Tag Archives: atherosclerosis

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.

 

 

 

 

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 Best Way to Fight Hunger Fights Terrorism As Well

The Best Way to Fight Hunger

Fights Terrorism As Well

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

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

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

How Glucose Creates Terrorism

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you Monsanto :(

Glycation – The Real Poisoning of America

The Real Poisoning of America – Glycation

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

According to Wikipedia;

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

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

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

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

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

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

These Are the Smoking Gun Articles Of

Evidence That The FDA Are Ignoring.

They’re Putting Your Health and Life at Risk.

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

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

Foundation of Glycation

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

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

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

Arthritis is a Result of Glycation From Inflammation

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

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

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

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

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

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

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

Glycation, Amyloid Plaque and Neurodegenerative Disorders

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

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

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

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

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

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

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

COPD, Lung Cancer and RAGE

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

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

Abstract

INTRODUCTION:

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

METHODS:

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

RESULTS:

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

CONCLUSIONS:

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

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

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

Skin Cancer and Glycation

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

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

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

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

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

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

Cataracts and Glycation

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

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

Cardiovascular Disease and RAGE

This study shows glycations implication in cardiovascular disease;

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

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

Dangers of Statins

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

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

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

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

Contraindications

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

According to a study completed in 1995;

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

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

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

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

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

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

Direct Influence of Glycation in Cancer

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

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

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

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

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

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

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

Breast Cancer and RAGE

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

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

“Abstract

BACKGROUND:

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

METHODS:

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

RESULTS:

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

CONCLUSIONS:

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

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

Evidence of bone density decline from glycation;

·        AdvancedGlycationEnd Products, Diabetes, and Bone Strength.

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

Evidence of Alzheimer’s disease from glycation;

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

“Abstract

BACKGROUND/AIMS:

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

METHODS:

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

RESULTS:

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

CONCLUSION:

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

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

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

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

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

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

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

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

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

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

Study Link

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

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

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

The following is evidence of glycations role in cardiovascular disease;

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

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

Evidence of glycation in mental disorders like schizophrenia;

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

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

Evidence of glycation in renal disease and kidney cancer;

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

“BACKGROUND:

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

METHODS:

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

RESULTS:

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

CONCLUSIONS:

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

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

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

Evidence of glycations influence in pancreatic cancer;

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

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

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

·        Glycationinduced generation of amyloid fibril structures by glucose metabolites.

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

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

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

“BACKGROUND:

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

METHODS:

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

RESULTS:

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

CONCLUSIONS:

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

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

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

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

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

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

“BACKGROUND:

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

METHODS:

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

RESULTS:

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

CONCLUSION:

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

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

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

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

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

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

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

 

Ovarian cancer is a consequence of glycation;

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

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

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

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

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

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

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

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

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

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

·       Collagen aging in vitro by nonenzymatic glycosylation and browning.

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

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

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

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

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

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

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

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

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

Study Link

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

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

·        Polymerisation and crosslinking of fibrin monomers in diabetes mellitus

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

From Wikipedia on Fibrinogen;

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

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

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

Study Link

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

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

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

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

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

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

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

BACKGROUND OF STUDY:

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

METHOD:

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

RESULT:

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

CONCLUSION:

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

More evidence of the role glucose plays in brain degradation;

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

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

J Clin Invest. 1984 Nov;74(5):1742-9.

Garlick RLMazer JSChylack LT JrTung WHBunn HF.

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

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

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

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

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

J Clin Invest. 1984 Nov;74(5):1742-9.

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

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

 

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

Garlick RLMazer JSChylack LT JrTung WHBunn HF.

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

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

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

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

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

You have two choices;

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

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

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

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

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

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

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

 

 

 

Documentaries worth watching;

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

Why No Warnings from the FDA About gluten and sugar?

FDA’s Assessment of Gluten and Sugar.

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

grunge-cracked-fda-approved-background-some-smooth-lines-69009424

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

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

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

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

Gluten

  1. Why is there a concern about gluten? 

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

  1. What does FALCPA require with regard to gluten?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

This is what I’m concerned about;

47,397 deaths daily from CVDs

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

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

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

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

According to The Guardian;

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

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

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

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

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

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

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

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

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

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

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

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

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

The scientists and executives involved are no longer alive.

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

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

The evidence is piling up.

The FDA can’t hide their complicity much longer.

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

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

According to the World Heart Association ;

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

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

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

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

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

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

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

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

42,657 dadeaths worldwide from cardiovascular disease

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

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

13,698 daily deaths globally from Alzheimer disease

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

11,232 deaths daily from cancer worldwide

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

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

The Iowa Corn Fed Beef Ruse

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

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

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

Monsanto, the USDA and the FDA

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

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

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

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

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

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

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

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

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

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

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

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

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

Sugar; America’s Worst Addiction,

Confessions of a Reformed Carboholic

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

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

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

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

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

Carbolism Should Be Treated Like Alcoholism

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

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

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

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

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

The Perfect Ruse

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

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

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

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

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

 

 

A Display of Dependence You Don’t Need


The Power of Being Thin Is Found By Eating Fat

The Power of Being Thin Is Found By Eating Fat

Most everybody wants to be thin simply to
look good,fat-thin-people-13593846 but the advantages of being thin go a lot further than just looking good. Being thin is not only highly beneficial for your looks but it’s crucial for your health and even more important for your brain’s health. Did you know that the fatter you are, the smaller your brain is? It’s true. That is directly from Dr Perlmutter’s book Grain Brain. Conversely, the thinner you are, the bigger your brain is. Don’t believe me? Look at the research studies and what Dr Perlmutter says in Grain Brain: 

“The dots connecting excessive body fat, obesity, and brain dysfunction are not hard to follow given the information you’ve already learned in this book. Excessive body fat increases not only insulin resistance, but also the production of inflammatory chemicals that play directly into brain degeneration. For this very reason, waist circumference is often a measurement of “health,” as it predicts future health challenges and mortality; the higher your waist circumference, the higher your risk for disease and death.”

danger-obesity-grim-reaper-touches-shoulder-happy-overweight-black-woman-big-cupcake-vector-illustration-health-41031554“It’s well documented that visceral fat is uniquely capable of triggering hormonal actions.  This, in turn, keeps the cascade of of negative effects from visceral fat going. In addition, visceral fat does more than just generate inflammation down the road through a chain of biological events; visceral fat itself becomes inflamed. This kind of fat houses tribes of inflammatory white blood cells. In fact, the hormonal and inflammatory molecules produced by visceral fat get dumped directly into the liver, which, as you can imagine, responds with another round of ammunition (i.e., inflammatory reactions and hormone-disrupting substances). Long story short: More than merely a predator lurking behind a tree, it is an enemy that is armed and dangerous. The number of health conditions now linked to visceral fat is tremendous, from the obvious ones such as obesity and metabolic syndrome to the not-so-obvious—cancer, autoimmune disorders, and brain disease.”

I copied and pasted the information above from Grain Brain for a reason. Obesity is a danger to more than just your body, by filling it with inflammation, it’s shrinking your brain by using these same process that creates plaque. I will show you exactly how obesity shrinks your brain and on the other hand, I’ll show you exactly how being thin can help your brain to grow in size. It all boils down to consumption of carbohydrates, mostly the high starchy carbs that you find in all pastries and breads, pastas, cereals, snack chips and crackers and some vegetables.

According to  Donald W. Miller, Jr., MD, Carbohydrates are the primary cause of weight gain, not fats. (Animals raised for food are fattened with carbohydrates.)” He goes on to say that eating fat is not only healthier than eating carbohydrates, it makes you thinner. “We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active” (Arch Int Med 1992;152:1271—2). It’s true,  I know from experience that eating fat makes you thin. It’s time for a new news alert;

Eating Fat Makes You Thin

Studies have shown that getting back to what our original metabolism likes for a diet and what our bodies are meant to digest means getting back to diet high in fats and low in carbohydrates. Low Carb diets date back to 1923 when the ketogenic diet was first created to help control epileptic seizures in infants. Dr Atkins came out with his low carb diet in 1958,  but it really got its boost when the Paleo diet came out early this century and with Dr Perlmutter’s recommendation for a ketogenic diet for optimal brain growth.

Wikipedia suggests, “we need to evaluate the low-carbohydrate diets over much longer periods of time, controlled studies as long as two years and survey studies as long as two decades.[7][13][14][15]” 

Dr Atkins was the first to promote a low carb diet as early as 1958, yet it seems that the carbohydrate addiction complex had already started its devious work in addicting our society to the ravages of the Wheat Belly saga. Too many members of our congress were sold on the notion that it is better to restrict our consumption fats, thinking that’s what was causing all the problem with obesity and diabetes. In all actuality, it is carbs that cause the fat that causes obesity and diabetes, not fat at all. You can find out how that happens in Carbs, The New Death Sentence. (I have to wonder who persuaded them to come to these conclusions, the grain industry?)

It’s all a matter of how they are digested. To digest carbohydrates, your body has to turn them into fat. This is because your body can’t run on glucose. It runs on fat. The studies showing this include,  Iris Shai, R.D., Ph.D. (July 2008), “Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet.” and New England Journal of Medicine 359 (3): 229–41. doi:10.1056/NEJMoa0708681.PMID 18635428, Low-carbohydrate-Diet Score and the Risk of Coronary Heart Disease an Omen, from The New England Journal of Medicineand the two others listed above ([14][15]). What this means is that when you eat carbohydrates, your body can’t use that as food because it burns fat.

When you eat fat, your body doesn’t have to convert that into anything else, so it can use it. Fats are digested in your small intestine unlike carbs that are digested cellularly with the help of insulin. That means that the glucose that carbs break down to, have to float around in your blood stream until they can enter a cell to be used as glycogen. This is where the problem begins. Anyone who’s been on a diet of carbohydrates for any amount of time has enough glycogen built up in their systems that they don’t need anymore, so the glucose turns into fat to be stored for future use.

The first place your body stores this fat is around your mid section, hence its name, belly fat or visceral fat. This is a dangerous fat to have in your body as this is where diabetes starts, along with a host of cancers and CVDs or heart diseases and most every kind of dementia, including Alzheimer’s Disease, Parkinson’s Disease and Huntington’s Disease.

Human biology hasn’t changed evolutionarily enough to allow humans to continue to eat carbohydrates in the massive amounts that everyone everywhere is eating them. The Paleo Diet  is a recent addition to the low carb diet choice. The ketogenic diet is the ultimate in a low carb diet and has already shown numerous benefits for better health. It’s the recommended diet for Celiac Disease since Celiac Disease is caused by the gluten that’s found in wheat, barley and rye and a few other grains. It’s also the oldest low carb diet, first designed in 1923, to help control seizures. The diet fell out of use when seizure medicines became more prevalent.

It turns out that a ketogenic diet is the healthiest diet that any human can eat and it brings with it, the most natural form of weight loss, possible. It goes back to the way our bodies have  metabolized food for the last 100,000 years. Simply because this diet is based on fat and not carbs, the diet provides much more efficient fuel for our bodies to use. A carbohydrate diet requires refueling every two hours or so and they has a tendency to gum up your body. It does it by creating plaque. That gets into to glycation of proteins and LDL cholesterol, which you can read about in Carbs, How They Cause AGEs

This plaque build up is the foundation of 75% of the deadliest and costliest diseases, known to man, ranging from breast cancer  to Atherosclerosis to 99% of all dementias, making carbohydrates some of the deadliest food that any human can eat. It’s not that this food just makes us fat, it kills us slowly and expensively, with an arm long list of  disorders. For this one reason alone, the power of being thin cannot be overspoken.

Studies have also shown the simple practice of calorie restriction to have multiple beneficial effects for the body, such as extended life. It’s amazing what just going hungry, can do for your body. It not only ramps up your immune system by boosting your anti-oxidants exponentially, it actually helps your brain grow, through a little protein known as BDNF, brain derived neurotrophic factor. This is what makes your brain grow and it doesn’t happen in obese people. This is part of the power of being thin.

The Power of MCTs and Coconut Oil

Calorie restriction on a carbohydrate diet is next to impossible. Yet I do it every day, quite easily and comfortably, while on my MCT ketogenic diet. MCT ketogenic diet is, in my estimation, the easiest low carbohydrate diet to get adjusted to. MCTs (Medium Chain Triglycerides) work differently in your body than LCTs (Long Chain Triglycerides). MCTs are a good way to actually lower your cholesterol because they build up the HDL cholesterol. Coconut oil and Palm kernel oil are optimal for this, as they contain lauric acid  and lauric acid is the foundation of HDL cholesterol, the good cholesterol.

Although curbing your carbs is the best way to lower your LDL cholesterol, adding coconut oil and other saturated fats to your diet will help curb your appetite for carbs, which in turn will cut down your LDL cholesterol and at the same time build up your HDL cholesterol.

Going back to what Dr Miller had included in his paper, “calorie restriction prolongs life as well as helps to make your brain grow.” This is the true power of being thin. It comes easiest from being on a high fat low carb diet.

What kind of fats then, do we need to eat, to be thinner? I mentioned before, MCTs. Medium chain triglycerides are the best, along with olive oil and avocado oil, palm kernel oil is also an excellent source of MCTs but coconut oil is by far the best MCT, in my opinion.

Coconut oil and palm Kernel oil have lauric acid in their chains of triglycerides, which is the foundation of HDL cholesterol. This means that a diet high in coconut oil or palm kernel oil MCTs helps build up HDL cholesterol, which in turn can help lower LDL cholesterol. Lauric acid is at the core of apolipoprotein A1, which in turn is at the core of HDL cholesterol. Studies have shown higher levels of HDL particles in the blood to be very beneficial for one’s health.

I can’t recommend staying away from dairy either. As I said before, all milk fats are MCTs. If you truly are lactose intolerant, then it may be best to limit your intake to nothing more than cheese. Cheese looses its lactose as the cheese hardens, so most cheeses have little to no lactose content in them. Just don’t choose the low fat cheeses.

Butter’s Back

butterFor MCTs, I like milk fats. All milk fats are MCTs. That means that all milk fats can help you lose weight. I’ll bet you didn’t expect that, did you? That means that low fat milk and skim milk actually help make you fatter by taking away the healthy MCTs in milk fat. That also means, butter is back! Wow, how much better can it be? Butter can help you lose weight. What a concept, the more milk fat you eat, the healthier you will be. I love it!!! Cause I love cheese, and cheese is a milk fat.

MCTs are so important, Neuropharmacology just completed a study in June 2013 showing the ability of MCTs to control epileptic seizures. All MCTs are saturated fats. Your body uses saturated fats and would much rather have it fed to it than have to make its own through the ingestion of carbohydrates.

That also means that I can go back to eating bacon. I love bacon. (As a matter of fact, I’ve already gone back to eating bacon. I just enjoyed about 6 slices.) Bacon may not be a medium chain triglyceride, but it’s a saturated fat and I still love it, and I’m not restricted from eating it by my religion, so I eat it and lots of it. I couldn’t do that though, if I ate carbs. That would lead to major problems like hypertensive heart disease.

Grass fed beef is always a good source of fats as well as protein. Lamb is always good also as it’s almost always grass fed. I’m sorry vegans, but a vegetarian diet is too carbohydrate laden to be a fully healthy diet, unless you get the bulk of your calories from healthy oils like olive oil, avocado oil, palm kernel oil, and most importantly coconut oil. Simply because carbohydrates are involved in a vegetarian diet, you’re going to be suffering the same consequences as everyone else on a high carbohydrate diet. It may take longer for the disorders to manifest, because your vegan diet is a little healthier than most high carbohydrate diets, but they will, simply because carbohydrates are involved. The science of metabolism doesn’t allow any variation on this rule.

Carbs, not fats create body fat, especially visceral  fat,  the kind that kills.

The secret is to get more of your calories from fat and fewer from carbohydrates. Fat has more calories per gram of usable food anyway, making it a much more efficient fuel. Like proteins, carbohydrates only give you 4 calories per gram of food, but fat gives you 9 calories per gram of food. That’s over twice as many calories for the same weight of the food you put in your body.

That means that you have to eat more than twice as many carbohydrates to get the same amount of calories. It’s no wonder that a carbohydrate diet is so fattening.

A high fat, low carb diet is like than running high octane gas in your car but it’s even better, for your body. What high octane gas does for your car, fat does more for your body. On the other hand, What sugar does for your car, it also does to your body. Only it does it much slower.If you know of anyone who has put sugar in a gas tank, you know what that did top the engine. The same thing happens in your body. It gums it up. Glucose is to akin too glue, to be healthy.

It does it slower because your body doesn’t burn fuel as fast or as hot as your car engine, so it takes it longer to gum up. But when it does, the results are exactly the same, disastrous. That is the curse of being on a carbohydrate diet.

It’s Time For A Cure

Carbs, How They Create A.G.E.s. Your ticket to Alzheimer’s Disease, Cancer, Heart Disease and more

How Carbs Create A.G.E.s. Your ticket to Alzheimer’s Disease, Cancer, Heart Disease and more

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

According to Wikipedia;

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

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

Wikipedia goes on to say,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Effects in aging

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

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

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

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

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

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

To summarize,

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

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

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