Consumption, the primary cause of glycation, why doesn’t the FDA say anything? The last study, submitted in November, 1989 shows how it causes inflammation and with inflammation a factor in so many diseases, it truly is a wonder that the FDA never even issued anything as simple as a warning. The FDA’s involvement in this issue is largely explained by the influence they receive from the one industry where they get a good portion of their execs from, Monsanto.

With having the evidence for over 30 years, why hasn’t the public been told about glycation or the AGEs they create? It’s those AGEs that are at the root of all modern diseases. If this was uncovered 30+ years ago, why have we just found out about it from the bestselling books from two doctors? They weren’t published in 2010 and 2012 and they had to dig this information our of the archives. Is someone trying to hide something? In who’s best interest would it be to hide this information? The grain industry? My guess is yes.

From every for of cancer (with the possible exception of brain cancer, which I suspect is influenced by glycation simply because of the inflammation factor) to Alzheimer’s disease to heart disease and cardiovascular disease to arthritis to hypertension to high cholesterol these food sources (sugar and grains) are responsible for each and every one of these disorders. These studies are proof of exactly what sugar does to the body. To cure the glycation factor in these diseases, the best way is to eliminate it as much as possible. To do that you must eliminate its source and to eliminate the source, you have to eliminate the grains and sugar. Thank you Dr Davis and Dr Perlmutter for bringing this to my attention. It would have been nice if someone could have done it 20 or 30 years ago. For that, I thank the FDA, the USDA and Monsanto. Don’t allow them to be in your driver’s seat. As long as you remain on your carbohydrate diet, they’re in the driver’s seat for your health. Give up the carbs and put yourself back in the driver’s seat. You are the only one who can change yourself. Enable yourself to do so.




Documentaries worth watching;

  1. Food, Inc
  2. Food Matters
  3. Food Beware (French)
  4. Genetically Modified Foods
  5. David vs Monsanto
  6. Of the Land
  7. Hungry for Change
  8. That Sugar Film
  9. Fathead
  10. Love Paleo
  11. Heal Yourself
  12. Fresh
  13. Who Wants to Live Forever
  14. Overfed and Undernourished
  15. My Big Fat Body
  16. Facing the Fat
  17. Fat
  18. Just Eat It; A Food Waste Story

Why No Warnings from the FDA About gluten and sugar?

FDA’s Assessment of Gluten and Sugar.

It would be nice if this was a problem with just the grain industry but it’s not. It also involves the FDA and what has influenced them to not issue warnings for this allergen. The more I look at it, the more I see that it is a problem with overextending corporate entities. Knowing the dealings that Monsanto has had in the past with competitors and their own judicial systems, it’s not hard to fathom at all the involvement they would have, in the cover up of these studies. It’s actually easy to see their involvement the same as the sugar industry. They didn’t just cover up the studies condemning gluten , they initiated reports themselves that showed gluten was healthy. That is a complete falsehood from the truth of what gluten does.


Gluten does the same thing as sugar. Why won’t the FDA recognize that? They have all the studies that point to it. Don’t they read them?

The following is an excerpt from an FDA study on Gluten as an allergen (1 of 173 studies).

What is the Food Allergen Labeling and Consumer Protection Act (FALCPA) of 2004? 

FALCPA is an amendment to the Federal Food, Drug, and Cosmetic Act and requires that the label of a food that contains an ingredient that is or contains protein from a “major food allergen ” declare the presence of the allergen in the manner described by the law.


  1. Why is there a concern about gluten? 

Gluten describes a group of proteins found in certain grains (wheat, barley, and rye.) It is of concern because people with celiac disease cannot tolerate it. Celiac disease (also known as celiac sprue) is a chronic digestive disease that damages the small intestine and interferes with absorption of nutrients from food. Recent findings estimate that 2 million people in the U.S. have celiac disease or about 1 in 133 people.

  1. What does FALCPA require with regard to gluten?

FALCPA requires FDA to issue a proposed rule that will define and permit the voluntary use of the term “gluten free” on the labeling of foods by August 2006 and a final rule no later than August 2008.

  1. What has FDA done in response to the FALCPA mandate?

FDA held a public meeting in August 2005 to obtain expert comment and consultation from stakeholders to help FDA develop a regulation to define and permit the voluntary use on food labeling of the term “gluten-free” (Public Meeting On: Gluten-Free Food Labeling). The meeting focused on food manufacturing, analytical methods, and consumer issues related to reduced levels of gluten in food.

FDA’s gluten-free definition, is that the food contain less than 20 ppm of gluten. It seems their concern is more with labelling than it is with safety. If it were with safety, they’d be warning us about the dangers that I’ve listed, yet they don’t, as if they were influenced by an outside source.

They consider wheat and gluten as undeclared allergens yet they refuse to acknowledge its allergenic properties to the extent that they won’t require a warning label for it. Yet they know what damage it does. All they require is a mention of wheat in the ingredients and nothing more. That is their warning. Consider this your warning; Grains are poison, and that includes wheat.

Their negligence in regards to our health in this manner is unconscionable. I can only assume that they’ve been influenced by the other side of the industry that provides crop seed for the farmers that grow the food that the FDA approves for us to eat. The other side of this industry, owned by the same corporations, is the pharmaceutical industry. They provide us with all of the drugs that we take to fight the disease caused by the food provided their sister pharmaceutical industry.

What I wonder is, what does the FDA consider stakeholders? Are they the corporate entities who have an interest in proliferating wheat and gluten? Since we now know that this happened with sugar, why wouldn’t the same thing happen with gluten? We know that gluten breaks down to nothing more than glucose (sugar), I can see where the same situation would exist today, that existed 50 -60 years ago. In fact, I believe it’s an ongoing problem.

Just like in the tobacco industry, “selling a product that is already sold for them as it’s addictive”, the same mantra is heard in the grain industry concerning their gluten.  “How can people refuse to buy our products? They’re addictive so people will want them more.

I salute the FDA for monitoring products claiming to be gluten free yet have more than a trace of gluten in them, such as the Investigation into General Mills for selling Cheerios that had more than the allowed limit of 20 ppm of gluten. Yet knowing what damage gluten does to the body, I have to wonder why do they still allow it to be marketed without any warnings? The tobacco companies can’t market their products without warnings. Why it the food industry allow to? The evidence lies within the vaults of the FDA, showing all the damage it does. Why do they ignore that evidence?

What evidence, you say? This evidence lies in the excerpts below, from three of their 173 studies on gluten;

  1. “Gluten is the protein that naturally occurs in wheat, rye, barley, and crossbreeds of these grains.Most people can eat gluten, but in people with celiac disease, gluten intake gradually damages the intestines, prevents the absorption of vitamins and minerals, and can lead to other health problems. Symptoms can include diarrhea, fatigue, headaches, abdominal pain, brain fog, rashes, nausea, vomiting, and other reactions.”
  2. “People who have an allergy to wheat run the risk of serious or life-threatening allergic reaction if they eat wheat. Symptoms may include swelling, itching or irritation of mouth or throat, difficulty breathing, nasal congestion, itchy or watery eyes, rash or hives, headaches, nausea, vomiting, cramps, diarrhea, or anaphylaxis, a potentially life-threatening reaction.”What I can’t understand, with this kind of disruption of bodily functions, why doesn’t this require a warning like cigarettes? It’s clearly killed more people.
  3. ”Unlike food allergies, clinical signs and symptoms do not appear to be reliable markers of disease activity because many individuals affected with celiac disease may be entirely asymptomatic. This tells me that a lot more people suffer from the disease than what have been diagnosed. Furthermore, although biomarkers of genetic susceptibility (e.g., presence of DQ2 and/or DQ8 HLA alleles) and gluten exposure [e.g., antibodies for gliadin (AGA), endomysial (EMA), and tissue transglutaminase (tTG)] have been defined for use in noninvasive diagnosis of individuals with celiac disease, these biomarkers have not been shown to correlate with disease severity nor to be useful in assessing daily responses to gluten exposures. Rather, evidence of intestinal mucosal inflammation is the gold standard biomarker for diagnosis of celiac disease and for assessment of disease severity. Intestinal mucosal inflammation may occur long before the development of clinical signs or a rise in antibody titers following a gluten challenge. Intestinal inflammation is assessed by intestinal biopsy, which is an invasive procedure, associated with false negatives (due to sampling error), and is impractical for frequent monitoring of disease activity or severity.”     Revised Threshold Report Page 58 of 108
  4. “Unpublished data described in Moneret-Vautrin and Kanny (2004) show that 83% of wheat allergic children reacted to less than 2 g of wheat flour while only 18% of wheat allergic adults responded at this level. Unpublished data described in Moneret Vautrin (2004) on wheat flourchallenges using 32 children and 32 adults with wheat allergy, reported a LOAEL of ≤ 1.8 mg protein for allergic children (the lowest tested dose) and 52.8 mg protein for allergic adults. Scibilia et al. (2006) reported that 2 of 13 responders reacted to the lowest dose of wheat flour tested (100 mg of a mix of bread and durum flour, approximately 15 mg protein) in DBPCFCs. In total, 31% of the patients who reacted did so to challenge doses less than or equal to 240 mg of wheat protein.” Approaches to Establish Thresholds for Major Food Allergens My question how many people eat this amount? Most people eat around 150mg of wheat products in a day, not enough to express symptoms of celiac disease, but enough to do unnoticed damage.
  5. “The foods of concern for individuals with, or susceptible to, celiac disease are the cereal grains that contain the storage proteins prolamin and glutelin (commonly referred to as glutens in wheat), including all varieties of wheat (e.g., durum, spelt, kamut), barley (where the storage proteins are called hordiens), rye (where the storage proteins are called secalins), and their cross-bred hybrids (such as triticale). The proportion of individuals with celiac disease that are also sensitive to the storage proteins in oats (avenins) has not been determined but is likely to be less than 1% (Kelly, 2005).”
  6. “The clinical manifestations of celiac disease are highly variable in character and severity. The reasons for this diversity are unknown but may depend on the age and immunological status of the individual, the amount, duration, or timing of exposure to gluten, and the specific area and extent of the gastrointestinal tract involved by disease (Dewar et al., 2004). These clinical manifestations can be divided into gastrointestinal, or “classic,” and non-gastrointestinal manifestations. Gastrointestinal manifestations usually present in children 4 to 24 months old and include abdominal pain and cramping, bloating, recurrent or chronic diarrhea in association with weight loss, poor growth, nutrient deficiency, and (in rare cases) a life-threatening metabolic emergency termed celiac crisis, characterized by hypokalemia and acidosis secondary to profuse diarrhea (Farrell and Kelly, 2002; Baranwal et al., 2003). Non-gastrointestinal manifestations are more insidious and highly variable and are the common presenting signs in older children and adults. These manifestations are frequently the result of long-term nutrient malabsorption, including iron deficiency anemia, short stature, delayed puberty, infertility, and osteoporosis or osteopenia (Fasano, 2003). In children, progressive malabsorption of nutrients may lead to growth, developmental, or neurological delays (Catassi and Fasano, 2004). Extra-intestinal manifestations such as dermatitis herpetiformis, hepatitis, peripheral neuropathy, ataxia, and epilepsy have also been associated with celiac disease (Fasano and Catassi, 2001). Individuals with untreated celiac disease are also at increased risk for potentially serious medical conditions, such as other autoimmune diseases (e.g., Type I diabetes mellitus) and intestinal cancers associated with high mortality (Farrell and Kelly, 2002; Peters et al., 2003; Catassi et al., 2002). For example, individuals with celiac disease have an 80-fold greater risk of developing adenocarcinoma of the small intestine, a greater than two-fold increased risk for intestinal or extra intestinal lymphomas (Green and Jabri, 2003) and a 20-fold greater risk of developing enteropathy-associated T cell lymphoma (EATL) (Catassi et al.,”
  7. “There is no standard protocol for gluten challenges, and challenge studies have varied greatly in amount and duration of gluten exposure. Although some studies have been designed to determine the acute effects (i.e., after 4 hours) of exposure to gluten (Sturgesset al., 1994; Ciclitiraet al., 1984), most challenges consist of an open challenge to a fixed or incremental dose of daily gluten over a minimum period of 4 weeks. Many challenge studies use a high exposure (≥ 10 g/day) to gluten, because this is believed to shorten time to disease confirmation or relapse and, therefore, to minimize discomfort to subjects (Rolles and McNeish, 1976). However, some studies have shown that low daily exposures to gluten also can elicit a disease response (Catassi et al., 1993; Laurin et al., 2002; Hamilton and McNeill, 1972).”      
  8. “At this time there is no correlative information on the efficacy of using these tests to predict or help prevent adverse effects in individuals with celiac disease.”
  9. “Although gluten-free diets are considered the only effective treatment for individuals with celiac disease, it has been recognized that it is difficult, if not impossible, to maintain a diet that is completely devoid of gluten (Collinet al., 2004). Therefore, several attempts have been made to define gluten-free in regulatory contexts. Efforts by the Codex Alimentarius to define an international standard for “gluten-free” labeling date back to 1981. At that time, due to the lack of sensitive, specific analytical methods, a threshold value of 0.05 g nitrogen per 100 g dry matter was set for wheat starch, on the assumption that wheat protein would be the only source of nitrogen in starch (Codex Standard 118-1981). The Codex Committee on Nutrition and Foods for Special Dietary Uses is developing a revised standard. The current draft proposal would define three categories of gluten-free foods: processed foods that are naturally “gluten-free” (≤ 20 ppm of gluten), products that had been rendered “gluten-free” by processing (≤ 200 ppm), and any mixture of the two (≤ 200 ppm). The Australia New Zealand Food Agency (ANZFA) defines gluten to mean “the main protein in wheat, rye, oats, barley, triticale and spelt relevant to the medical conditions, Coeliac disease and dermatitis hepetiformis.” ANZFA recognizes two classes of foods, gluten-free foods (” …no detectable gluten”) and low-gluten foods (” …no more than 20 mg gluten per 100 gm of the food”) (ANZFA Food Code Standard 1.2.8). The Canadian standard for “gluten-free” is more general, simply stating that “No person shall label, package, sell or advertise a food in a manner likely to create an impression that it is a “gluten-free” food unless the food does not contain wheat, including spelt and kamut, or oats, barley, rye, triticale or any part thereof” (Canadian Food and Drugs Act Regulation B.24.018).”     Approaches to Establish Thresholds for Major Food Allergens and for Gluten in Food. III, IV, V.Now that you know what grains this involves you can get an idea of what not to eat.
  10. ”Like food allergies, celiac disease affects only a small proportion of the U.S. population (estimated at 1%, 3.1 million) (NIH, 2004). Susceptibility to celiac disease is genetically determined and is linked to the presence of the DQ2 or DQ8 HLA alleles. However, carrying these alleles does not necessarily lead to celiac disease. Both acute and chronic morbidity have been well documented for individuals with symptomatic celiac disease. A gluten-free diet has been shown to greatly reduce the risk for cancer and overall mortality for these individuals. The potential benefit of a gluten-free diet has not been established for individuals with silent or latent celiac disease.”

I submit that this is a disease of a much grander scale, meaning a lot more people suffer from it than what’s reported, as far too often this disease goes completely unrecognized and thus undiagnosed. I hear complaints from many carboholics about many of the disorders at the top of this list. That tells me that they each have an allergic intolerance to gluten and they don’t even know it.  Because of its addictive nature, they’ll never know it, unless they can give it up.

The above paragraphs apply to those with celiac disease, yet I contend that everyone experience some of the above reactions to some degree. This happens even more so if you consume more of their products. I thought I could eat this food for 58 years until I learned that I had allergies to it. Now I know that I have allergic intolerances to this food. It presents itself every time I try to eat it again.

My guess is 90% of the population is exactly the same as I am, allergic to the protein in gluten. I contend that the obesity and diabetes rates that exist today confirm this. The death rates of all the diseases caused by gluten prove it. That forces me to ask, with all the evidence available in your archives, why doesn’t this food require a warning?

This is what the FDA claims they’re concerned about;

“In 21 Code of Federal Regulations (CFR) part 117 (part 117), we have established our regulation entitled “Current Good Manufacturing Practice, Hazard Analysis, and Risk Based Preventive Controls for Human Food.” We published the final rule establishing part 117 in the Federal Register of September 17, 2015 (80 FR 55908). Part 117 establishes requirements for current good manufacturing practice for human food (CGMPs), for hazard analysis and risk-based preventive controls for human food (PCHF), and related requirements.”

After reviewing over half of the documents available and an examination of all the titles of the documents, I see nothing that bans the inclusion of any of these dangerous foods in our food products made for public consumption (processed foods, including bread). It seems their interest lies only in compliance with the labeling of the product. They want to make sure that a package that’s sold as gluten free has to have less than 20ppm gluten in the product.

They don’t even feel that it’s important enough to warn you that a product contains gluten, yet they don’t feel it important enough to warn you of the dangers of gluten on the package, like they do with the dangers of cigarettes. They recognize the danger of tobacco, why can’t they recognize the dangers of gluten and wheat? It seems that they’re content with warning you how  much a product is gluten free, but not how much gluten it has in it, as if it does no harm at all. “C’MON MAN.” I have access to the same studies they have. They’re all located at PUBMED.COM and they all explain the dangers this food presents. If I can learn about what this food does, they have to know. Why are they so willing to ignore it? Why are they so willing to treat this food as though there’s nothing wrong with it.

The first page of studies I opened brought me to this study, the twelfth study out of 1797 studies on the list and reveals the dangers of just breathing the dust from these cereal grains. The grain induced asthma which affects those who work in the various fields in the grain industry, as stated by the Allergy, Asthma & immunology Research:

“Asthma caused by allergy to proteins from cereal grains is one of the most common types of occupational asthma (OA) and its prevalence does not seem to be declining.1 The main professions affected are: bakers, confectioners, pastry factory workers, millers, farmers, and cereal handlers. Although wheat is the most commonly involved cereal, other grains (e.g. rye, barley, rice) also play a role. In addition, flour from other sources (e.g. soya, lupin), pests, and several flour additives used in the baking industry to improve fermentation and elasticity of the dough, as well as to improve storage of the bread, may also give rise to IgE-mediated allergy.”  “This disorder has been classically considered a form of allergic asthma mediated by IgE antibodies specific to cereal flour antigens, mainly wheat, rye and barley,”

In the tenth study the on list published, in July 2009, it’s been found that the globulins in wheat can cause type 1 diabetes. T1D is an autoimmune disorder that was thought to have no cause. At least, all the studies I’ve looked at didn’t reveal this. According to BioMed Central;

“Taken together, the results indicate that a diverse group of globulins exists in wheat, some of which could be associated with the  pathogenesis of T1D in some susceptible individuals.Taken together, the results indicate that a diverse group of globulins exists in wheat, some of which could be associated with the pathogenesis of T1D in some susceptible individuals. These data expand our knowledge of specific wheat globulins and will enable further elucidation of their role in wheat biology and human health.

I have read elsewhere that it might be thought that an allergen might trigger an autoimmune response that shuts down the hormones that trigger insulin manufacture in the pancreas. It appears that this is that finding. Wheat can be responsible for type 1 diabetes. Have you seen any warnings for that? I haven’t. Have any been issued? I haven’t seen them. Why haven’t they been issued? How many parents have fed their kids bread to find out that their children are diabetic because of this auto-immune disorder? Why is bread still considered by so many to be a necessity of life?  It doesn’t appear so. It appears more likely to be a destroyer of life.

This is what I’m concerned about;

47,397 deaths daily from CVDs

47,397 people died each day, worldwide, from cardiovascular disease in 2013.  That breaks down to over 1800 Americans that died every day from cardiovascular disease in 2013. That’s 17.3 million annually, worldwide. That was up from 12.3 million (25.8%) in 1990According to Wikipedia“Coronary artery disease and stroke account for 80% of CVD deaths in males and 75% of CVD deaths in females.[1] Most cardiovascular disease affects older adults. In the United States 11% of people between 20 and 40 have CVD, while 37% between 40 and 60, 71% of people between 60 and 80, and 85% of people over 80 have CVD.[10] The average age of death from coronary artery disease in the developed world is around 80 while it is around 68 in the developing world.” This rate is increasing each year by

This points to the fact the this food which is eaten on a daily basis does so little damage incrementally to the consumer that it’s never noticed until it’s too late. The disease has already manifested itself and the price is now being paid for a lifetime of consumption. The question I keep asking myself is why does this have to keep happening? Why hasn’t the FDA warned us about the dangers of this food? They have access to all of the same reports that I do, yet they still refuse to acknowledge that this food is dangerous.

Does their interest lie elsewhere? Is there corporate influence involved with this like there was with sugar?

The sugar industry actively took steps for years to influence public’s perception of the nutritional value of their product, when they clearly knew of the dangers it posed. “Food companies have spent billions of dollars to cover up the link between sugar consumption and health problems. That’s the conclusion of a new report from the Center for Science and Democracy at the Union of Concerned Scientists (UCS).”

According to The Guardian;

Sugar lobby paid scientists to blur sugar’s role in heart disease – report

“New report highlights battle by the industry to counter sugar’s negative health effects, and the cushy relationship between food companies and researchers”. ” Influential research that downplayed the role of sugar in heart disease in the 1960s was paid for by the sugar industry, according to a report released on Monday.

This actions are responsible for more deaths that all the world wars combined. Their actions have killed, hurt or harmed more than 500,000,000 people in the last 30 years alone. (At 17.3 million for heart disease alone, 500 million is a lowball estimate for death coming from cancer and  dementia as well.) All total, the death rate for ECC is over 24,000,000 each year. That’s over 65,753 deaths each day, simply from excessive carbohydrate consumption. (Remember carbs = sugar.)

With backing from a sugar lobby, scientists promoted dietary fat as the cause of coronary heart disease instead of sugar, according to a historical document review published in JAMA Internal MedicineThis was criminal, yet nothing was done about it.

Though the review is nearly 50 years old, it also showcases a decades-long battle by the sugar industry to counter the product’s negative health effects. Why isn’t this agency being held accountable?

The findings come from documents recently found by a researcher at the University of San Francisco, which show that scientists at the Sugar Research Foundation (SRF), known today as the Sugar Association, paid scientists to do a 1967 literature review that overlooked the role of sugar in heart disease. Wasn’t that a clear case of bribery that should have been prosecuted?

SRF set an objective for the review, funded it and reviewed drafts before it was published in the New England Journal of Medicine, which did not require conflict of interest disclosure until 1984. The three Harvard scientists who wrote the review made what would be $50,000 in today’s dollars from the review. Because of this bribery, over 500,000,000 have suffered from this diseases that sugar is responsible for. From diabetes to heart disease to arthritis to cancer to…you should know the list by now.

“Marion Nestle, a nutrition, food studies and public health professor at New York University, said the food industry continues to influence nutrition science, in an editorial published alongside the JAMA report When will it stop? Never, until we let this industry know that we won’t accept their definition of healthy food and stop buying their versions of it.

 “Today, it is almost impossible to keep up with the range of food companies sponsoring research – from makers of the most highly processed foods, drinks, and supplements to producers of dairy foods, meats, fruits, and nuts – typically yielding results favorable to the sponsor’s interests,” Nestle said. “Food company sponsorship, whether or not intentionally manipulative, undermines public trust in nutrition science, contributes to public confusion about what to eat, and compromises Dietary Guidelines in ways that are not in the best interest of public health.”

The cushy relationship between food companies and researcher has been captured in recent investigations by the Associated Press and New York Times.The AP revealed in June that candy trade groups were funding research into sweets. And in 2015, the New York Times showed how Coca-Cola has funded millions in research to downplay the link between sugary beverages and obesity.

The Sugar Association said in a statement that SRF “should have exercised greater transparency” in its research, but also accused the study authors of having an “anti-sugar narrative”.

“We question this author’s continued attempts to reframe historical occurrences to conveniently align with the currently trending anti-sugar narrative, particularly when the last several decades of research have concluded that sugar does not have a unique role in heart disease,” the Sugar Association said. “Most concerning is the growing use of headline-baiting articles to trump quality scientific research – we’re disappointed to see a journal of JAMA’s stature being drawn into this trend.”

The findings were based on documents found by Cristin Kearns, a postdoctoral fellow at UCSF, in library archives.

The scientists and executives involved are no longer alive.

In recent years, the link between fat and heart disease has become a more contentious topic – a 2010 review of scientific studies of fat in the American Journal of Clinical Nutrition found that “there is no convincing evidence that saturated fat causes heart disease”. The role of sugar in heart disease is still being debated.”

Even according to Mother Jones“The industry’s tactics—similar to those used by Big Tobacco in downplaying the adverse health effects of smoking—were explored by Gary Taubes and Cristin Kearns Couzens in the 2012 Mother Jones investigation “Big Sugar’s Sweet Little Lies.” But this latest report draws on some newly released documents submitted as evidence in a recent federal court case involving the two biggest players in the sweetener industry: the Sugar Association and the Corn Refiners Association (the trade group for manufacturers of high fructose corn syrup). ”

The evidence is piling up.

The FDA can’t hide their complicity much longer.

Even according to Mother Jones“The industry’s tactics—similar to those used by Big Tobacco in downplaying the adverse health effects of smoking—were explored by Gary Taubes and Cristin Kearns Couzens in the 2012 Mother Jones investigation “Big Sugar’s Sweet Little Lies.” But this latest report draws on some newly released documents submitted as evidence in a recent federal court case involving the two biggest players in the sweetener industry: the Sugar Association and the Corn Refiners Association (the trade group for manufacturers of high fructose corn syrup). ”

“Obesity and diabetes mellitus are often linked to cardiovascular disease,[53] as are a history of chronickidney disease and hypercholesterolaemia.[54] In fact, cardiovascular disease is the most life-threatening of the diabetic complications and diabetics are two- to four-fold more likely to die of cardiovascular-related causes than nondiabetics.”

According to the World Heart Association ;

“Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided.[65]“ Their goal is 25 by 25. “25×25, achieving a 25% relative reduction in overall mortality from cardiovascular disease, cancer, diabetes or chronic respiratory disease by 2025. In September 2011, the United Nations held a High-Level Meeting in New York on the subject of NCDs, including cardiovascular disease (CVD), cancers, diabetes and chronic respiratory diseases.“

They’re actively taking steps to lower the death rate of CVDs by recommending everyone to eat right, quit smoking, and exercise, all of which will lower this number one killer of people. Eating right, in my opinion is by far the best way to combat CVDs, diabetes, obesity, hypertension, high cholesterol (which is really a problem of unbalanced cholesterol), arthritis and worst of all, dementia and Alzheimer disease.

In all of my research, I can’t find anything that says to limit the use of bread and starchy carbohydrates made from grains. Yet all research I’ve look at from PubMed and even the FDA show that this food does cause these disorders. Every time I look at the data, I’m forced to ask myself, why hasn’t’ the FDA, WHA, or the ADA condemned this food? These agencies have to know what’s going on, yet they refuse to act. Who is blocking this action?

After researching my book It’s Time For A Cure, I’ve learned that this food is at the base of all of the diseases listed above, forcing me to ask, why hasn’t the FDA, or the WHF warned us of this food. The only reason I can come up with is that it is being protected from prosecution by the industry that provides the crop seed for the farmer as well as the drugs to combat the arthritis caused by what their seed grows into.

From PubMed’s study; Characterization of Proteins from Grain of Different Bread and Durum Wheat Genotypes: “Wheat is unique among the edible grains because wheat flour has the protein complex called “gluten” that can be formed into dough with the rheological properties required for the production of leavened bread [9]. The rheological properties of gluten are needed not only for bread production, but also in the wider range of foods that can only be made from wheat, viz., noodles, pasta, pocket breads, pastries, cookies, and other products [10]. The gluten proteins consist of monomeric gliadins and polymeric glutenins. Glutenins and gliadins are recognized as the major wheat storage proteins, constituting about 75–85% of the total grain proteins with a ratio of about 1:1 in common or bread wheat [3,11] and they tend to be rich in asparagine, glutamine, arginine or proline [12] but very low in nutritionally important amino acids lysine, tryptophan and methionine [13].”

“Very low in nutritionally important amino acids” interests me. Amino acids are proteins. When you take away the protein, you’re left with little else but carbohydrates. This fact combined with the fact that gliadins have been shown to provoke the body to release anti-gliadin antibodies, which also have been shown to have the ability to attach themselves to Purkinje cells in the cerebellum, make this food suspect, at the least.

When an anti-gliadin antibody attaches itself to a cell in the cerebellum, the brain renders that cell useless and discards it. Although many parts of your brain can grow new cells to replace discarded cells, this area of the brain can’t. That means whenever an anti-gliadin antibody attaches itself to a purkinje cell, that part of the brain never comes back. Yes, that does mean brain damage for those who release these anti-gliadin antibodies.

The question this brings up is how many of us release these antibodies? Judging from the amount of Alzheimer’s disease invading the civilized world, I would say a majority of people display this form of intolerance….a rather large majority.  The next question this congers is, am I one of them? Are you one of them? I found out that I am. Have you yet?

42,657 dadeaths worldwide from cardiovascular disease

Heart disease kills more people every year than any other single cause. Over 42,000 people die from this disease and every day and the only reason it exists is the high amount of sugar we put into our bodies. It brings about the glycation ECC is responsible for and it’s this glycation that is responsible 42,000 deaths from cardiovascular disease every day.

But that’s not all it is responsible for. We have to look at Alzheimer’s disease and dementia. We have to consider cancer, and we have to worry about the amount of high blood pressure and high cholesterol ECC is responsible for. All of these disorders are money producing the diseases that this industry generates, simply for the sake of profit. It’s this profit that is killing everyone

13,698 daily deaths globally from Alzheimer disease

13.698 die each day, worldwide, due to Alzheimer disease alone. That amounts to over 500 deaths daily in the US alone, which means that at least 20 people in this country will die this hour alone, due to Alzheimer disease. Nothing contributes to Alzheimer disease as much as bread consumption. It’s the starchy carbs that break down to glucose, and it’s the glucose that glycates the cholesterol and protein that builds up the plaque and inflammation in your blood that leads to Alzheimer disease, cancer, arthritis, Atherosclerosis as well as most all other CVDs, as well as hypertension and high cholesterol.

11,232 deaths daily from cancer worldwide

11,232 people die every day globally due to some form of cancer and with all the evidence available that wheat contributes to the spread of multiple forms of cancer, why hasn’t the FDA made any statements about the dangers this food presents to the human body. Evidence shows these devastating effects going back to the bones of earliest cavemen that have been discovered.

I recently watched a Nova program on a 5,000 year old iceman mummy that had been frozen in an ice flow until he was discovered in 1991. They found remnants of einkorn wheat in his upper digestive tract suggesting his last meal was bread made from the flour of einkorn wheat. His bones also showed “disease of a modern lifestyle”, as they like to call it. What is this disease of a modern lifestyle? Arthritis. This is evidence of the glycation that occurred in this man from eating the carb loaded bread made from einkorn wheat. Even as difficult as it was to digest einkorn wheat at that time, due to its fibrous nature, it still did the same damage then, that it does today to everyone who continues to eat this food.

Copied from NOVA on PBS concerning a 5,000 year old frozen mummy ;

“Oeggl reconstructed the Iceman’s last meal from his microscopic analysis of a tiny sample removed from the mummy’s transverse colon, the part of the intestine just beyond the stomach. When the Iceman was discovered in 1991, x-rays and CAT-scans of the corpse revealed that his internal organs had shrunken so drastically in the 5,300 years in the glacier that Dr. Dieter Zur Nedden, the radiologist who examined the images, could barely distinguish them. Instead of filling the chest cavity with their billowy white form, the lungs looked like wisps of clouds.

But at the top of the colon, Zur Nedden made out a slight bulge, which the radiologist suspected was a clump of half-processed food. The progress of the food indicated that the Iceman had last eaten about eight hours before he died, possibly of hypothermia, on the Hauslabjoch pass, which cuts over the main Alpine ridge dividing Austria from Italy at 10,500 feet above sea level.

Not until several years after the discovery did the Innsbruck scientists finally cut a hole into the mummy, insert an endoscope, and snip out about .004 ounces from the colon. Dr. Werner Platzer, the University of Innsbruck anatomist then in charge of research on the corpse, gave .0016 ounces milligrams of the material to Oeggl, who had already been studying the rich botanical finds from the site.

Pollen provided a snapshot of the environment the Iceman was exposed to in the hours before his death

Oeggl’s sample was barely the size of his little fingernail. Under the microscope, he quickly identified the flake-like, semi-digested material that made up the bulk of the sample as einkorn, the most important wheat of the Neolithic, the period of prehistory in which people lived in semi-permanent settlements and survived by agriculture and keeping animals. The discovery of einkorn, which does not occur naturally in Europe, in the Iceman’s intestinal tract suggested that he had contact with an agricultural community. The dominance of bran in the sample led Oeggl to believe that the wheat had been finely ground into meal and made into bread, rather than eaten as a porridge, where the grains would have been eaten whole and found in larger pieces in the colon. But the bread would have been little like modern breads. In order to get bread to rise when yeast is added, the wheat grains must contain a high level of gluten, which lends the dough a durable elasticity and therefore holds the pockets of air. Einkorn has low levels of gluten, so the bread made with it was probably hard, somewhat like a cracker, and rather tough on the teeth.

Using an electron microscope Oeggl also spotted tiny particles of charcoal attached to the bran, probably remnants of the baking process on a hot rock, or next to a fire. In addition to the einkorn, the cells of at least one other plant, possibly some herb, were present in the sample, and Oeggl concluded that they, too, had been part of his meal. He also found a tiny muscle fiber and a burned bit of bone, evidence that the Iceman might also have eaten a meat. What kind of meat Oeggl cannot yet say, nor can he determine how much of the meal the sample represented.


Not everything passing through the Iceman’s gut had been swallowed intentionally, or was even desirable. Oeggl also found the eggs of the human whipworm. Many people alive today who do not live in areas with flush toilets also carry the worm, which can cause unpleasant symptoms like stomach ache and diarrhea, or even lead to malnutrition. The scientists have no way of knowing whether the Iceman had any such complaints.

Scientists may never know what prompted the Iceman to leave the relatively hospitable valley with no water or food to speak of

The sample also contained many different varieties of pollen, whose strange and beautiful forms Oeggl saw under the electron microscope. Though some peoples are known to eat pollen, Oeggl believed that the quantity in his colon was too small to represent a meal. Instead, the pollen accidentally ended up in the man’s stomach because they either had landed in food or water he ingested, or were inhaled and became trapped in saliva which he then swallowed. Scientists had long wondered where the Iceman was coming from and where he was headed, but until the discovery of the pollen inside the corpse, no scientist had any convincing documentation for his last day. But the pollen provided a snapshot of the environment the Iceman was exposed to in the hours before his death.

The majority of the pollen came from the hop hornbeam tree, which grows in a warm environment. As soon as Oeggl recognized it under his microscope lens, he not only knew which side of the mountain the Iceman had been on shortly before his death, but also the season in which he died. The hop hornbeam tree blooms between March and June, and because the sperm inside the pollen grain, which normally decays after a short exposure to air or water, was still intact, Oeggl believed it had to have been absorbed relatively soon after its release from the tree. The nearest stands of that tree could have grown to the south of the Hauslabjoch, at least five or six hours away by foot. The high valleys to the north are just too cold to sustain it.

The pollen of this particular tree was, therefore, one key to understanding the Iceman’s last hours. It meant that the Iceman was almost certainly in the valley within half a day of his death. Previously scientists had speculated that the Iceman had died in the late summer, when he was surprised by an early storm while trying to cross the pass.

Oeggl readily acknowledges that scientists may never know what prompted the Iceman to leave the relatively hospitable valley with no water or food to speak of (a single sloe berry was found with his remains) and try to cross the mountain at a time of year when several feet of snow easily could have obscured the topography of the steep and rocky Alpine ridge. But his own interest in the Iceman’s demise is not yet exhausted. He expects that his meticulous analysis of the botanical and archaeological material recovered from the bottom of the shallow in which the man died will soon reveal more details about the circumstances of the Iceman’s death.

This feature originally appeared on the site for the NOVA program Ice Mummies.”

Although not shown in this excerpt, the iceman did show signs of modern day disease in his bones. it was evident mostly around his joints in the form of arthritis. This arthritis is directly due to his diet of einkorn wheat. As it does now, in glycating all cholesterol it comes in contact with causing arthritis, it did so then. It just did it slower, due to the indigestibility of the einkorn wheat, but it occurred never-the-less.

The damage it did at that time was much less than what it does now, due to the lack of fiber it has in today’s strains of wheat, mostly the bread wheat made of Triticum aestivum, and spelt, durum, and emmer, as well. Even though arthritis seldom kills its victim, the damage it does, doesn’t go away, ever. It’s stuck to you like paint on a wall and you can’t scrape it off. Most of today’s wheat has more gluten protein than its ever had in its history, making it gluier and stickier, which make it that much more dangerous , as this is what builds up the plaque in your system and you already know what damage plaque does.

Perhaps the biggest question this brings up is, with all of this information available for this many years, why hasn’t the FDA warned us that this food has these capabilities to do this kind of damage to the human body. Should the public be able to make an informed decision as to whether or not to continue to eat this food? Or should the FDA continue to ignore the evidence and fail to even let the public know what this food does? The question I want to ask, was there outside influence in their decision to not expose this information?

Someone is trying to hide this information. They’re want to leave it up to an uneducated public to automatically know what these studies have shown. In whose best interest would it be to keep this information hidden? Whose business would hurt the most if bread and corn and wheat products all of a sudden became taboo?  The grain industry?  Monsanto? The more I look into this, the more it spells out cover-up and because this is how the FDA treats this, it instills a lot of fear in me as to how healthy the rest of our food supply is.

The FDA has to know of the damage these grains do to the body when ingested, so why do they allow these industries continue to peddle their wares as if they’re healthy?

The Iowa Corn Fed Beef Ruse

Food, Inc. is a 2008 American documentary film directed by filmmakerRobert Kenner.[4] The Academy Award-nominated film examines corporate farming in the United States, concluding that agribusiness produces food that is unhealthy, in a way that is environmentally harmful and abusive of both animals and employees. The film is narrated by Michael Pollan and Eric Schlosser.[5][6]

The film received positive responses and was nominated for several awards, including the Academy Award and the Independent Spirit Awardsin 2009, both for Best Documentary Feature.

The film’s first segment examines the industrial production of meat (chicken, beef, and pork), calling it inhumane and economically and environmentally unsustainable. The second segment looks at the industrial production of grains and vegetables (primarily corn and soy beans), again labeling this economically and environmentally unsustainable. The film’s third and final segment is about the economic and legal power, such as food labeling regulations, of the major food companies, the profits of which are based on supplying cheap but contaminated food, the heavy use of petroleum-based chemicals (largely pesticides and fertilizers), and the promotion of unhealthy food consumption habits by the American public.[4][7] It shows companies like Wal-Mart transitioning towards organic foods as that industry is booming in the recent health movement.

Monsanto, the USDA and the FDA

Food, Inc is an eye opening documentary that deals with the agricultural industry’s influence in the USDA and the FDA, concentrating on the meat packing industry’s influence. In 2008 the Chief of Staff for the USDA was a former chief lobbyist for the beef industry. The head of the FDA was a former executive vice president for the national food processors Association. A majority of the staff at both the FDA and the USDA came from Monsanto or its subsidiaries, posing clear conflicts of interests when it comes to protecting consumers. These industries of Monsanto, the USDA and the FDA are responsible for more death and disease than all violence, which includes war and crime, as well as automobile accidents, all other addictions, including heroin, emphetimines and alcohol.

These industries and agencies are directly responsible for over 43,000,000 deaths each and every year.  That total continues to climb and it will continue until everyone decides that it’s time for a cure.

Decisions have been made in the past that clearly benefited industry while presenting clear dangers to humans. By not only allowing contaminated the food with worthless nutrition values or food contaminated by bacteria to sneak into our food supply, but by polluting our rivers and lakes in the process as well, with contaminated ground water from runoff from chemical fertilizers, pesticides and herbicides.

This is just a taste of how unsustainable this is and it all starts with the grain industry, and our insatiable appetites for high sugar food, which is all forced upon up by this industry, the corn producers, wheat growers, and the crop seed companies owned by Monsanto, Novartis, Syngenta, Bayer et al.. Because there food require treatment with medications that this industry controls, they have full control over what happens inside your body, when you bend to their will and buy their products.

The grain industry in Iowa promoted the Iowa corn fed beef, to sell more corn, their largest industry. This had multiple, unforeseen consequences that not only damaged our food supply, but it polluted our resources more than what could have ever been foreseen. Because of our propensity to feed our addiction to sugar, the products that this industry has devised to get us to eat more of their junk food, are putting everyone who is suckered into this cycle, in the hospital with serious disorders. These disorders range from arthritis to cancer to HBP to CVDs and much more.

This is clearly a case where this self policing doesn’t work. It’s killing Americans right now because it doesn’tt. Evidence can be seen in the number of heart disease deaths, cancer deaths, Alzheimer’s deaths, not to mention all the pain, discomfort, and drug abuse caused by the pain. Although this is nice for the profits Monsanto, Syngenta and Bayer who also make drugs that treat the diseases there foods cause, it’s leading our country down a path of destruction that we’ll never recover from if we keep eating the food they advertise. They are playing on the addiction that they’ve inflicted upon the American people as well as the world to pad their profits and boost the influence.

This industry makes sure that sugar gets into baby food, to make sure that every baby who eats it becomes addicted to it, making them lifetime users of their poison. This unwilling addiction to sugar has brought this industry to a level of evil that’s never been seen in any industry. This industry is so intent on keeping us addicted to its lure, simply to increase your profits, that they are now responsible for over 65,753 deaths, worldwide daily. Yes I said 65,753 deaths daily. If this doesn’t bother you, then you have no conscience. Yes this is something to be appalled about and appalled I am and you should be too. This is simply more proof that it’s time for a cure.

50,000 food safety inspections in 1972 to just over nine thousand of them in 2008, the FDA is failing us big time. This is directly related to departmental cutbacks reducing the number of agents available to do the inspections. This is how conservative politicians think this industry and all other industries should police themselves. It would be nice if corporate America but was concerned about more than just their profits, but unfortunately the bottom line is what wins here and the bottom line is greed.

If the FDA can allow a food this dangerous through its monitoring, I’m afraid to even think about what else has snuck through?  The beef industry is already displayed their contempt for regulation through the mass production of beef that their industry is gone last 50 years

Couldn’t this dispute, at least, be closed that wheat can kill? What I would rather ask, was there outside influence in their decision to not issue any warnings? It was recently revealed that the sugar industry took steps to cover up the reports of damage that their food offered, so why wouldn’t it make sense that this closely  related industry, the grain industry, would take those same steps to cover up the same information about what their foods provided?

Was this another case of the industry policing itself and its watchdog, as well? Does this make a solid argument for self policing for corporate entities instead of government regulations? Our health is at stake here and we’ve allowed the FDA to escape judgment. That in my estimation is borderline criminal. 2893 deaths nationally, each day from CVDs, cancer, and Alzheimer disease combined. All three of these disorders are directly due to ECC, excessive carbohydrate consumption, which can be controlled. That’s enough people to wipe out 4 towns, the same size I grew up in. That’s unconscionable and we let it happen. Is that a shame on us for allowing it to happen?

We have direct control of these disorders. We don’t have to let this continue, but we do, simply to feed our addiction. We have a societal addiction to glucose, because it’s not just sugar, it’s what breaks down to glucose, and that includes not only sugar but all carbohydrates that break down to their most basic molecule, glucose. It’s our addiction to this glucose that clouds our judgment, masks our emotions, and controls our desires by gumming up the neurons in our brains every time we eat this food. This is exactly makes it addictive and hands total control over to the glucose, every time we eat it.

Yes, we do have full control over this, and we can stop it, but we have to stop the celebration of our addiction, to stop the addiction itself. To do that we need to instill taxes on the damage it’s doing when you eat this food. It’s time to hit abusers in the pocket book where it hurts the most. This has been successful with cigarettes, why can’t we make it just as successful with glucose? Why can’t we add a glucose tax to sugary drinks and bread and pasta products? These are the products that do the most damage, outside of alcohol which already has its own tax. Why shouldn’t these products have a tax also? When people start to see the real expense in their pocketbooks, they can then equate that expense to the real expense of the devastating effects this food has, that leads to cancer, heart disease, diabetes and dementia. This may be the only manner in which this addiction can be curbed.

Sugar; America’s Worst Addiction,

Confessions of a Reformed Carboholic

Sugar, I love it. I grew up loving it. Because I grew up loving it, I’m now addicted to it. It’s an addiction that was forced upon me by our food industry, telling my mother that she had to make refined and whole grains the most prevalent food in my diet. She fed me this food, supposedly, to keep me healthy. Aren’t whole grains supposed to make you healthy? That was 60 years ago. I’m paying the price for that now, with my arthritis. I was paying the price for it just 30 months ago, by carrying 30 lbs more than what I carry right now and being borderline diabetic and in pain all the time. I’m about to debunk this myth that whole grains are healthy. There is a price to be paid for eating a (starchy) carbohydrate diet and you’re paying it with every sandwich you eat, every corn chip you munch, and every noodle you eat.

My sisters are paying the price for it now, also. They are both obese and diabetic. My father has always exercised to keep his weight down. He’s was always able to burn off the excess glucose, until he was about 35. Even though he’s always jogged every day, since I was in 7th grade, he couldn’t run away from this. After being borderline diabetic he couldn’t change his downhill spiral. He’s now taking an anti-diabetes drug which has several side effects that are initially so small that they aren’t noticed but after time, start to inflict other harm to the body, due to the effects of the chemical changes caused by the medication. His carb diet is starting to lead him down the same path as my mother, who passed away 4 months ago. My mother, in trying to be the best mother and wife she could be, went along with what the FDA, the USDA and the ADA told her because she wanted to do what was right for her family. Guidelines from the ADA telling her that grains needed to be at the base of her all of her meals was what drove her to do this to our family. This is what doomed us to our current list of ailments, ailments like obesity and diabetes, arthritis, cancer, stomach ailments galore, and now, side effects from treatment for those ailments. It all comes along with a carbohydrate diet because all carbs break down into glucose. Even yet, MyPlate.gov suggests that whole grains be a part of a healthy diet. The evidence I’m going to show you is completely contrary to this notion.

Because sugar addiction is America’s biggest addiction, that makes it, its worst addiction. It’s an addiction that everybody grew up with and into. It’s an addiction that’s been with us for as long as we’ve been eating it. It’s an addiction that’s become far worse than it’s ever been, since we’ve been eating it over its 10,000 year history. It’s an addiction that’s built scores of empires, and then tore them all down. This addiction is far worse than any other addiction that plagues America. Whether it be today, yesterday or tomorrow, this addiction is the worst that Man has ever faced or may ever face. This is simply due to its propensity to expand its influence across the whole world. It’s also driven by the greed of those condemned to this addiction. Their desire to feed their own addiction drives them to impose this addiction on the rest of the world, simply so they can make an extra buck. This addiction is at the root of almost every known form of dementia, heart disease, diabetes and everything that comes along with that, like cancers, cardiovascular diseases. The list is endless because sugar’s worst instigator of inflammation, AGEs, or glycation is at the base of an arm long list of disorders.

All of these disorders can be curbed simply by curbing carbohydrate consumption but addiction keeps this from happening. That’s why fighting this addiction in particular is so important. It’s life saving at its simplest, just remove contaminating factors from the food source and the diseases cannot manifest themselves. The contaminating factor in this case? You guessed it, sugar. Sugar addiction is leading our society to the brink of destruction because of the nature of its addiction and what it does to the body. Its continued use only leads to discomfort and death. It’s only redeeming factor is that it tastes good and satiates quickly. This is what makes it so deadly, though.

That’s sad. I have to live with it too. I can’t have what I love, what I’ve been addicted to. I have to say no, to stay healthy. So do you. I know that’s exactly the opposite of what you’ve been told, but what you were told is wrong. For us it’s dead wrong. It should have never been pushed upon us to eat it in the quantities that it was. But pushed upon us it was. And we bought it. We bought into it big time and we’re paying for it now. This is evidenced by the proliferation of Alzheimer’s disease. How many lives does it have to take, before people wake up? How many families does it have to destroy, before people wake up?

Carbolism Should Be Treated Like Alcoholism

We need clinics for sugar addiction and they should be financed by the food industrial complex that imposed this diet on the people who now suffer from the consequences of it. The administration of the clinic though, should be done by trained medical professionals, because this is an addiction and should be treated as such.

Is this something that should be investigated? Should an industry be held accountable for the ruse that’s been pulled on the American people, and now the world? The ruse is that this is healthy food, when it’s really not. Why are they still allowed to claim that it’s healthy? Why are they still, allowed to advertise that it’s healthy? It’s clearly not, and it’s clearly at the root of almost all of the deadliest diseases, that we’re actively fighting right now. Diseases like Atherosclerosis, Endocarditis and Hypertensive heart disease. That’s just the CVD’s. We haven’t even covered the cancers, or dementias. Those lists are much longer.

Can anyone tell me why this is still allowed to be advertised like it is today? It starts with what’s put in baby food for starches and fillers and sweeteners. These fillers satiate babies quickly often putting them right to sleep after a short burst of energy. This is the first indication of sugar addiction and it starts at a young age. This is done for a purpose. That purpose is to addict you to its lure, so you’ll buy into it when you’re an adult.

It continues with your introduction to breakfast cereals and the load of sugars they carry when you see them advertised with the Saturday morning cartoons. I can remember for commercials for Sugar Pops, Sugar Frosted Flakes, and Captain Crunch. It starts young, real young and continues through your youth with candy and soda, and into your adult years with bread and baked goods (cakes, crackers, cookies).

It’s been forced upon us. Nobody has had a choice in this addiction and that is what makes it so lethal. That also makes it profitable for the Pharmaceutical industry. This is what scares me. The Pharmaceutical industry used to be owned by the same industry the provided the crop seed for the farmers that grew the grain that provided the flour to bake all of those loaves of bread that causing so much disease.

The Perfect Ruse

It’s almost the perfect scam. Sell crop seed to farmers that’s been genetically modified, so that it feeds your customer base, food that will require them, in the future to purchase medications from your other companies. How convenient we’ve made it for this industry to take our money. We should be ashamed.

We would be ashamed if we knew that this was done intentionally, especially if it was done for nothing more than profit. That is why this is something that should be investigated. Regardless of how long it takes, we need to know who is responsible. This is a lesson that cannot be lost, like every other study done on these concerns, we cannot allow this to be swept under the rug. Even if they’re no longer around, we need to hold their companies’ accountable. This is the only way we can prevent this from happening in the future.

For 1,000s of years, we’ve been treating the symptoms of the diseases and disorders that carbohydrate digestion cause. Because of our addiction to it, we’ve never looked at the prospect of eliminating the cause completely. When a whole society is addicted to a staple that they’ve eaten their whole lives, how does one tell the truth about something that is so important to everyone on the planet? How does one tell everyone that what they’re eating is killing them slowly, expensively, painfully, and worst of all, undignified because of all the lost memories from brain damage? How does one tell a whole society that a staple that they’ve lived on for close to 10,000 years has been, and continues to be, the one food that creates more disease and illness than any other one food in their diet? How does a world break their addiction, when the addicted are the majority of the world and only 5% of that population can recognize their addiction?

Dr Perlmutter is trying to tell the people and continues to do so. I honestly feel that he thinks as I do, that if we don’t dispel the consumption of these foods, our society is doomed. From what I’ve learned, since I’ve broken the addiction, I see a collapse, due to out of control emotions, due to the wild glucose swings in the blood, making people under the control of a carbohydrate diet, under the control of those who impose this diet on the American public. It’s in their interest to keep America addicted and the best way they can do this, is to tell you that it’s healthy and what you need to keep your body healthy. Only those who want to buy their pharmaceuticals, from them in the future, are ones who should to buy their food products now, because, they eventually will.

By following what little advice I offer, to curb your carbs dramatically and as completely as possible, you can dramatically slow down if not eliminate many of the disorders and diseases within these pages. If it can’t eliminate your disease, it will reduce the expression of your disorder. If it doesn’t cure you, it will definitely extend your life. My goal is to extend it a minimum of 20 years. I would like to see everyone live to be 100 years old, or more. I know this diet lifestyle can do that (depending on your age and degree of addiction of course). To know this yourself, though, you have to change your diet.



A Display of Dependence You Don’t Need

Carbs and Arthritis

Carbs and Arthritis

Carbs cause arthritis?
You Bet!!

Nothing else in the body creates inflammation, more than carbohydrates in our diet and arthritis is a disease of inflammation.

Carbs are the foundation of inflammation. They are the sole internal source of inflammation. Inflammation wouldn’t even exist  (except for external injuries) without carbohydrates.

Inflammation is caused by glucose and cholesterol coming together and glycating. It happens because of the massive amounts of glucose in the blood. Fat, by itself,  doesn’t cause inflammation. It needs glucose to do that. Protein, by itself, doesn’t cause inflammation. It needs glucose to do so, also.

That makes glucose, the bad actor in this drama, the drama of inflammation in the body and how it’s made. Every manifestation has an equation, or a set amount of variables that make up that which is being manifested.

With that said, we’re going to look at the variables that make up the equation of arthritis, the variables that cause inflammation in the body, because after all, arthritis is a disease of inflammation.

Arthritis is the expression of inflammation in the body and it shows up mostly in the joints, first, where movement take place. That’s because this is where the macrophages get deposited, because this is where the blood flows.

There’s another expression of inflammation the body and it’s called a common cold. The funny thing about inflammation is that because it exists everywhere the blood flows, it effects every system in the body. A common cold, for example, expresses itself with inflammation in the sinuses. I know that this may be hard to believe, but if you remove the instigator of inflammation, carbohydrates, a common cold becomes much easier to endure. Actually, common colds are not experienced in people on a ketogenic diet nearly as much s much as they are in carbolics, those on a carbohydrate diet. This is because of the amount of inflammation that carbs cause. Viruses may play a part in the spread of a common cold, but without the glucose in the system, the expression of inflammation can’t take place.  Unfortunately, this can only be proven by elimination carbs from the diet, completely.

It’s basically the same with arthritis, because blood flows throughout the entire body and the inflammation exists in the blood, The inflammation is going to effect every system that blood flows through, including the joints of all limbs.

Before we can continue with arthritis, started we need to know what Wikipedia says about it;

“Arthritis (from Greek arthro-, joint + -itis, inflammation; plural: arthritides) is a form of joint disorder that involves inflammation in one or more joints.[1][2] There are over 100 different forms of arthritis.[3][4] The most common form of arthritis is osteoarthritis (degenerative joint disease), a result of trauma to the joint, infection of the joint, or age. Other arthritis forms are rheumatoid arthritis, psoriatic arthritis, and related autoimmune diseases. Septic arthritis is caused by joint infection.”

If the definition of arthritis is joint inflammation, We already know where inflammation comes from, and it comes from carbohydrates, as explained in Carbs, the New Death SentenceThat makes glucose the bad actor here, because without the free glucose roaming through your blood, inflammation wouldn’t exist.

It’s glucose that glycates the unused proteins and fats, by attaching themselves to these cells. The glucose is looking for insulin to turn itself into fat so it can join one of the LDL particles in your blood. if it finds a protein particle or cholesterol particle (almost always LDL particles) to attach itself to, it’ll do so, and this is where the problem of inflammation begins. When this happens, the glucose, glycates the cholesterol or protein and its these misshaped proteins and glycated cholesterol that forms plaque and creates inflammation.

This is where I think it gets really interesting, if the lipid that makes up the particle comes from carbohydrates, it attaches itself to an apolipoprotein B and forms LDL cholesterol to be used as fuel for the body.

If the lipid comes from fat, it associates with apolipoprotein A, the foundation of high density particles or HDL cholesterol. Learn how the HDL and LDL work in your body by reading The value of balancing your cholesterol and The foundations of LDL cholesterol, apolipoprotein B.

It’s the LDL particles that cause most of the damage because of their loose form. Hence the name, low density lipoprotein. These glycated particles are at the base of over half of all cancers, CVDs, brain damage and arthritis.

According to Wikipedia, “Arthritis is predominantly a disease of the elderly, but children can also be affected by the disease. More than 70% of individuals in North America affected by arthritis are over the age of 65″

This tells me that arthritis is going to happen to everyone on a carbohydrate diet, regardless of how many carbs they consume each day. Remember that 90% of the population is gluten sensitive. This is something that can only be reversed by the industry that feeds us. As long as we have to eat the food they provide us and encourage us to eat, this problem will not subside. It’s in the science, the science of inflammation.

That explains why our addiction to these vile substances must come to an end.
As a society, we need to change this pattern.

The problem of arthritis goes deeper than just inflammation, though, it rides on the amount of vitamin D in the system, as well. vitamin is crucial to the transport of cholesterol into  the cells, so it can be used.

Again, according to Wikipedia;

“Vitamin D refers to a group of fat-soluble secosteroids responsible for enhancing intestinal absorption of calcium, iron, magnesium, phosphate, and zinc. In humans, the most important compounds in this group are vitamin D3 (also known as cholecalciferol) and vitamin D2 (ergocalciferol).[1]

Vitamin D deficiency is more common in people with rheumatoid arthritis than in the general population.[36][37] However, whether vitamin D deficiency is a cause or a consequence of the disease remains unclear.[38] 1α,25-dihydroxyvitamin D3 (1,25D), an active metabolite of vitamin D, affects bone metabolism indirectly through control of calcium and phosphate homeostasis. Interaction between 1,25D and the vitamin D receptor (VDR) affects the production of RANKL and delays osteoclastogenesis.[39] Some trials have found a decreased risk for RA with vitamin D supplementation while others have not.[37]

If Rheumatoid arthritis sufferers have a deficiency of vitamin D in their bodies, that tells me that vitamin D helps to control the expression of Rheumatoid arthritis by allowing the cholesterol particle admittance into the cell so it can be used. (No conductor, no admittance.)

This action prevents the cholesterol from becoming glycated and turned into inflammation, because with lower levels of vitamin D in the body, the arthritis is more prevalent. That tells me why lower levels of vitamin D increases Rheumatoid Arthritis. It’s the one-two punch that hits everyone with arthritis; carbs raise LDL particles, raising total cholesterol throwing up flags that cholesterol must be lowered. when that’s the worst thing you can do. Your cholesterol doesn’t need to be lowered (that leads to disease), it needs to be balanced, so you can continue to use your cholesterol to feed your cells the nutrients they need to function properly. See the value of balancing your cholesterol to learn how to balance yours.

Most vitamin D is produced in our skin by ultraviolet rays acting on cholesterol;

“Vitamin D3 is produced photochemically from 7-dehydrocholesterol in the skin of most vertebrate animals, including humans.[106] The precursor of vitamin D3, 7-dehydrocholesterol is produced in relatively large quantities. 7-Dehydrocholesterol reacts with UVB light at wavelengths between 270 and 300 nm, with peak synthesis occurring between 295 and 297 nm.[107] These wavelengths are present in sunlight, as well as in the light emitted by the UV lamps in tanning beds (which produce ultraviolet primarily in the UVA spectrum, but typically produce 4% to 10% of the total UV emissions as UVB). Exposure to light through windows is insufficient because glass almost completely blocks UVB light.[108][109]

With vitamin D actually being a fat, in the body, as it comes from cholesterol and cholesterol is made up of lipids, that makes makes me wonder if it comes from digested fats or ingested fats. A look at 7-dehydrocholesterol revealed nothing as to where it comes from, so I have to be content just knowing it’s a lipid.

Being a lipid gives it access to the cellular structure of all organs, including the skin, bones, and most importantly, your brain. 

This places the importance of vitamin D even higher than what I thought before. Vitamin D is a fat that delivers calcium to your bones, making it that important to bone growth and structure. Yet it’s also important in your brain, where it acts as an a conductor for cell signaling proteins, cytokines and adipokines and hormones.

According to Pubmed;
“Vitamin D receptor in the brain

It should be noted that 1,25(OH)2D signaling is conducted through the VDR, which shares its structural characteristics with the broader nuclear steroid receptor family.11 In 1992, Sutherland et al12 provided the first evidence that the VDR is expressed in the human brain. Using radiolabeled complementary deoxyribonucleic acid probes, the authors showed that VDR messenger ribonucleic acid is expressed in the postmortem brains of patients with AD or Huntington’s disease. In a landmark study, Eyles et al13 described that both the VDR and CYP27B1 are widespread in important regions of the human brain including the hippocampus, which is particularly affected by neurodegenerative disorders.1417 Furthermore, the VDR is also expressed in the prefrontal cortex, cingulate gyrus, basal forebrain, caudate/putamen, thalamus, substantia nigra, lateral geniculate nuclei, hypothalamus, and cerebellum.18 Importantly, VDR gene polymorphisms are associated with cognitive decline,19,20 AD,2124 Parkinson’s disease,2529 and multiple sclerosis.30

Showing how important vitamin D is in the brain, it’s become evident that it’s as important as the cell signaling can’t take place efficiently without it, as it’s the conductor. Without enough vitamin D in your system, the conduction is going to be poor, at best. Could it be that this is where cell degradation begins, and inflammation introduces its ugly face? Whether or not it is, we know that vitamin D is crucial for hormones and cell signaling proteins to get their signals through the cell membrane, as that’s what conductors do, they transmit signals.

That tells me, if the pathway is blocked, due to vitamin D deficiency, the cells can’t perform their intended function, because their fuel, lipoproteins cam’t get through the cells, due to the lack of a conductor, vitamin D, so they’re left floating around in the blood waiting to be used.

This is where the problem begins because there’s also massive amounts of glucose floating in the blood, waiting to be turned into fat, This gives us the equation  that nobody wants, Glucose + cholesterol =  glycation. Glycation is the start is the start of inflammation.

According to PubMed; “Vitamin D lipid-lowering effects appear limited to statin-treated patients and are likely due to decreased cholesterol absorption.” Cholesterol plays a much bigger part in this play, than what seemed apparent a few minutes ago. If statin drugs lower total cholesterol and vitamin D, I can only imagine what damage that is reeking on the bodies of those who are condemned to use them. That tells me that those on statin drugs, are condemned to more inflammation, more disease, and more arthritis, can this be true?

This is exactly why it’s so important to balance your cholesterol instead of just lowering it. The value of balancing cholesterol tells us that raising HDL cholesterol will help lower LDL cholesterol and  control the inflammation by limiting the source of the inflammation, LDL cholesterol. Knowing that raising HDL particles can lower LDL particles help makes it easier to lower LDL particles. Fewer LDL particles in the blood lowers inflammation lessening the effects of arthritis in the body.

Now that we know that , We also know that lowering carb intake lowers LDL cholesterol as it’s carbs that create LDL cholesterol. So curbing carbs, even though it can’t restore, immediately, the damage that’s already been done, it can reverse its current effects, and in the future work to restore at least some of the damage. But it can only restore that which isn’t already too far damaged.

This forces me again to ask, why is this food even on our grocery shelves and  why doesn’t it come with a warning?