Tag Archives: glycation

Calories

Calories, Do You Worry About Them?

Calories, do you worry about how many you eat? If you do, you’re not alone. A lot of people do the very same thing, they count their calories. If you’re one of those who do, I have a suggestion for you. To help make your job easier and you healthier; it’s not how many calories you eat, that’s important. What’s important is where the calories come from.

Calories are essential to survive, so they’re absolutely necessary and yes if you eat more, you weigh more. If you eat less, of course, you weigh less. That does make eating fewer calories crucial yet eating less to control them can be very difficult at the least if you’re on a carb diet. The simple reason for this is because carbs make you hungry. They create and maintain a hunger cycle that you have no control over, without removing them. That makes, where you get your calories from, more important than how many you eat.

Are the calories you get from the food you eat most from carbohydrates or are they calories from protein and fat? If you’re eating calories from carbohydrates, under the guise of healthy energy, you’re allowing those carbs to make the fat that your body needs to use for that energy. If you’re getting your calories from fat and protein, you’re feeding your body exactly what it needs to survive and thrive. Eating fats and protein also allows your body to heal itself from virtually anything. There is very little our bodies cannot heal from, as long as they don’t have the influence of the glycation that’s the result of carbohydrates contaminating their systems. That means if your body needs glucose, let it make its own.

Whatever glucose you can get from carbs, your body can supply, on its own. When your brain (which is the only part of your body that uses glucose) needs glucose, it can supply the brain with all it needs through a process of gluconeogenesis. Your body reformulates the glycogen in your body to pull glycose out of it to use whenever the brain needs the glucose. (Remember, glycose used to be the name for glucose.)The interesting thing about this little-known fact is that your body makes this glucose, regardless of how much you already have in your body from the carbs you eat.

This all points to the fact that your body will make the nutrients it needs, provided you feed it the proper foods to begin with and carbs are not in that group. Carbs make your body make its own fat. It makes that fat out of the carbs you eat with the hormone insulin. (That’s an enzyme you don’t want to be inhibited.) A healthier way to live is to allow your body to make its own glucose instead of fat. This does wonders for the body. As long as you eat enough protein to compensate for the loss in muscle tissue from gluconeogenesis, you’ll never lose vital muscle tissue.

This is why long fasts help you lose so much weight. After your body uses up its own fat to fuel your body, it resets your body to produce growth hormones that not only help keep you thinner; they keep you healthier by repairing your systems for you (usually without the need for medication).

It does this by changing your hormones. The way in which many hormones work is affected by eliminating carbs from the diet. Insulin is soon replaced by glucagon which regulates the gluconeogenesis that takes place in your body whenever it needs glucose. This hormone regulates how fat is burned in your body, whereas insulin controls how fat is stored in your body. As long as you’re eating carbs you’re creating insulin and it’s instructing all the fat you’re making to be stored, instead of to be used. When you remove the carbs from your body; your body changes, from increasing its production of insulin to increasing the production of glucagon which in turn ramps up the burning of your fat. This is why keto diets work so good. It’s also why carb diets work so bad.

That means when you continue a diet of carbs, you’re forcing your body to make its own fat out of those carbs and this is where your problem lies. The fat your body turns the glucose into is not a clean burning fat. It’s a dirty fat at best. It leaves glycated residue wherever it’s burned. That, in turn, gums up your cells…all of them, including your brain cells, your heart cells, your kidney cells, liver cells, every cell that blood flows through including the blood vessels they flow through. This is the true danger in carbohydrate consumption. This danger has been magnified by the glyphosate herbicide Roundup, with its enzyme inhibiting chemicals.

Some of the enzymes that get affected are enzymes that influence behavior. Some of these behavioral enzymes influence your appetite, as well as digestion, making this enzyme inhibitor responsible for more of your hunger and less of your nutrition. (It could actually detract from your nutrition.)

Could that be why Monsanto is so vehement about their product being safe? They must know, cutting the use of enzyme inhibitors in crops will cut down on the need for medication for the changes those enzyme inhibitors impose on the body. If news like that were to leak out to the world, what do you think that would to the profits of the pharmaceutical corporations they used to own? What would happen to the profits of the food producers that depend on the grain industry to provide them with their flour? Don’t you think that would have a major influence on them if everyone knew that it was actually all of the grain products that Monsanto is responsible for that is making them need the very medications that Monsanto’s old pharmaceutical companies make?

I’m sure the pharmaceutical companies are still customers of Monsanto chemical division now, buying the same enzyme inhibitors to use in heart medication as well as many cancer medications. This practice leads only to more and more drug need by their consumers and this is how you get hooked. If you eat grains in any form you’re one of their consumers.

This is what happened to my mother and continues to happen to over 20,000 mothers every day. This vicious cycle is courtesy of Monsanto’s crop seed companies, Monsanto’s herbicide companies through the production of Roundup, and what used to be Monsanto’s corporate partner, Pharmacia.

Cutting down on the use of these herbicides will also cut down on the need to use these same chemicals they need to produce to make those medicines and this is the doom they’ve condemned our society too. Their greed is more important to them than the health and safety of all America. Their glyphosate ensures this for Monsanto even after their patent expired. It also ensures that America is not free, but still under the control of this industry and Monsanto.

According to Wikipedia; Glyphosate kills plants by interfering with the synthesis of the aromatic amino acids phenylalaninetyrosine, and tryptophan. It does this by inhibiting the enzyme 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), which catalyzes the reaction of shikimate-3-phosphate (S3P) and phosphoenolpyruvate to form 5-enolpyruvyl-shikimate-3-phosphate (EPSP). Glyphosate is absorbed through foliage and minimally through roots, meaning that it is only effective on actively growing plants and cannot prevent seeds from germinating. After application, glyphosate is readily transported around the plant to growing roots and leaves and this systemic activity is important for its effectiveness. Inhibiting the enzyme causes shikimate to accumulate in plant tissues and diverts energy and resources away from other processes. While growth stops within hours of application, it takes several days for the leaves to begin turning yellow.

This makes your body waste a lot more energy, converting those carbs into fat, so it can use them. If you feed your body fat in the first place, you don’t need to convert anything as the fat is “ready to use”. This last little factor is what’s important to know because it doesn’t require your body to make fat out of the sugar. This is what drains your pancreas from its supply of insulin. It also glycates your blood and it’s this glycation, that leads to more modern disease than any other one thing. If you can control glycation, you control all inflammation. Controlling all inflammation means that you’re controlling all modern diseases created by inflammation.

This fact combined with the fact that Roundup affects the enzymes phenylalaninetyrosine, and tryptophan, means that they’re also affecting your hunger patterns and your digestion. That creates a double dipper for the food industry and pharmaceutical industry. And they do this legally, thanks to a patent law from 1954 and a ruling from an old Monsanto lawyer saying that modifying seeds for any purpose, is legal. I’m sure they didn’t realize the consequences at the time, their actions would have on humanity.

One of the enzymes affected in your body is Phenylalanine, is a precursor to tyrosine; the monoamine neurotransmitters dopaminenorepinephrine  (noradrenaline), and epinephrine (adrenaline); and the skin pigment melanin. Affecting the phenylalanine is going to affect how your other hormones work that are influenced by these enzymes. Tryptophan is an enzyme that influences your hunger by influencing enzymes that affect hormones that are influenced by what you eat. This is why your hunger is greater now than it ever was in the past and this is why the obesity epidemic, diabetes epidemic, CVD epidemic, cancer epidemic and dementia epidemics have worsened alongside the increase of glyphosate sprayed on American crops.

That means you must get your calories from healthy fats and protein. These are the foods your body prefers. It can live on carbs but carbs are only supposed to be used in times when we can’t get the protein or fat. The healthiest fats to partake of are MCT fats, Medium Chain Triglycerides. They’ll balance your cholesterol which is much healthier than just lowering it. Balancing is will actually lower your LDL by increasing your HDL. It’s the HDL that cleans out your cells of the spent LDL that’s been fed into it. If your body can’t clean out the burned LDL out of your cells, the LDL backs up in your blood increasing your overall cholesterol. What’s worse? If you accumulated this LDL from eating carbs, it’s dirty LDL, which is going to leave a residue inside your cells and this is what turns carbs into poison. That residue is what leads to all the modern diseases known to man. If you can cut down on that residue, you can control all disease.

Protein and fat have been the basis of our diet as far back as our species dates. We’re not going to change that overnight by converting to a diet of carbs. That’s insanity in my opinion. Homo Sapiens went through well over 100,000 years eating protein and fat supplementing it with carbs. Today, the basis of our diet is carbs and we supplement it with protein and fat. This practice urged on by a grain industry that’s interested only in profits and not public health, has proven deadly for all Americans. Since the expansion of the use of Roundup, this practice has become the deadliest practice that anyone can take part in. Not even the extensive exercise our ancestors had from running all the time could have saved them from the ravages of this weed killer.

This weed killer has turned into a people killer, through its enzyme inhibiting functions and this is something Monsanto continues to deny. (They’ve made lying to the public legal, with their placements in the USDA, FDA, EPA and probably the CDC all to ensure their success in carrying out that grandiose ruse that grains are healthy to eat and that you need to eat more of them. Hold on to that thought because we’re going to look into why they’re pushing this on the public like they are.

Thousands of years ago in our Paleolithic state, we were primarily carnivores. Just like bears we developed the ability to digest plant food making us omnivorous instead of just carnivorous. However, eating carbohydrates has its bad side, and it’s called glycation. Protein can’t create glycation. Fat can’t create glycation. They both need the glucose to do that. That makes glucose a natural poison that we’ve been eating for over 10,000 years, only to be ramped up in the last 50 years or so to where the proliferation of its use is now sending hoards of people to their premature deaths. It’s also making these same people very sick for extended periods of time before they die. It also makes people sick while they continue to eat, what now are really dirty carbs, due to the glyphosate herbicide sprayed on them as many as four times before they reach your table. Think about that for a minute.

The bread you make your sandwich with has been poisoned, right under your nose without your consent, or knowledge, which forces you to need the pharmaceuticals that this same company produces. Who knew that this addiction that’s been forced upon you claims your health with every bite you take? You should know what addiction this is, by now and what you can do about it. What they’re selling as safe has escalated death rates from diabetes to brain cancer, from Alzheimer’s to atherosclerosis, all evidenced by the rise in cancer rates in the farmers that use this weed killer.

It’s also evidenced by the rise in autism since the start of spraying, 40 years ago. Autism rates climbed steadily for 15 – 20 years from the early 70’s, when they started using glyphosate, until they too, skyrocketed in the 90’s, when glyphosate usage multiplied. Now glyphosate is at an all time high with every rate of modern disease at an all time high as well. Yet Monsanto and its industry refuse to acknowledge the true damage they’re doing to our society. It’s their greed that’s driving every pandemic known to modern man. From destroying our health to destroying the environment, Monsanto is leaving quite possibly the largest footprint on our ecosystem, medical system, pharmaceutical system as well as our agricultural system, . They have industrialized legal covert terrorism on an unsuspecting public, by saturating our diets with poisonous food, without telling us. What they should have shared with us, was that they were using us as guinea pigs, for their experiment on the impact glyphosate has on human physiology.

Their experiment has been disastrous for the American people, as well as the world, as glyphosate is breaking records in sales every year, especially since the patent expired 16 years ago. But this isn’t supposed to be about glyphosate. This is about the calories you eat and where you get them from. The glyphosate sprayed grains just tells you, not to get your carbs from that source as that source is now tainted, severely.

Do you get them from dirty sources like carbs or do you get them from efficient foods like protein and fats? Remember where I said that a gram of sugar has 4 calories and that a gram of fat has 9 calories? That only points to the fact that fat is 225% more efficient as a food source. (This is something Monsanto has lied to you, for about 30 years .) With fat being that much more efficient than sugar, it’s no wonder that it’s that much healthier.

Eating the proper fats feeds your body exactly what it’s been running on ever since we’ve been running as a species. A running we did in our Paleolithic years. We ran all day long, either hunting food, tracking down food, or just running down our food. The funny thing about this is, they were all running on empty stomachs, all day long, and not running out of energy. They could only do this by not eating many carbs. Their bodies had to run on ketones and fat, ramped up by adiponectin and other hormones in their bodies that set their brains to grow.

It was this constant practice of exercising every day that made their bodies produce the hormones that allowed them to advance faster than the other species. It was our ability to sweat and cool our bodies that allowed our ancestors to run down their game to feed their families. It was this kind of diet that our bodies ate for 1,000’s of years. Not until the last 60 years or so did we become sedentary and start eating more of what used to take us a half a day of gathering to eat. Most people now get their calories without the gathering or the hunting or the running so they never burn up those calories. They store them. This is the nature of a carbohydrate diet. The same hormone (insulin) instructs the fat it just made to store itself as visceral fat around your midsection until you need it. Your problem is, you seldom need it so it stays as fat.

The bad thing about that is that this fat you just made out of your carbs is going to demand more fat to join it. Fat in your body shuts down the action of leptin, the satiety hormone. When this hormone isn’t working right to tell you when to put down your spoon, it‘s demanding that your body consume more carbs to satisfy it. This leptin resistance leads directly to you needing to eat more and more, just to produce enough leptin to satisfy your addiction. And this is precisely why you should get your calories from protein and a much more efficient fat, rather than carbs.  This is metabolic syndrome, a precursor to diabetes. This is why the keto diet is taking off so much. It’s not only a fat burning diet, it’s a brain growing, muscle growing diet that truly gives you the best body and brain you can have.

You’re probably asking, what kind of fat is good to eat? I’ve always been told that fat is bad. Until I learned that it isn’t at all. It’s healthy. Actually, it’s very healthy. The industry that told you it was bad had an interest in selling you that idea so you would eat more carbs. They even recommended for you to eat them over the fat. That’s because the grain industry is behind the recommendations for what you eat and they’re interest is in supplying more grains for you to consume.

Later they found out that a diet of fat won’t lead you to any drug use. That’s reserved for the carb diet and that may have been why this industry dissuaded everyone from consuming a diet of fat. Just like the sugar industry the grain industry has been lying to the public for greater than 60 years about the safety in eating their food. Now, they’ve amplified its danger by dousing it with more and more glyphosate right up until two weeks before harvest. How safe do you really think that makes the food you eat?

Remember the thought I asked you to hold on to earlier in this article, why Monsanto has been pushing the idea that grains are healthy to eat? The answer to that question, is because this is crop that can be marketed to farmers as making them more money by producing more crop. Yet they need to spread more Roundup, to do this, according to Monsanto. (This is something many farmers don’t agree with and are actively trying to resist. Monsanto’s push to own every farmer on North American soil has taken many of these farmers to court where Monsanto has tied them up for years at a time, often, to get them to use their own gmo seed.) This includes Canada where a majority of canola is grown, which happens to be another Monsanto glyphosated crop. This is another one that they like to spray with Roundup right before harvesting to save the lower oil pods that drop off the crop and shatter losing much of the valuable canola oil. (For the farmer it’s Roundup to the rescue. For the consumer it’s Roundup to the dinner table where it can continue it enzyme inhibiting actions in the bodies of your family.

Right after Monsanto patented their first seed in 1980, they purchased GD Searle chemicals, makes of NutraSweet in 1985. This was about 14 years after they patented Roundup. (They probably patented the glycation of America.) Their Roundup has done a bang-up job of bringing the senescence of glyphosate to humans. Roundup is advertised as working through senescence, on how it kills weeds. That senescence is rubbing off on our population. It was 7 years after they patented seeds that they patented Celebrex setting themselves up to be a provider of foods that require an early departure to drugs and a never ending cycle that never lets up until a premature death.

This current cycle of disease, disorder and death can be tracked back to 1954 and the the plant act. That’s when they made it legal to patent seeds, later leading to genetic modifying of crop seed, later leading to genetically modifying crop seed to survive multiple uses of an enzyme inhibiting herbicide that induces senescence in humans. This is the genetic modifying of humans by modifying their food. This food that gets modified just happens to be an addictive food that’s been made more addictive by its modifying. If this isn’t criminal, I don’t know what is.

To prevent your premature death, look to make fat and protein the core of your diet. You don’t have to eat nearly as much, or as often, as it’s that dreaded hunger cycle that never appears in the keto diet. That’s because the arguably worst manifestation of a carbohydrate diet, is the hunger cycle that’s tied to it. I don’t know anyone who would want that. Especially when that hunger gets magnified by what’s been sprayed on it multiple times.

It’s clear to me that the more glyphosate that Monsanto sells, the more disease the public is going to fight. From autism to Alzheimer’s, all modern diseases have increased right alongside the increase of glyphosate usage. The only blessing here is that we don’t have to eat it. We can say no to glyphosate by not eating any grains, including sugar.

To learn exactly why you should avoid glyphosate, see The New Dangers of Grain Consumption at www.saveourdignity.org 

Full Details:

 

Extended Details:

Basic Warning:

Glycation-The Real Poisoning of America (Why You Can’t Lose Weight)

The Real Poisoning of America – Glycation

Glycation has everything to do with the consumption of glucose. Keep that in mind as you read through this article. You have the power to control this all too common of a process. Glycose is at the root of all glycation unless it’s made in your body from gluconeogenesis as that’s the only way you can obtain clean glucose. (This is why Metformin is so dangerous. It shuts down your body’s only source of clean glucose. We’ll get into more of that in the next book.)

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. In industrialized nations the proportion is much higher, reaching 90%. Thus, albeit indirectly, biological aging(senescence) is by far the leading cause of death. Whether senescence as a biological process itself can be slowed down, halted, or even reversed is a subject of current scientific speculation and research.

2001 figures

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.)

who-dataThe top 10 causes of death, ones caused by Excessive Carbohydrate Consumption are in red ;
According to the World Health Organization’s top ten causes of death, ECC plays a role in 70% of them.

  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@1.6mil
  6. HIV/AIDS@1.5mil
  7. Diarrheal diseases@1.5mil
  8. Diabetes mellitus@1.5mil
  9. Road injury@1.3mil
  10. Hypertension@1.1mil

The Link Between Carbohydrate Consumption and Death

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.

Although not directly responsible for some of these cancers, they would not exist in the glycation didn’t exist. This 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 80% 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 is ignoring.

In doing so, they’re

putting your health and life at risk.

30 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.

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

This report can be found on PubMed at Receptor for advanced glycation end‐products‐mediated inflammation and diabetic vascular complications. It explains how glycation turns your body’s fuel into AGEs before it can be used for fuel. These AGEs are responsible for almost all modern diseases and thus, are the reason for this article.

“Exposure of amino residue of proteins to reducing sugars, such as glucose, glucose 6phosphate, fructose, ribose and intermediate aldehydes, results in nonenzymatic glycation, which forms reversible Schiff bases and Amadori compounds. A series of further complex molecular rearrangements then yield irreversible advanced glycation endproducts (AGE). The aldehydes, highly reactive AGE precursors, are produced by both enzymatic and nonenzymatic 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

The following report is the evidence of glucose’s involvement in arthritis. By being responsible for glycation, the glucose from broken down from carbs, again, is directly responsible for arthritis

 “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

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 cataracts 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.”

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).

“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 an AGE (advanced glycation endproduct), as near as I can tell.

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

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

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

Has anyone asked yet about removing the glycating products from our diets?

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

This study shows glycations implication in 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 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.”

More evidence of its influence in cancer;

“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

This is evidence of glycations effect on the kidneys:

“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

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

“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

Evidence of bone density decline from glycation;

“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;

“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

More evidence of cancer-causing agents from glycation;

“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

Evidence of glycation causing agents in baby food, This is where your addiction starts;

“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 gastrointestinal 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

Here’s your proof that glucose is responsible for diabetes;

“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 aging;

“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;

“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;

“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;

“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. All rights reserve” Study Link

Methylglyoxal is the link from glucose to disease through its conversion to AGEs, advanced glycation endproducts as explained by this study;

“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;

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

Amyloid plaque is at the root of most modern diseases, ranging from cancer to heart disease to arthritis to Alzheimer’s disease;

“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.”

More evidence of glycations involvement 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;

·        “The false alarm hypothesis: Food allergy is associated with high dietary advanced glycation end-products and proglycating dietary sugars that mimic alarmins.

“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 “alarming.” 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

Evidence of the influence of glycation in dementia;

“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. For permissions, please e-mail: journals.permissions@oup.com.”        Study Link

Evidence of glycation in lung cancer;

“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;

  • IL-1β/HMGB1 signaling promotes the inflammatory cytokines release via TLR signaling in human intervertebral disc cells.

“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;

“OBJECTIVE:

To investigate the expression of advanced glycation end products (AGEs) and the receptor for AGE (RAGEs) in maternal blood, umbilical blood and placental tissues in women with severe preeclampsia (sPE) as well as any association with inflammatory processes.

METHODS:

The expressions of AGEs, RAGE, tumor necrosis factor-alpha (TNF)-α and vascular cell adhesion molecule-1 (VCAM)-1 in placental tissues were measured using immunohistochemistry. The levels of AGEs, RAGE, TNF-α and VCAM-1 in maternal blood, umbilical blood and placental extracts were assessed using enzyme-linked immunosorbent assays. Placental RAGE, TNF-α and VCAM-1 mRNA expression levels were determined by PCR. Placental AGEs, RAGE, TNF-α and VCAM-1 protein levels were determined by western blotting.

RESULTS:

The levels of AGEs, TNF-α and VCAM-1 in the maternal tissues and umbilical blood were significantly higher in the sPE group than in the normal pregnancy (NP) controls (p < 0.05). The serum level of sRAGE in the umbilical blood was lower in the sPE group than in the NP controls (p < 0.05), while sRAGE was higher in the maternal blood of sPE than in the NP (p < 0.05). The maternal serum levels of AGEs were positively correlated with that of TNF-α and VCAM-1 in the maternal blood. There were no correlations between the levels of RAGE, TNF-α or VCAM-1 in maternal blood or umbilical serum. There were no correlations between the levels of sRAGE and TNF-α or VCAM-1 in maternal blood or umbilical serum. The levels of AGEs were positively correlated with those of TNF-α and VCAM-1 in placental lysates.

CONCLUSION:

AGEs and RAGE appear to act as important mediators in regulating the inflammatory pathways of preeclampsia.”

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 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 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

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 ).

From every form of cancer to Alzheimer disease to heart disease and cardiovascular disease to arthritis to hypertension to high cholesterol this food source (sugar and grains) is responsible for each and every one of them. These studies are proof of exactly what sugar does to the body.

If these foods were removed from the diet, the impact would be astounding for public health. By removing the food from your shelves, you’d be removing any reason for glycation. Remove the glycation and you remove the cause of the disease. Removing the glucose from the diet will remove the glycation and inflammation. Can it be that hard to understand? It’s really very plain and simple. Thank you, Dr. Davis. Thank you, Dr. Perlmutter. Although I would have felt the results of my abstinence, (because I had already quit when I read your books) I would have never known why or been able to tell anyone else about the wonders of living without sugar, had I not read them. Thank you again.

Full Details:

 

Extended Details:

Basic Warning:

Where are the warnings from the FDA on gluten and sugar?

FDA’s take on gluten.

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 the same as the sugar industry not just covered up the studies condemning sugar, but they initiated reports themselves that sugar was healthy. That is a complete falsehood of the truth of what sugar 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?

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.

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

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.regulatory-guidelines-business-cartoon-books-floating-air-librarian-saying-to-patron-have-all-kinds-floating-55414961

FDA’s gluten-free definition is that the food contains less than 20 ppm of gluten.

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. This is evidenced by the report that I sent you yesterday. All they require is a mention of wheat in the ingredients and nothing more. That is their warning.

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 into 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 allowed 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 flour challenges 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 1990. According 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.

Where does the FDA’s interest lie?

History has shown us that there has been corporate influence in the sugar industry, was it involved with the grain industry, as well?

woman-holds-anti-fda-gmo-sign-rally-asheville-nc-may-yound-carries-saying-compromised-monsanto-s-pack-31230844The 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).”

“Obesity and diabetes mellitus are often linked to cardiovascular disease,[53] as are a history of chronic kidney 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 looked 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 daily deaths 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 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.

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?

“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.

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.

These 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.

These actions are responsible for more deaths than 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.

Is someone trying to hide this information? Or are they just leaving 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 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.

If the FDA can allow a food this despicable through its monitoring, I’m afraid to even think about what else has snuck through?  Shouldn’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 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 pocketbook 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.

 

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