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.

OBJECTIVE:

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.

RESEARCH DESIGN AND METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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.

BACKGROUND:

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.

OBJECTIVE:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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?

Abstract

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.

Abstract

BACKGROUND:

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.

CONCLUSIONS:

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.

Abstract

OBJECTIVE:

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.

CONCLUSIONS:

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.

BACKGROUND:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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

Abstract

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.

Abstract

PURPOSE:

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.

EXPERIMENTAL DESIGN:

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.

RESULTS:

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.

CONCLUSION:

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.

Abstract

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;

Abstract

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;

Abstract

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;

Abstract

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;

Abstract

BACKGROUND:

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.

OBJECTIVE:

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

METHODS:

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

RESULTS:

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.

CONCLUSIONS:

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?

Abstract

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;

Abstract

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;

Abstract

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

Abstract

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;

Abstract

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;

Abstract

BACKGROUND:

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.

METHODS:

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.

RESULTS:

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).

CONCLUSIONS:

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.

Abstract

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;

Abstract

BACKGROUND:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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.

Abstract

BACKGROUND:

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.

METHOD:

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.

RESULTS:

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.

CONCLUSIONS:

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;

BACKGROUND:

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.

OBJECTIVE:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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.

Abstract

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.

Conclusion

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;

Abstract

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;

Abstract

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;

Abstract

BACKGROUND:

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.

CONCLUSIONS:

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;

Abstract

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.

Abstract

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;

Abstract

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).

Abstract

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;

Abstract

PURPOSE:

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.

METHODS:

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).

FINDINGS:

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.

IMPLICATIONS:

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.

BACKGROUND:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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.

Background

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.

Methods

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.

Results

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.

Conclusion

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.

The Glucose Ruse to Feed You Disease, Compliments of the Grain and Pharmaceutical Industries

The Glucose Ruse to Feed You Disease

This is a matter of your health being engineered without your knowledge or consent. The engineering in this case is not good. Actually it’s creating pain where none should exist. Our food supply industry may be the most important industry concerned, when it comes to our health. As everyone knows, ‘you are what you eat’, so it’s vital that what you eat won’t make you sick. Unfortunately, for those who still masturbate their taste buds with their addiction to sugar this couldn’t be further from the truth. Our food supply has been hijacked by the same industry that treats you for the illness their food supplies. Granted the health care industry is vital to our health, but I submit that it wouldn’t be as important as it is today, if we paid more attention to what we eat. Because I now watch what I eat, I can change the “we” to “you”, meaning “you” have to watch what you eat. (All that means is that you still have an addiction to break, I don’t, I broke mine three years ago.) Because of this addiction, you’ve doomed yourself unwittingly to a lifetime of medications. That is unless you’re one of the .05% who shows no ill effects from glycation. I have yet to meet one of them. If you eat at a restaurant or buy groceries at a grocery store, you’re subject to this addiction. It’s in their food everywhere you look. You actually look for it because you love to eat it. You love their advertising. What’s not to love, it’s full of attractive people selling you what appears to provide health, but in all reality provides nothing but the opposite, as it’s responsible for most all pain, most all disease, all brain damage, all atherosclerosis, all diseases affiliated with inflammation, and this is just for starters.

Monsanto has politically engineered their dominance of your food supply and subsequent health by forcing as many farmers as they can to use Monsanto’s seed companies’ GMO seed to grow their crops. Monsanto has many seed companies. Their control over the seed industry is mirrored by their control over the pharmaceutical industry because they can use the seed companies to influence the profits of their drug companies. , owns 15 crop seed companies all selling GMO seed for their contracted farmers to grow. Five of these companies sell seed for wheat crops. That’s the seed that grows the wheat that’s ground into flour for your bread and crackers. Their contracted farmers have to grow Monsanto’s GMO seed at risk of facing legal action, if caught growing anything else. This is how Monsanto controls what goes on your table to eat. This is also how Monsanto forces you into purchasing the Celebrex, made by GD Searle Pharmaceuticals. Searle has been part of Monsanto since 1985. The Celebrex is what your doctor prescribes for your arthritis that’s caused by the glycation set up from the grain diet you’ve been on all your life. After you get the arthritis that you will inevitably get from eating their GMO grains, you’ll be begging your doctor for that prescription for the Celebrex. Then you’ll get to deal with the side effects of the Celebrex that it inevitably has and presents to the body. That’s the damage to your body from the drug side of their industry.  The damage from the crop seed side includes crops that are not only GMO seed, they are laden with Roundup, the glyphosate herbicide that works by inhibiting enzymes from doing what they supposed to do by instructing cells how to operate. Even though Monsanto claims that these enzyme inhibitors affect only targeted enzymes, the rise in cancer alone, that the nation has seen since the mid to late 80’s, has told a completely different story. The rise in these disorders is directly caused by an increase in the glycation that occurs in the blood by the high glucose laden grains this company forces their farmers to grow. That means that the food going on your table is engineered to make you need the medications that the pharmaceutical side of Monsanto’s companies sell.

 According to Wikipedia; “In December, 1997 Monsanto merged with Pharmacia and Upjohn.[14] The agricultural division became a wholly owned subsidiary of the “new” Pharmacia; Monsanto’s medical research division, which included products such as Celebrex.[61]

GD Searle and Pharmacia are the other side of Monsanto’s multinational chemical companies,  that includes now,  Pfizer and Upjohn, as well. GD Searle was purchased by Monsanto in 1985 two years after Monsanto started dabbling in GMO crops.  In 1993 GD Searle file for a patent for Celebrex, its widely used arthritis drug. I’ll bet you didn’t know that it is Monsanto’s seed companies that force their contracted farmers to grow GMO seed designed to make you need their Celebrex. Is this what you thought you were buying when you bought those corn chips last time? Was this what you thought you were buying when you purchased those pretzels? Whether it was or not, that’s what you got. You also got all the rest of the damage that glycation does to the body, which includes cataracts, atherosclerosis, cancer and dementia as well. You’re also subjecting yourself to the hunger cycle, probably the worst manifestation of a carb diet. The more carbs you eat, the hungrier your get. That’s a cycle that can’t be broken if you don’t stop the fuel that feeds it. Stopping the fuel is the only way to stop the glycation. That means that it’s the only way to stop the inflammation, which means it’s the only way to stop the illness and disorder that glycation is responsible for.

This study done on glycative effects and Alzheimer’s disease was completed in 2005. Glycation of cholesterol into amyloid plaque was researched in this study. It showed that the plaque was responsible for Alzheimer’s disease. Where were the warnings then? It’s now 15 years later and millions of people have died from Alzheimer’s disease. The question I ask is why? Why weren’t we notified of this revelation 14 years ago? It’s been in the archives of PubMed since then. Why the delay? How many more must die before this news of the glycative effects of glucose, is released to the media to inform the public of this devastating news?

5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) attenuates the expression of LPS- and Aβ peptide-induced inflammatory mediators in astroglia

J Biol Chem. 1985 Sep 5;260(19):10629-36.

Glycation of amino groups in protein. Studies on the specificity of modification of RNase by glucose.

Watkins NGThorpe SRBaynes JW.

This study done on the effects of glucose on glycation was done in September 1985. Have you seen or heard of any part of this report prior to today? I haven’t. I had to search for it. The question I have is why wasn’t the public notified of this revelation? Were the research results suppressed so as to hide the truth from the public? I have to wonder.

About this same time, according to Wikipedia; In 1985, Monsanto acquired G. D. Searle & Company, a life sciences company focusing on pharmaceuticals, agriculture and animal health. In 1993, its Searle division filed a patent application for Celebrex,[42][43] which in 1998 became the first selective COX‑2 inhibitor to be approved by the U.S. Food and Drug Administration (FDA).[44] Celebrex became a blockbuster drug and was often mentioned as a key reason for Pfizer‘s acquisition of Monsanto’s pharmaceutical business in 2002.[45]

What wasn’t disclosed publicly was the benefit that the stockholders retained when the merger was finalized. Stockholders of Pharmacia retained 23% of their control in the new Pfizer. You wouldn’t think that would have an influence in what they do to grow their customer base to sell more drugs, would you? Regardless of what you think, it does, and they do care. Monsanto sends this industry most of their customers just from the damage their food does to those who eat it. This industry has grown to accommodate those customers, mostly with their diabetes industry and ever expanding interests in dementia. Inflammation,  cancer and atherosclerosis, just for starters.

Was it coincidence? I have to wonder. Since then Monsanto has made moves to control all of the grain industry in America, by contracting farmers to grow no other seed than their own GMO seed. This forces the farmers who do this, to spray massive amounts of herbicide on those crops. The herbicide they spray is Monsanto’s Roundup, a glyphosate herbicide that works by inhibiting the actions of enzymes. Enzymes are important proteins in the body as they’re cell signaling proteins that instruct cells how to operate. This is important because it’s that instruction that the cells need to not become glycation. Otherwise, without that enzyme, you create inflammation. Inflammation is the foundation of all modern diseases. This is why grains are slowly killing those who eat them, cutting their lives short, to the tune of 2,684 deaths every day, that can be attributed to these killing field grains. These signaling cells are cells like hormones and cytokines that affect your body’s functions. If these aren’t working because of any enzyme inhibitor floating around in your blood, it’s going to lead to glycation and disease. This is the scary part of this story, if you eat bread, crackers, corn chips or anything flour is used in (whether it’s wheat flour or corn flour), your eating this herbicide along with your bread and cornpone.

Did you have any idea that this was being done to you without your consent or knowledge? I didn’t until I did this research. Did you have time to do your research? Why not? If you couldn’t, wouldn’t you think that we need some regulation in the field? The FDA and the USDA are supposed to provide that. With Monsanto’s control of each of those agencies, how much honest regulation do you think could take place? The regulation that does take place, takes place only for the benefit of Monsanto and Pfizer, not the consumer. We end up the lab rats in  this experiment. In my opinion, this is a failed experiment and should be shut down as soon as possible.

This study was complete in September 1985, about the same time Monsanto acquired G.D. Searle Pharmaceuticals. 8 years later they filed for a patent for Celebrex, their arthritis pain killer drug. Celebrex is a Cox 2 NSAID with the following side effects and concerns, according to Searle, and I’m listing all of them;

Contraindications

NSAIDs may be used with caution by people with the following conditions:[6]

Irritable bowel syndrome[6]

  • Persons who are over age 50, and who have a family history of GI (gastrointestinal) problems[6]
  • Persons who have had past GI problems from NSAID use[6]

NSAIDs should usually be avoided by people with the following conditions:[6]

Adverse effects

The widespread use of NSAIDs has meant that the adverse effects of these drugs have become increasingly common. Use of NSAIDs increases risk of having a range of gastrointestinal(GI) problems.[16] When NSAIDs are used for pain management after surgery they cause increased risk of kidney problems.[17]

An estimated 10–20% of NSAID patients experience dyspepsia. In the 1990s high doses of prescription NSAIDs were associated with serious upper gastrointestinal adverse events, including bleeding.[18] Over the past decade, deaths associated with gastric bleeding have declined.

NSAIDs, like all drugs, may interact with other medications. For example, concurrent use of NSAIDs and quinolones may increase the risk of quinolones’ adverse central nervous system effects, including seizure.[19][20]

There is argument over the benefits and risks of NSAIDs for treating chronic musculoskeletal pain. Each drug has a benefit-risk profile [21] and balancing the risk of no treatment with the competing potential risks of various therapies is the clinician’s responsibility.

Combinational risk

If a COX-2 inhibitor is taken, a traditional NSAID (prescription or over-the-counter) should not be taken at the same time.[22][not in citation given] In addition, people on daily aspirin therapy (e.g., for reducing cardiovascular risk) must be careful if they also use other NSAIDs, as these may inhibit the cardio protective effects of aspirin.

Rofecoxib (Vioxx) was shown to produce significantly fewer gastrointestinal adverse drug reactions (ADRs) compared with naproxen.[23] This study, the VIGOR trial, raised the issue of the cardiovascular safety of the coxibs. A statistically significant increase in the incidence of myocardial infarctions was observed in patients on rofecoxib. Further data, from the APPROVe trial, showed a statistically significant relative risk of cardiovascular events of 1.97 versus placebo[24]—which caused a worldwide withdrawal of rofecoxib in October 2004.

Use of methotrexate together with NSAIDS in rheumatoid arthritis is safe, if adequate monitoring is done.[25]

Cardiovascular

NSAIDs aside from aspirin, both newer selective COX-2 inhibitors and traditional anti-inflammatories, increase the risk of myocardial infarction and stroke.[26][27] They are not recommended in those who have had a previous heart attack as they increase the risk of death and/or recurrent MI.[28]Evidence indicates that naproxen may be the least harmful out of these.[27][29]

NSAIDs aside from (low-dose) aspirin are associated with a doubled risk of heart failure in people without a history of cardiac disease.[29] In people with such a history, use of NSAIDs (aside from low-dose aspirin) was associated with a more than 10-fold increase in heart failure.[30] If this link is proven causal, researchers estimate that NSAIDs would be responsible for up to 20 percent of hospital admissions for congestive heart failure. In people with heart failure, NSAIDs increase mortality risk (hazard ratio) by approximately 1.2–1.3 for naproxen and ibuprofen, 1.7 for rofecoxib and celecoxib, and 2.1 for diclofenac.[31]

On 9 July 2015, the FDA toughened warnings of increased heart attack and stroke risk associated with nonsteroidal anti-inflammatory drugs (NSAID). Aspirin is an NSAID but is not affected by the new warnings.[32]

Possible erectile dysfunction risk

A 2005 Finnish study linked long term (over 3 months) use of NSAIDs with an increased risk of erectile dysfunction.[33] This study was correlational only, and depended solely on self-reports (questionnaires).

A 2011 publication [34] in the Journal of Urology received widespread publicity.[35] According to this study, men who used NSAIDs regularly were at significantly increased risk of erectile dysfunction. A link between NSAID use and erectile dysfunction still existed after controlling for several conditions. However, the study was observational and not controlled, with low original participation rate, potential participation bias, and other uncontrolled factors. The authors warned against drawing any conclusion regarding cause.[36]

Gastrointestinal

The main adverse drug reactions (ADRs) associated with NSAID use relate to direct and indirect irritation of the gastrointestinal (GI) tract. NSAIDs cause a dual assault on the GI tract: the acidic molecules directly irritate the gastric mucosa, and inhibition of COX-1 and COX-2 reduces the levels of protective prostaglandins. Inhibition of prostaglandin synthesis in the GI tract causes increased gastric acid secretion, diminished bicarbonate secretion, diminished mucus secretion and diminished trophic[clarification needed] effects on epithelial mucosa.

Common gastrointestinal ADRs include:[5]

Clinical NSAID ulcers are related to the systemic effects of NSAID administration. Such damage occurs irrespective of the route of administration of the NSAID (e.g., oral, rectal, or parenteral) and can occur even in patients with achlorhydria.[38]

Ulceration risk increases with therapy duration, and with higher doses. To minimise GI ADRs, it is prudent to use the lowest effective dose for the shortest period of time—a practice that studies show is often not followed. Recent studies show that over 50% of patients who take NSAIDs have sustained some mucosal damage to their small intestine.[39]

There are also some differences in the propensity of individual agents to cause gastrointestinal ADRs. Indomethacinketoprofen and piroxicam appear to have the highest prevalence of gastric ADRs, while ibuprofen (lower doses) and diclofenac appear to have lower rates.[5]

Certain NSAIDs, such as aspirin, have been marketed in enteric-coated formulations that manufacturers claim reduce the incidence of gastrointestinal ADRs. Similarly, some believe that rectal formulations may reduce gastrointestinal ADRs. However, consistent with the systemic mechanism of such ADRs, and in clinical practice, these formulations have not demonstrated a reduced risk of GI ulceration.[5]

Commonly, gastric (but not necessarily intestinal) adverse effects can be reduced through suppressing acid production, by concomitant use of a proton pump inhibitor, e.g., omeprazoleesomeprazole; or the prostaglandin analogue misoprostol. Misoprostol is itself associated with a high incidence of gastrointestinal ADRs (diarrhea). While these techniques may be effective, they are expensive for maintenance therapy.

Inflammatory bowel disease

NSAIDs should be used with caution in individuals with inflammatory bowel disease (e.g., Crohn’s disease or ulcerative colitis) due to their tendency to cause gastric bleeding and form ulceration in the gastric lining. Pain relievers such as paracetamol (also known as acetaminophen) or drugs containing codeine (which slows down bowel activity) are safer medications for pain relief in IBD.[citation needed]

Renal

NSAIDs are also associated with a fairly high incidence of renal adverse drug reactions (ADRs). The mechanism of these renal ADRs is due to changes in renal haemodynamics (kidney blood flow), ordinarily mediated by prostaglandins, which are affected by NSAIDs. Prostaglandins normally cause vasodilation of the afferent arterioles of the glomeruli. This helps maintain normal glomerular perfusion and glomerular filtration rate (GFR), an indicator of renal function. This is particularly important in renal failure where the kidney is trying to maintain renal perfusion pressure by elevated angiotensin II levels. At these elevated levels, angiotensin II also constricts the afferent arteriole into the glomerulus in addition to the efferent arteriole it normally constricts. Prostaglandins serve to dilate the afferent arteriole; by blocking this prostaglandin-mediated effect, particularly in renal failure, NSAIDs cause unopposed constriction of the afferent arteriole and decreased RPF (renal perfusion pressure).

Common ADRs associated with altered renal function include:[5]

Salt (Sodium) and fluid retention

Hypertension(high blood pressure)

These agents may also cause renal impairment, especially in combination with other nephrotoxic agents. Renal failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor (which removes angiotensin II’s vasoconstriction of the efferent arteriole) and a diuretic (which drops plasma volume, and thereby RPF)—the so-called “triple whammy” effect.[40]

In rarer instances NSAIDs may also cause more severe renal conditions:[5]

Interstitial nephritis

Nephrotic syndrome

Acute renal failure

Acute tubular necrosis

Renal papillary necrosis

NSAIDs in combination with excessive use of phenacetinand/or paracetamol (acetaminophen) may lead to analgesic nephropathy.[41]

Photosensitivity

Photosensitivity is a commonly overlooked adverse effect of many of the NSAIDs.[42] The 2-arylpropionic acids are the most likely to produce photosensitivity reactions, but other NSAIDs have also been implicated including piroxicamdiclofenac and benzydamine.

Benoxaprofen, since withdrawn due to its hepatotoxicity, was the most photoactive NSAID observed. The mechanism of photosensitivity, responsible for the high photoactivity of the 2-arylpropionic acids, is the ready decarboxylation of the carboxylic acid moiety. The specific absorbance characteristics of the different chromophoric 2-aryl substituents, affects the decarboxylation mechanism. While ibuprofen has weak absorption, it has been reported as a weak photosensitising agent.[citation needed]

During pregnancy

NSAIDs are not recommended during pregnancy, particularly during the third trimester. While NSAIDs as a class are not direct teratogens, they may cause premature closure of the fetal ductus arteriosus and renal ADRs in the fetus. Additionally, they are linked with premature birth[43] and miscarriage.[44][45] Aspirin, however, is used together with heparin in pregnant women with antiphospholipid antibodies.[46] Additionally, Indomethacin is used in pregnancy to treat polyhydramnios by reducing fetal urine production via inhibiting fetal renal blood flow.

In contrast, paracetamol (acetaminophen) is regarded as being safe and well-tolerated during pregnancy, but Leffers et al. released a study in 2010 indicating that there may be associated male infertility in the unborn.[47][48] Doses should be taken as prescribed, due to risk of hepatotoxicity with overdoses.[49]

In France, the country’s health agency contraindicates the use of NSAIDs, including aspirin, after the sixth month of pregnancy.[50]

Allergy/allergy-like hypersensitivity reactions

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, i.e. unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug.[51] Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE-mediated urticarial skin eruptions, angioedema, and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2)Comparatively mild to moderately severe T cell-mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rashfixed drug eruptionsphotosensitivity reactions, delayed urticaria, and contact dermatitis; or 3) far more severe and potentially life-threatening t-cell mediated delayed systemic reactions such as the DRESS syndromeacute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis. Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites and/or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1)exacerbations of asthmatic and rhinitis (see aspirin-induced asthma) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals and/or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema.[15]

Contraindications

NSAIDs may be used with caution by people with the following conditions:[6]

Irritable bowel syndrome[6]

Persons who are over age 50, and who have a family history of GI (gastrointestinal) problems[6]

Persons who have had past GI problems from NSAID use[6]

NSAIDs should usually be avoided by people with the following conditions:[6]

Peptic ulceror stomach bleeding[6]

Uncontrolledhypertension[6]

Kidney disease[6]

People that suffer with inflammatory bowel disease (Crohn’s disease or ulcerative colitis)[6]

Pasttransient ischemic attack (excluding ibuprofen)[6]

Paststroke (excluding ibuprofen)[6]

Pastmyocardial infarction (excluding ibuprofen)[6]

Coronary artery disease(excluding ibuprofen)[6]

Undergoingcoronary artery bypass surgery[6]

Taking ibuprofen for heart[6]

Congestive heart failure(excluding low-dose ibuprofen)[12]

In third trimester of pregnancy[6]

Persons who have undergonegastric bypass surgery[13][14]

Persons who have a history of allergic or allergic-typeNSAID hypersensitivity reactions, e.g. aspirin-induced asthma[15]

Adverse effects

The widespread use of NSAIDs has meant that the adverse effects of these drugs have become increasingly common. Use of NSAIDs increases risk of having a range of gastrointestinal(GI) problems.[16] When NSAIDs are used for pain management after surgery they cause increased risk of kidney problems.[17]

An estimated 10–20% of NSAID patients experience dyspepsia. In the 1990s high doses of prescription NSAIDs were associated with serious upper gastrointestinal adverse events, including bleeding.[18] Over the past decade, deaths associated with gastric bleeding have declined.

NSAIDs, like all drugs, may interact with other medications. For example, concurrent use of NSAIDs and quinolones may increase the risk of quinolones’ adverse central nervous system effects, including seizure.[19][20]

There is argument over the benefits and risks of NSAIDs for treating chronic musculoskeletal pain. Each drug has a benefit-risk profile [21] and balancing the risk of no treatment with the competing potential risks of various therapies is the clinician’s responsibility.

Combinational risk

If a COX-2 inhibitor is taken, a traditional NSAID (prescription or over-the-counter) should not be taken at the same time.[22][not in citation given] In addition, people on daily aspirin therapy (e.g., for reducing cardiovascular risk) must be careful if they also use other NSAIDs, as these may inhibit the cardioprotective effects of aspirin.

Rofecoxib (Vioxx) was shown to produce significantly fewer gastrointestinal adverse drug reactions (ADRs) compared with naproxen.[23] This study, the VIGOR trial, raised the issue of the cardiovascular safety of the coxibs. A statistically significant increase in the incidence of myocardial infarctions was observed in patients on rofecoxib. Further data, from the APPROVe trial, showed a statistically significant relative risk of cardiovascular events of 1.97 versus placebo[24]—which caused a worldwide withdrawal of rofecoxib in October 2004.

Use of methotrexate together with NSAIDS in rheumatoid arthritis is safe, if adequate monitoring is done.[25]

Cardiovascular

NSAIDs aside from aspirin, both newer selective COX-2 inhibitors and traditional anti-inflammatories, increase the risk of myocardial infarction and stroke.[26][27] They are not recommended in those who have had a previous heart attack as they increase the risk of death and/or recurrent MI.[28]Evidence indicates that naproxen may be the least harmful out of these.[27][29]

NSAIDs aside from (low-dose) aspirin are associated with a doubled risk of heart failure in people without a history of cardiac disease.[29] In people with such a history, use of NSAIDs (aside from low-dose aspirin) was associated with a more than 10-fold increase in heart failure.[30] If this link is proven causal, researchers estimate that NSAIDs would be responsible for up to 20 percent of hospital admissions for congestive heart failure. In people with heart failure, NSAIDs increase mortality risk (hazard ratio) by approximately 1.2–1.3 for naproxen and ibuprofen, 1.7 for rofecoxib and celecoxib, and 2.1 for diclofenac.[31]

On 9 July 2015, the FDA toughened warnings of increased heart attack and stroke risk associated with nonsteroidal anti-inflammatory drugs (NSAID). Aspirin is an NSAID but is not affected by the new warnings.[32]

Possible erectile dysfunction risk

A 2005 Finnish study linked long term (over 3 months) use of NSAIDs with an increased risk of erectile dysfunction.[33] This study was correlational only, and depended solely on self-reports (questionnaires).

A 2011 publication[34] in the Journal of Urology received widespread publicity.[35] According to this study, men who used NSAIDs regularly were at significantly increased risk of erectile dysfunction. A link between NSAID use and erectile dysfunction still existed after controlling for several conditions. However, the study was observational and not controlled, with low original participation rate, potential participation bias, and other uncontrolled factors. The authors warned against drawing any conclusion regarding cause.[36]

Gastrointestinal

The main adverse drug reactions (ADRs) associated with NSAID use relate to direct and indirect irritation of the gastrointestinal (GI) tract. NSAIDs cause a dual assault on the GI tract: the acidic molecules directly irritate the gastric mucosa, and inhibition of COX-1 and COX-2 reduces the levels of protective prostaglandins. Inhibition of prostaglandin synthesis in the GI tract causes increased gastric acid secretion, diminished bicarbonate secretion, diminished mucus secretion and diminished trophic[clarification needed] effects on epithelial mucosa.

Common gastrointestinal ADRs include:[5]

Nausea/vomiting

Dyspepsia

Gastric ulceration/bleeding[37]

Diarrhea

Clinical NSAID ulcers are related to the systemic effects of NSAID administration. Such damage occurs irrespective of the route of administration of the NSAID (e.g., oral, rectal, or parenteral) and can occur even in patients with achlorhydria.[38]

Ulceration risk increases with therapy duration, and with higher doses. To minimise GI ADRs, it is prudent to use the lowest effective dose for the shortest period of time—a practice that studies show is often not followed. Recent studies show that over 50% of patients who take NSAIDs have sustained some mucosal damage to their small intestine.[39]

There are also some differences in the propensity of individual agents to cause gastrointestinal ADRs. Indomethacinketoprofen and piroxicam appear to have the highest prevalence of gastric ADRs, while ibuprofen (lower doses) and diclofenac appear to have lower rates.[5]

Certain NSAIDs, such as aspirin, have been marketed in enteric-coated formulations that manufacturers claim reduce the incidence of gastrointestinal ADRs. Similarly, some believe that rectal formulations may reduce gastrointestinal ADRs. However, consistent with the systemic mechanism of such ADRs, and in clinical practice, these formulations have not demonstrated a reduced risk of GI ulceration.[5]

Commonly, gastric (but not necessarily intestinal) adverse effects can be reduced through suppressing acid production, by concomitant use of a proton pump inhibitor, e.g., omeprazoleesomeprazole; or the prostaglandin analogue misoprostol. Misoprostol is itself associated with a high incidence of gastrointestinal ADRs (diarrhea). While these techniques may be effective, they are expensive for maintenance therapy.

Inflammatory bowel disease

NSAIDs should be used with caution in individuals with inflammatory bowel disease (e.g., Crohn’s disease or ulcerative colitis) due to their tendency to cause gastric bleeding and form ulceration in the gastric lining. Pain relievers such as paracetamol (also known as acetaminophen) or drugs containing codeine (which slows down bowel activity) are safer medications for pain relief in IBD.[citation needed]

Renal

NSAIDs are also associated with a fairly high incidence of renal adverse drug reactions (ADRs). The mechanism of these renal ADRs is due to changes in renal haemodynamics (kidney blood flow), ordinarily mediated by prostaglandins, which are affected by NSAIDs. Prostaglandins normally cause vasodilation of the afferent arterioles of the glomeruli. This helps maintain normal glomerular perfusion and glomerular filtration rate (GFR), an indicator of renal function. This is particularly important in renal failure where the kidney is trying to maintain renal perfusion pressure by elevated angiotensin II levels. At these elevated levels, angiotensin II also constricts the afferent arteriole into the glomerulus in addition to the efferent arteriole it normally constricts. Prostaglandins serve to dilate the afferent arteriole; by blocking this prostaglandin-mediated effect, particularly in renal failure, NSAIDs cause unopposed constriction of the afferent arteriole and decreased RPF (renal perfusion pressure).

Common ADRs associated with altered renal function include:[5]

Salt (Sodium) and fluid retention

Hypertension(high blood pressure)

These agents may also cause renal impairment, especially in combination with other nephrotoxic agents. Renal failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor (which removes angiotensin II’s vasoconstriction of the efferent arteriole) and a diuretic (which drops plasma volume, and thereby RPF)—the so-called “triple whammy” effect.[40]

In rarer instances NSAIDs may also cause more severe renal conditions:[5]

Interstitial nephritis

Nephrotic syndrome

Acute renal failure

Acute tubular necrosis

Renal papillary necrosis

NSAIDs in combination with excessive use of phenacetinand/or paracetamol (acetaminophen) may lead to analgesic nephropathy.[41]

Photosensitivity]

Photosensitivity is a commonly overlooked adverse effect of many of the NSAIDs.[42] The 2-arylpropionic acids are the most likely to produce photosensitivity reactions, but other NSAIDs have also been implicated including piroxicamdiclofenac and benzydamine.

Benoxaprofen, since withdrawn due to its hepatotoxicity, was the most photoactive NSAID observed. The mechanism of photosensitivity, responsible for the high photoactivity of the 2-arylpropionic acids, is the ready decarboxylation of the carboxylic acid moiety. The specific absorbance characteristics of the different chromophoric 2-aryl substituents, affects the decarboxylation mechanism. While ibuprofen has weak absorption, it has been reported as a weak photosensitising agent.[citation needed]

During pregnancy

NSAIDs are not recommended during pregnancy, particularly during the third trimester. While NSAIDs as a class are not direct teratogens, they may cause premature closure of the fetal ductus arteriosus and renal ADRs in the fetus. Additionally, they are linked with premature birth[43] and miscarriage.[44][45] Aspirin, however, is used together with heparin in pregnant women with antiphospholipid antibodies.[46] Additionally, Indomethacin is used in pregnancy to treat polyhydramnios by reducing fetal urine production via inhibiting fetal renal blood flow.

In contrast, paracetamol (acetaminophen) is regarded as being safe and well-tolerated during pregnancy, but Leffers et al. released a study in 2010 indicating that there may be associated male infertility in the unborn.[47][48] Doses should be taken as prescribed, due to risk of hepatotoxicity with overdoses.[49]

In France, the country’s health agency contraindicates the use of NSAIDs, including aspirin, after the sixth month of pregnancy.[50]

Allergy/allergy-like hypersensitivity reactions

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, i.e. unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug.[51] Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE-mediated urticarial skin eruptions, angioedema, and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2)Comparatively mild to moderately severe T cell-mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rashfixed drug eruptionsphotosensitivity reactions, delayed urticaria, and contact dermatitis; or 3) far more severe and potentially life-threatening t-cell mediated delayed systemic reactions such as the DRESS syndromeacute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis. Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites and/or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1)exacerbations of asthmatic and rhinitis (see aspirin-induced asthma) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals and/or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema.[15]

Other

Common adverse drug reactions (ADR), other than listed above, include: raised liver enzymesheadachedizziness.[5]Uncommon ADRs include: hyperkalaemia, confusion, bronchospasm, rash.[5] Rapid and severe swelling of the face and/or body. Ibuprofen may also rarely cause irritable bowel syndrome symptoms. NSAIDs are also implicated in some cases of Stevens–Johnson syndrome.

Most NSAIDs penetrate poorly into the central nervous system(CNS). However, the COX enzymes are expressed constitutively in some areas of the CNS, meaning that even limited penetration may cause adverse effects such as somnolence and dizziness.

In very rare cases, ibuprofen can cause aseptic meningitis.[52]

As with other drugs, allergies to NSAIDs might exist. While many allergies are specific to one NSAID, up to 1 in 5 people may have unpredictable cross-reactive allergic responses to other NSAIDs as well.[53]

Drug interactions

NSAIDs reduce renal blood flow and thereby decrease the efficacy of diuretics, and inhibit the elimination of lithium and methotrexate.[54]

NSAIDs cause hypocoagulability, which may be serious when combined with other drugs that also decrease blood clotting, such as warfarin.[54]

NSAIDs may aggravate hypertension (high blood pressure) and thereby antagonize the effect of antihypertensives,[54] such as ACE Inhibitors.[55]

NSAIDs may interfere and reduce efficiency of SSRIantidepressants.[56][57]

Various widely used nonsteroidal anti-inflammatory drugs (NSAIDs) enhance endocannabinoid signaling by blocking the anandamide-degrading membrane enzyme fatty acid amide hydrolase (FAAH).[58]

How’s that for a warning label?  Did it have enough side effects for you? Think you might need more meds after taking this one? That label was 4094 words long. How many of those do you read? How do you know what you’re doing to your body if you don’t know what you’re putting into it? Do you think it coincidence that Monsanto started their GMO seed about the same time that glycation started being researched? Since much of this kind of research is funded by the industry it affects, I wouldn’t doubt that Monsanto had a hand in this research. This would allow them to immediately file these studies on glycation so that doctors and other scientists couldn’t find them to review. Yet each and every one of these 17,000+ studies have been vetted and examined by the NIH and PubMed. What I want to know is, why weren’t warnings about the glycative affects of glucose revealed at that time? Did Monsanto have anything to do with it?

The above list is the warning label for the adverse effects of Celebrex. Do you take Celebrex? Have you read the above warnings? Use of this drug can only lead to the use of more and more drugs. What do you think that would do for the profits for Monsanto? Do you still think this is coincidence? From renal failure, to the increased risk of myocardial infarction and stroke,[26][27] this drug brings on more drug use, simply so people can get away from their pain, pain caused by consumption of Monsanto’s grains. To me this is completely an unsustainable cycle. It’s a cycle of death and disease, leaving only, people in pain. Where is the sense in keeping this addiction?

Celebrex isn’t the only drug that leads to this interdependent drug abuse orchestrated by Monsanto, Pfizer, Bayer and Syngenta. There is a profitable reason that this cycle continues. Boatloads of investors depend on it. Too bad they don’t know what it’s doing to the society that they have to life in and with.

I propose that we tell Monsanto how we feel about this, not with our voices, but with our mouths in what we eat. Quit eating grains. They’re responsible for nearly all the pain you experience (with the exception of physical injuries).Grains and the glycation they bring, bring also all inflammation that influences all diseases. Stop buying bread, crackers, cookies, anything that flour is used in, stop using it, forever. That’s the only way you can start to free yourself from the addiction. You have to stop buying their junk food. Their junk food is making you sick. It’s making you sicker by the day. Stop it, you have the power to stop it and by stopping it, it gives you power, far more power than what you ever could have imagined you would have.

According to the BJM (British Medical Journal) on Cox 2 inhibitors such as Celebrex,  Selective COX 2 inhibitors are associated with a moderate increase in the risk of vascular events, as are high dose regimens of ibuprofen and diclofenac, but high dose naproxen is not associated with such an excess. How often do you need to take an Advil for your headache? Were you aware of what that painkiller does to your kidneys and liver or how much it increased your odds of having a heart attack? Why weren’t you made aware of that when it was sold to you? Maybe it was. Every drug commercial is primarily a dissertation of the adverse effects and precautions and contraindications each drug has. They all have to include this in all advertising. You’d think that that would dissuade anyone from buying into what has turned out to be nothing more than a perception of health. What drug use leads to is really not relief but continued drug use. It’s called ongoing treatment. Every hospital takes part in it. This is the effect of a society on carbohydrates….a society on drugs.

In all, there were 11,833 studies on PubMed, on the effects of glucose glycating proteins, hemoglobin, and cholesterol dating back to March, 1984. {There were 17628 studies done on PMC.) 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 and advice that it was the AGEs that were hindering my recovery. Again, I have to thank you, Dr Perlmutter.

With having the evidence for over 30 years, why hasn’t the public been told about glycation or the AGEs they create prior to Dr Perlmutter’s book, Grain Brain? 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? Was someone trying to hide something? My guess is yes.

This is Monsanto’s path to power and freedom. Their freedom is to wreak whatever havoc they can on your health by masturbating your taste buds with their glucose laden products, so you’ll be buying their pharmaceuticals in the near future. By near, I mean, it only takes a couple days before you’re indebted (addicted). If you want true power and freedom, you can have it in two weeks. That’s how long it takes to break the addiction. Or you can do it with a fast in 3 days.

THE WAY FORWARD – FASTING AND KETOSIS

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.