Glutenology: No grain no pain
(too old to reply)
2017-04-25 17:35:46 UTC
Rejected Man
2017-04-25 22:06:52 UTC
Post by Taka
I've have wondered if the use of sour dough might reduce the risk of wheat inciting celiac. I saw a paper on Pubmed making the suggestion.
2017-05-18 07:18:30 UTC
Do You Need Specific Genes to Have Gluten Sensitivity?

Unlike celiac disease, gluten sensitivity doesn't seem to require exact genetics

Although research into non-celiac gluten sensitivity is just beginning and studies showing it's a distinct condition haven't yet been replicated, preliminary results indicate that you don't need to carry either of the so-called celiac disease genes in order to develop gluten sensitivity.

Those with celiac disease, the best understood of the five different types of gluten "allergy," almost always carry one of two very specific genes.

In fact, doctors routinely use gene testing to rule out celiac disease — if you don't have the gene required to develop celiac, they say, you almost certainly don't have the condition.

The genetics of non-celiac gluten sensitivity are far less clear.
Quick Celiac Disease Genetics Lesson

Hang on — this is like genetic alphabet soup.

The "celiac disease genes" appear in about 35 to 40% of the overall population, and the fact that you have the genes doesn't mean you'll necessarily develop celiac disease — it simply means you have the genetic potential to do so.

The genes that predispose you to celiac disease are known as the HLA-DQ genes, and they're found on the HLA-class II complex of our DNA. Everyone gets one copy of an HLA-DQ gene from their mother and a second copy of an HLA-DQ gene from their father.

There are four general types of HLA-DQ genes, known as HLA-DQ1, HLA-DQ2, HLA-DQ3 and HLA-DQ4.

HLA-DQ1 is further broken down into HLA-DQ5 and HLA-DQ6, while HLA-DQ3 is further broken down into HLA-DQ7, HLA-DQ8 and HLA-DQ9.

Since everyone gets two HLA-DQ genes (one from their mother and one from their father), a person can have any one of many, many different gene combinations. Some of these genes predispose you to celiac disease, while preliminary research indicates other genes may predispose you to gluten sensitivity.

We know that the vast majority of people with biopsy-proven celiac disease carry either HLA-DQ2 or HLA-DQ8 (a subset of HLA-DQ3). However, since about 35% or 40% of the population carries one or both of those celiac disease genes, having the genes doesn't mean you'll definitely get celiac — there are other (mainly undiscovered) factors involved.
So What Genes Are Involved In Gluten Sensitivity?

When it comes to gluten sensitivity, it appears that the celiac disease genes aren't much in play, according to some preliminary research.

In the gluten sensitivity research study released in early 2011 by University of Maryland celiac researcher Dr. Alessio Fasano, the authors analyzed the genes of those diagnosed with gluten sensitivity, and compared them with another group of people who all had a so-called "gold standard" celiac disease diagnosis through blood tests and biopsy.

The researchers found that only 56% of those diagnosed as gluten sensitive carried DQ2 or DQ8, indicating that those genes are far less involved in the development of gluten sensitivity than they are in the development of celiac disease. However, the genes did appear more often in those with gluten sensitivity than they do in the general population, so perhaps they may play some role in gluten sensitivity — it's just not clear what role they may play.

Of course, many physicians want to see Dr. Fasano's findings replicated before they agree that gluten sensitivity exists. Dr. Fasano currently is working to identify biomarkers that could lead to a test for gluten sensitivity.
Other Genes Potentially Involved In Gluten Intolerance

Dr. Kenneth Fine, who developed the EnteroLab gluten sensitivity testing process, says he believes that everyone with the genes HLA-DQ2 and HLA-DQ8 "will present gluten to the immune system for reaction — i.e., be gluten sensitive."

But those with HLA-DQ2 and HLA-DQ8 aren't alone in their gluten sensitivity, Dr. Fine says.

He believes everyone with HLA-DQ1 and HLA-DQ3 also is predisposed to having gluten sensitivity. That means only people with two copies of HLA-DQ4 (less than 1% of the U.S. population) are immune from genetically induced gluten sensitivity, according to Dr. Fine. In his opinion, the rest have the genetic potential to develop the condition.

People with two copies of specific genes, such as HLA-DQ7 (a form of HLA-DQ3 that's similar to HLA-DQ8), risk very strong reactions to gluten, just as people with two copies of HLA-DQ2 can develop very severe celiac disease, he says.

Remember, Dr. Fine's research hasn't been replicated by others studying the genetics of celiac and gluten sensitivity, so it's not clear if it will be validated or not. However, if his predictions turn out to be accurate, that would mean almost everyone in the U.S. has some of the basic genes needed to develop gluten sensitivity. However, since not everyone does have the condition (see my article How Many People Have Gluten Sensitivity?), there must be other factors and genes involved.
Much More Research Needed on Gluten Intolerance Genes

Other researchers still need to confirm these preliminary results and hypotheses for them to be widely accepted in the medical community, and there's plenty of skepticism among physicians on whether gluten sensitivity exists at all. Based on all of this, gene testing for gluten sensitivity is unlikely to become helpful or practical in the real world at this time, if ever.

Still, both Dr. Fasano and Dr. Fine, among others, continue to study the issue of gluten sensitivity genetics. Their research indicates that even if your celiac gene test was negative, you still could have a problem with gluten.

SOURCE: https://www.verywell.com/gluten-sensitivity-genes-562967

MORE: https://www.enterolab.com/StaticPages/Faq.aspx

PMID: 11922565
DOI: 10.1111/j.1572-0241.2002.05471.x
2017-05-26 07:03:41 UTC
What is the world’s healthiest diet?

I can tell you that the longest-lived are getting 95% of their calories from plants and only 5% from animal products. Contrary to what the paleo or Atkins diet says, these folks actually eat a high carb diet. About 65% of their diet is whole grains, beans and starchy tubers. No matter where you go, the snack of choice is nuts. People who eat nuts live 2-3 years longer than non-nut eaters.

Is there any such thing as a “Longevity Food?”

Yes and no. There’s no one food that is going to assure you’ll live longer or healthier; it’s about the combination. In the “Blue Zone” of Costa Rica, we found almost the perfect food combination in corn, beans and squash—these three provide all the proteins necessary for life. In Okinawa, sweet potatoes—high in beta-carotene—fueled centenarians for nearly half of their lives. And in Sardinia, a sourdough bread, leavened with lactobacillus, actually lowers insulin response to a meal.

MORE: https://bluezones.com/2015/04/the-blue-zones-solution-secrets-of-the-worlds-healthiest-people-9-questions-for-dan-buettner/


Apparently gluten is no problem for the centenarians. Are all the centenarians HLA-DQ free?

2017-06-07 07:37:47 UTC
Post by Taka
Are all the centenarians HLA-DQ free?
The Dark Side of Wheat - New Perspectives On Celiac Disease and Wheat Intolerance

The globe-spanning presence of wheat and its exalted status among secular and sacred institutions alike differentiates this food from all others presently enjoyed by humans. Yet the unparalleled rise of wheat as the very catalyst for the emergence of ancient civilization has not occurred without a great price. While wheat was the engine of civilization’s expansion and was glorified as a "necessary food," both in the physical (staff of life) and spiritual sense (the body of Christ), those suffering from celiac disease are living testimony to the lesser known dark side of wheat. A study of celiac disease and may help unlock the mystery of why modern man, who dines daily at the table of wheat, is the sickest animal yet to have arisen on this strange planet of ours.

The Celiac Iceberg

Celiac disease (CD) was once considered an extremely rare affliction, limited to individuals of European descent. Today, however, a growing number of studies indicate that celiac disease is found throughout the world at a rate of up to 1 in every 100 persons, which is several orders of magnitude higher than previously estimated.

These findings have led researchers to visualize CD as an iceberg. The tip of the iceberg represents the relatively small number of the world’s population whose gross presentation of clinical symptoms often leads to the diagnosis of celiac disease. This is the classical case of CD characterized by gastrointestinal symptoms, malabsorption and malnourishment. It is confirmed with the "gold standard" of an intestinal biopsy. The submerged middle portion of the iceberg is largely invisible to classical clinical diagnosis, but not to modern serological screening methods in the form of antibody testing. This middle portion is composed of asymptomatic and latent celiac disease as well as "out of the intestine" varieties of wheat intolerance. Finally, at the base of this massive iceberg sits approximately 20-30% of the world’s population – those who have been found to carry the HLA-DQ locus of genetic susceptibility to celiac disease on chromosome 6.*

The "Celiac Iceberg" may not simply illustrate the problems and issues associated with diagnosis and disease prevalence, but may represent the need for a paradigm shift in how we view both CD and wheat consumption among non-CD populations.

First let us address the traditional view of CD as a rare, but clinically distinct species of genetically-determined disease, which I believe is now running itself aground upon the emerging, post-Genomic perspective, whose implications for understanding and treating disease are Titanic in proportion.

It Is Not In the Genes, But What We Expose Them To
Despite common misconceptions, monogenic diseases, or diseases that result from errors in the nucleotide sequence of a single gene are exceedingly rare. Perhaps only 1% of all diseases fall within this category, and Celiac disease is not one of them. In fact, following the completion of the Human Genome Project (HGP) in 2003 it is no longer accurate to say that our genes "cause" disease, any more than it is accurate to say that DNA alone is sufficient to account for all the proteins in our body. Despite initial expectations, the HGP revealed that there are only 20,000-25,000 genes in human DNA (genome), rather than the 100,000 + believed necessary to encode the 100,000 + proteins found in the human body (proteome).
The "blueprint" model of genetics: one gene → one protein → one cellular behavior, which was once the holy grail of biology, has now been supplanted by a model of the cell where epigenetic factors (literally: "beyond the control of the gene") are primary in determining how DNA will be interpreted, translated and expressed. A single gene can be used by the cell to express a multitude of proteins and it is not the DNA alone that determines how or what genes will be expressed. Rather, we must look to the epigenetic factors to understand what makes a liver cell different from a skin cell or brain cell. All of these cells share the exact same 3 billion base pairs that make up our genome, but it is the epigenetic factors, e.g. regulatory proteins and post-translational modifications, that make the determination as to which genes to turn on and which to silence, resulting in each cell’s unique phenotype. Moreover, epigenetic factors are directly and indirectly influenced by the presence or absence of key nutrients in the diet, as well as exposures to chemicals, pathogens and other environmental influences.
In a nutshell, what we eat and what we are exposed to in our environment directly affects our DNA and its expression.
Within the scope of this new perspective even classical monogenic diseases like cystic fibrosis (CF) can be viewed in a new, more promising light. In CF many of the adverse changes that result from the defective expression of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene may be preventable or reversible, owing to the fact that the misfolding of the CFTR gene product has been shown to undergo partial or full correction (in the rodent model) when exposed to phytochemicals found in turmeric, cayenne, and soybean Moreover, nutritional deficiencies of seleniun, zinc, riboflavin, vitamin e, etc. in the womb or early in life, may "trigger" the faulty expression or folding patterns of the CFTR gene in cystic fibrosis which might otherwise have avoided epigenetic activation. This would explain why it is possible to live into one’s late seventies with this condition, as was the case for Katherine Shores (1925-2004). The implications of these findings are rather extraordinary: epigenetic and not genetic factors are primary in determining disease outcome. Even if we exclude the possibility of reversing certain monogenic diseases, the basic lesson from the post-Genomic era is that we can’t blame our DNA for causing disease. Rather, it may have more to do with what we choose to expose our DNA to.
Celiac Disease Revisited

What all of this means for CD is that the genetic susceptibility locus, HLA-DQ, does not by itself determine the exact clinical outcome of the disease. Instead of being 'the cause,' the HLA genes may be activated as a consequence of the disease process. Thus, we may need to shift our epidemiological focus from viewing this as a classical "disease" involving a passive subject controlled by aberrant genes, to viewing it as an expression of a natural, protective response to the ingestion of something that the human body was not designed to consume.

If we view celiac disease not as an unhealthy response to a healthy food, but as a healthy response to an unhealthy food, classical CD symptoms like diarrhea may make more sense. Diarrhea can be the body’s way to reduce the duration of exposure to a toxin or pathogen, and villous atrophy can be the body’s way of preventing the absorption and hence, the systemic effects of chronic exposure to wheat.

I believe we would be better served by viewing the symptoms of CD as expressions of bodily intelligence rather than deviance. We must shift the focus back to the disease trigger, which is wheat itself.

People with celiac disease may actually have an advantage over the apparently non-afflicted because those who are "non-symptomatic" and whose wheat intolerance goes undiagnosed or misdiagnosed because they lack the classical symptoms and may suffer in ways that are equally or more damaging, but expressed more subtly, or in distant organs. Within this view celiac disease would be redefined as a protective (healthy?) response to exposure to an inappropriate substance, whereas "asymptomatic" ingestion of the grain with its concomitant "out of the intestine" and mostly silent symptoms, would be considered the unhealthy response insofar as it does not signal in an obvious and acute manner that there is a problem with consuming wheat.

It is possible that celiac disease represents both an extreme reaction to a global, species-specific intolerance to wheat that we all share in varying degrees. CD symptoms may reflect the body’s innate intelligence when faced with the consumption of a substance that is inherently toxic. Let me illustrate this point using wheat germ agglutinin (WGA), as an example.

WGA is classified as a lectin and is known to play a key role in kidney pathologies, such as IgA nephropathy. In the article: "Do dietary lectins cause disease?" the Allergist David L J Freed points out that WGA binds to "glomerular capillary walls, mesangial cells and tubules of human kidney and (in rodents) binds IgA and induces IgA mesangial deposits," indicating that wheat consumption may lead to kidney damage in susceptible individuals. Indeed, a study from the Mario Negri Institute for Pharmacological Research in Milan Italy published in 2007 in the International Journal of Cancer looked at bread consumption and the risk of kidney cancer. They found that those who consumed the most bread had a 94% higher risk of developing kidney cancer compared to those who consumed the least bread. Given the inherently toxic effect that WGA may have on kidney function, it is possible that in certain genetically predisposed individuals (e.g. HLA-DQ2/DQ8) the body – in its innate intelligence – makes an executive decision: either continue to allow damage to the kidneys (or possibly other organs) until kidney failure and rapid death result, or launch an autoimmune attack on the villi to prevent the absorption of the offending substance which results in a prolonged though relatively malnourished life. This is the explanation typically given for the body’s reflexive formation of mucous following exposure to certain highly allergenic or potentially toxic foods, e.g. dairy products, sugar, etc? The mucous coats the offending substance, preventing its absorption and facilitating safe elimination via the gastrointestinal tract. From this perspective the HLA-DQ locus of disease susceptibility in the celiac is not simply activated but utilized as a defensive adaptation to continual exposure to a harmful substance. In those who do not have the HLA-DQ locus, an autoimmune destruction of the villi will not occur as rapidly, and exposure to the universally toxic effects of WGA will likely go unabated until silent damage to distant organs leads to the diagnosis of a disease that is apparently unrelated to wheat consumption.

Loss of kidney function may only be the "tip of the iceberg," when it comes to the possible adverse effects that wheat proteins and wheat lectin can generate in the body. If kidney cancer is a likely possibility, then other cancers may eventually be linked to wheat consumption as well. This correlation would fly in the face of globally sanctioned and reified assumptions about the inherent benefits of wheat consumption. It would require that we suspend cultural, socio-economic, political and even religious assumptions about its inherent benefits. In many ways, the reassessment of the value of wheat as a food requires a William Boroughs-like moment of shocking clarity when we perceive "in a frozen moment….what is on the end of every fork." Let’s take a closer look at what is on the end of our forks.

Our biologically inappropriate diet

In a previous article, I discussed the role that wheat plays as an industrial adhesive (e.g. paints, paper mache’, and book binding-glue) in order to illustrate the point that it may not be such a good thing for us to eat. The problem is implicit in the word gluten, which literally means "glue" in Latin and in words like pastry and pasta, which derives from wheatpaste, the original concoction of wheat flour and water which made such good plaster in ancient times. What gives gluten its adhesive and difficult-to-digest qualities are the high levels of disulfide bonds it contains. These same sulfur-to-sulfur bonds are found in hair and vulcanized rubber products, which we all know are difficult to decompose and are responsible for the sulfurous odor they give off when burned.

There will be 676 million metric tons of wheat produced this year alone, making it the primary cereal of temperate regions and third most prolific cereal grass on the planet. This global dominance of wheat is signified by the Food & Agricultural Organization’s (FAO) (the United Nation’s international agency for defeating hunger) use of a head of wheat as its official symbol. Any effort to indict the credibility of this "king of grains" will prove challenging. As Rudolf Hauschka once remarked, wheat is "a kind of earth-spanning organism." It has vast socio-economic, political, and cultural significance. For example, in the Catholic Church, a wafer made of wheat is considered irreplaceable as the embodiment of Christ. .

Our dependence on wheat is matched only by its dependence on us. As Europeans have spread across the planet, so has this grain. We have assumed total responsibility for all phases of the wheat life cycle: from fending off its pests; to providing its ideal growing conditions; to facilitating reproduction and expansion into new territories. We have become so inextricably interdependent that neither species is sustainable at current population levels without this symbiotic relationship.

It is this co-dependence that may explain why our culture has for so long consistently confined wheat intolerance to categorically distinct, "genetically-based" diseases like "celiac." These categorizations may protect us from the realization that wheat exerts a vast number of deleterious effects on human health in the same way that "lactose intolerance" distracts attention from the deeper problems associated with the casein protein found in cow’s milk. Rather than see wheat for what it very well may be: a biologically inappropriate food source, we "blame the victim," and look for genetic explanations for what’s wrong with small subgroups of our population who have the most obvious forms of intolerance to wheat consumption, e.g. celiac disease, dermatitis herpetiformis, etc. The medical justification for these classifications may be secondary to economic and cultural imperatives that require the inherent problems associated with wheat consumption be minimized or occluded.

In all probability the celiac genotype represents a surviving vestigial branch of a once universal genotype, which through accident or intention, have had through successive generations only limited exposure to wheat. The celiac genotype, no doubt, survived through numerous bottlenecks or "die offs" represented by a dramatic shift from hunted and foraged/gathered foods to gluten-grain consumption, and for whatever reason simply did not have adequate time to adapt or select out the gluten-grain incompatible genes. The celiac response may indeed reflect a prior, species-wide intolerance to a novel food source: the seed storage form of the monocotyledonous cereal grasses which our species only began consuming 1-500 generations ago at the advent of the Neolithic transition (10-12,000 BC). Let us return to the image of the celiac iceberg for greater clarification.

Our Submerged Grain-Free Prehistory
The iceberg metaphor is an excellent way to expand our understanding of what was once considered to be an extraordinarily rare disease into one that has statistical relevance for us all, but it has a few limitations. For one, it reiterates the commonly held view that Celiac is a numerically distinct disease entity or "disease island," floating alongside other numerically distinct disease "ice cubes" in the vast sea of normal health. Though accurate in describing the sense of social and psychological isolation many of the afflicted feel, the celiac iceberg/condition may not be a distinct disease entity at all.
Although the HLA-DQ locus of disease susceptibility on chromosome 6 offers us a place to project blame, I believe we need to shift the emphasis of responsibility for the condition back to the disease "trigger" itself: namely, wheat and other prolamine rich grains, e.g. barley, rye, spelt, and oats. Without these grains the typical afflictions we call celiac would not exist. Within the scope of this view the "celiac iceberg" is not actually free floating but an outcropping from an entire submerged subcontinent, representing our long-forgotten (cultural time) but relatively recent metabolic prehistory as hunters-and-gatherers (biological time), where grain consumption was, in all likelihood, non-existent, except in instances of near-starvation.
The pressure on the celiac to be viewed as an exceptional case or deviation may have everything to do with our preconscious belief that wheat, and grains as a whole are the "health foods," and very little to do with a rigorous investigations of the facts.
Grains have been heralded since time immemorial as the "staff of life," when in fact they are more accurately described as a cane, precariously propping up a body starved of the nutrient-dense, low-starch vegetables, fruits, edible seeds and meats, they have so thoroughly supplanted (c.f. Paleolithic Diet). Most of the diseases of affluence, e.g. type 2 diabetes, coronary heart disease, cancer, etc. can be linked to the consumption of a grain-based diet, including secondary "hidden sources" of grain consumption in grain-fed fish, poultry, meat and milk products.
Our modern belief that grains make for good food, is simply not supported by the facts. The cereal grasses are within an entirely different family: monocotyledonous (one leafed embryo) than that from which our body sustained itself for millions of years: dicotyledonous (two leafed embryo). The preponderance of scientific evidence points to a human origin in the tropical rainforests of Africa where dicotyledonous fruits would have been available for year round consumption. It would not have been monocotyledonous plants, but the flesh of hunted animals that would have allowed for the migration out of Africa 60,000 years ago into the northern latitudes where vegetation would have been sparse or non-existent during winter months. Collecting and cooking grains would have been improbable given the low nutrient and caloric content of grains and the inadequate development of pyrotechnology and associated cooking utensils necessary to consume them with any efficiency. It was not until the end of the last Ice Age 20,000 years ago that our human ancestors would have slowly transitioned to a cereal grass based diet coterminous with emergence of civilization. 20,000 years is probably not enough time to fully adapt to the consumption of grains. Even animals like cows with a head start of thousands of years, having evolved to graze on monocotyledons and equipped as ruminants with the four-chambered fore-stomach enabling the breakdown of cellulose and anti-nutrient rich plants, are not designed to consume grains. Cows are designed to consume the sprouted mature form of the grasses and not their seed storage form. Grains are so acidic/toxic in reaction that exclusively grain-fed cattle are prone to developing severe acidosis and subsequent liver abscesses and infections, etc. Feeding wheat to cattle provides an even greater challenge:
"Beef: Feeding wheat to ruminants requires some caution as it tends to be more apt than other cereal grains to cause acute indigestion in animals which are unadapted to it. The primary problem appears to be the high gluten content of which wheat in the rumen can result in a "pasty" consistency to the rumen contents and reduced rumen motility."
(source: Ontario ministry of Agriculture food & Rural affairs)
Seeds, after all, are the "babies" of these plants, and are invested with not only the entire hope for continuance of its species, but a vast armory of anti-nutrients to help it accomplish this task: toxic lectins, phytates and oxalates, alpha-amalyase and trypsin inhibitors, and endocrine disrupters. These not so appetizing phytochemicals enable plants to resist predation of their seeds, or at least preventing them from "going out without a punch."
Wheat: An Exceptionally Unwholesome Grain
Wheat presents a special case insofar as wild and selective breeding has produced variations which include up to 6 sets of chromosomes (3x the human genome worth!) capable of generating a massive number of proteins each with a distinct potentiality for antigenicity. Common bread wheat (Triticum aestivum), for instance, has over 23,788 proteins cataloged thus far. In fact, the genome for common bread wheat is actually 6.5 times larger than that of the human genome!
With up to a 50% increase in gluten content of some varieties of wheat, it is amazing that we continue to consider "glue-eating" a normal behavior, whereas wheat-avoidance is left to the "celiac" who is still perceived by the majority of health care practitioners as mounting a "freak" reaction to the consumption of something intrinsically wholesome.
Thankfully we don’t need to rely on our intuition, or even (not so) common sense to draw conclusions about the inherently unhealthy nature of wheat. A wide range of investigation has occurred over the past decade revealing the problem with the alcohol soluble protein component of wheat known as gliadin, the sugar-binding protein known as lectin (Wheat Germ Agglutinin), the exorphin known as gliadomorphin, and the excitotoxic potentials of high levels of aspartic and glutamic acid found in wheat. Add to these the anti-nutrients found in grains such as phytates, enzyme inhibitors, etc. and you have a substance which we may more appropriately consider the farthest thing from wholesome.
The remainder of this article will demonstrate the following adverse effects of wheat on both celiac and non-celiac populations: 1) wheat causes damage to the intestines 2) wheat causes intestinal permeability 3) wheat has pharmacologically active properties 4) wheat causes damage that is "out of the intestine" affecting distant organs 5) wheat induces molecular mimicry 6) wheat contains high concentrations of excitoxins.
Gliadin is classified as a prolamin, which is a wheat storage protein high in the amino acids proline and glutamine and soluble in strong alcohol solutions. Gliadin, once deamidated by the enzyme Tissue Transglutaminase, is considered the primary epitope for T-cell activation and subsequent autoimmune destruction of intestinal villi. Yet gliadin does not need to activate an autoimmune response, e.g. Celiac disease, in order to have a deleterious effect on intestinal tissue.
In a study published in GUT in 2007 a group of researchers asked the question: "Is gliadin really safe for non-coeliac individuals?" In order to test the hypothesis that an innate immune response to gliadin is common in patients with celiac disease and without celiac disease, intestinal biopsy cultures were taken from both groups and challenged with crude gliadin, the gliadin synthetic 19-mer (19 amino acid long gliadin peptide) and 33-mer deamidated peptides. Results showed that all patients with or without Celiac disease when challenged with the various forms of gliadin produced an interleukin-15-mediated response. The researchers concluded:
"The data obtained in this pilot study supports the hypothesis that gluten elicits its harmful effect, throughout an IL15 innate immune response, on all individuals [my italics]."
The primary difference between the two groups is that the celiac disease patients experienced both an innate and an adaptive immune response to the gliadin, whereas the non-celiacs experienced only the innate response. The researchers hypothesized that the difference between the two groups may be attributable to greater genetic susceptibility at the HLA-DQ locus for triggering an adaptive immune response, higher levels of immune mediators or receptors, or perhaps greater permeability in the celiac intestine. It is possible that over and above the possibility of greater genetic susceptibility, most of the differences are from epigenetic factors that are influenced by the presence or absence of certain nutrients in the diet. Other factors such as exposure to NSAIDs like naproxen or aspirin can profoundly increase intestinal permeability in the non-celiac, rendering them susceptible to gliadin’s potential for activating secondary adaptive immune responses. This may explain why in up to 5% of all cases of classically defined celiac disease the typical HLA-DQ haplotypes are not found. However, determining the factors associated greater or lesser degrees of susceptibility to gliadin’s intrinsically toxic effect should be a secondary to the fact that it is has been demonstrated to be toxic to both non-celiacs and celiacs.
Gliadin upregulates the production of a protein known as zonulin, which modulates intestinal permeability. Over-expression of zonulin is involved in a number of autoimmune disorders, including celiac disease and Type 1 diabetes. Researchers have studied the effect of gliadin on increased zonulin production and subsequent gut permeability in both celiac and non-celiac intestines, and have found that "gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules."10 These results indicate, once again, that a pathological response to wheat gluten is a normal or human, species specific response, and is not based entirely on genetic susceptibilities. Because intestinal permeability is associated with wide range of disease states, including cardiovascular illness, liver disease and many autoimmune disorders, I believe this research indicates that gliadin (and therefore wheat) should be avoided as a matter of principle.
Gliadin can be broken down into various amino acid lengths or peptides. Gliadorphin is a 7 amino acid long peptide: Tyr-Pro-Gln-Pro-Gln-Pro-Phe which forms when the gastrointestinal system is compromised. When digestive enzymes are insufficient to break gliadorphin down into 2-3 amino acid lengths and a compromised intestinal wall allows for the leakage of the entire 7 amino acid long fragment into the blood, glaidorphin can pass through to the brain through circumventricular organs and activate opioid receptors resulting in disrupted brain function.
There have been a number of gluten exorphins identified: gluten exorphin A4, A5, B4, B5 and C, and many of them have been hypothesized to play a role in autism, schizophrenia, ADHD and related neurological conditions. In the same way that the celiac iceberg illustrated the illusion that intolerance to wheat is rare, it is possible, even probable, that wheat exerts pharmacological influences on everyone. What distinguishes the schizophrenic or autistic individual from the functional wheat consumer is the degree to which they are affected.
Below the tip of the "Gluten Iceberg," we might find these opiate-like peptides to be responsible for bread’s general popularity as a "comfort food", and our use of phrases like "I love bread," or "this bread is to die for" to be indicative of wheat’s narcotic properties. I believe a strong argument can be made that the agricultural revolution that occurred approximately 10-12,000 years ago as we shifted from the Paleolithic into the Neolithic era was precipitated as much by environmental necessities and human ingenuity, as it was by the addictive qualities of psychoactive peptides in the grains themselves.
The world-historical reorganization of society, culture and consciousness accomplished through the symbiotic relationship with cereal grasses, may have had as much to do with our ability to master agriculture, as to be mastered by it. The presence of pharmacologically active peptides would have further sweetened the deal, making it hard to distance ourselves from what became a global fascination with wheat.
An interesting example of wheat’s addictive potential pertains to the Roman army. The Roman Empire was once known as the "Wheat Empire," with soldiers being paid in wheat rations. Rome’s entire war machine, and its vast expansion, was predicated on the availability of wheat. Forts were actually granaries, holding up to a year’s worth of grain in order to endure sieges from their enemies. Historians describe soldiers’ punishment included being deprived of wheat rations and being given barley instead. The Roman Empire went on to facilitate the global dissemination of wheat cultivation which fostered a form of imperialism with biological as well as cultural roots.
The Roman appreciation for wheat, like our own, may have had less to do with its nutritional value as "health food" than its ability to generate a unique narcotic reaction. It may fulfill our hunger while generating a repetitive, ceaseless cycle of craving more of the same, and by doing so, enabling the surreptitious control of human behavior. Other researchers have come to similar conclusions. According to the biologists Greg Wadley & Angus Martin:
"Cereals have important qualities that differentiate them from most other drugs. They are a food source as well as a drug, and can be stored and transported easily. They are ingested in frequent small doses (not occasional large ones), and do not impede work performance in most people. A desire for the drug, even cravings or withdrawal, can be confused with hunger. These features make cereals the ideal facilitator of civilization (and may also have contributed to the long delay in recognizing their pharmacological properties)."
Wheat contains a lectin known as Wheat Germ Agglutinin which is responsible for causing direct, non-immune mediated damage to our intestines, and subsequent to entry into the bloodstream, damage to distant organs in our body.
Lectins are sugar-binding proteins which are highly selective for their sugar moieties. It is believed that wheat lectin, which binds to the monosaccharide N-acetyl glucosamine (NAG), provides defense against predation from bacteria, insects and animals. Bacteria have NAG in their cell wall, insects have an exoskeleton composed of polymers of NAG called chitin, and the epithelial tissue of mammals, e.g. gastrointestinal tract, have a "sugar coat" called the glycocalyx which is composed, in part, of NAG. The glycocalyx can be found on the outer surface (apical portion) of the microvilli within the small intestine.
There is evidence that WGA may cause increased shedding of the intestinal brush border membrane, reduction in surface area, acceleration of cell losses and shortening of villi, via binding to the surface of the villi. WGA can mimic the effects of epidermal growth factor (EGF) at the cellular level, indicating that the crypt hyperplasia seen in celiac disease may be due to a mitogenic reponse induced by WGA. WGA has been implicated in obesity and "leptin resistance" by blocking the receptor in the hypothalamus for the appetite satiating hormone leptin. WGA has also been shown to have an insulin-mimetic action, potentially contributing to weight gain and insulin resistance.15 And, as discussed earlier, wheat lectin has been shown to induce IgA mediated damage to the kidney, indicating that nephropathy and kidney cancer may be associated with wheat consumption.
Gliadorphin and gluten exporphins exhibit a form of molecular mimicry that affects the nervous system, but other wheat proteins effect different organ systems. The digestion of gliadin produces a peptide that is 33 amino acids long and is known as 33-mer which has a remarkable homology to the internal sequence of pertactin, the immunodominant sequence in the Bordetella pertussis bacteria (whooping cough). Pertactin is considered a highly immunogenic virulence factor, and is used in vaccines to amplify the adaptive immune response. It is possible the immune system may confuse this 33-mer with a pathogen resulting in either or both a cell-mediated and adaptive immune response against Self.
John B. Symes, D.V.M. is responsible for drawing attention to the potential excitotoxicity of wheat, dairy, and soy, due to their exceptionally high levels of the non-essential amino acids glutamic and aspartic acid. Excitotoxicity is a pathological process where glutamic and aspartic acid cause an over-activation of the nerve cell receptors (e.g. NMDA and AMPA receptor) leading to calcium induced nerve and brain injury. Of all cereal grasses commonly consumed wheat contains the highest levels of glutamic acid and aspartic acid. Glutamic acid is largely responsible for wheat’s exceptional taste. The Japanese coined the word umami to describe the extraordinary "yummy" effect that glutamic acid exerts on the tongue and palate, and invented monosodium glutamate (MSG) to amplify this sensation. Though the Japanese first synthesized MSG from kelp, wheat can also be used due to its high glutamic acid content. It is likely that wheat’s popularity, alongside its opiate-like activity, has everything to do with the natural flavor-enhancers already contained within it. These amino acids may contribute to neurodegenerative conditions such as multiple sclerosis, Alzhemier disease, Huntington’s disease, and other nervous disorders such as epilepsy, attention deficit disorder and migraines.
In this article I have proposed that celiac disease be viewed not as a rare "genetically-determined" disorder, but as an extreme example of our body communicating to us a once universal, species-specific affliction: severe intolerance to wheat. Celiac disease reflects back to us how profoundly our diet has diverged from what was, until only recently a grain free diet, and even more recently, a wheat free one. We are so profoundly distanced from that dramatic Neolithic transition in cultural time that "missing is any sense that anything is missing." The body, on the other hand, cannot help but remember a time when cereal grains were alien to the diet, because in biological time it was only moments ago.
Eliminating wheat, if not all of the members of the cereal grass family, and returning to dicotyledons or pseudo-grains like quinoa, buckwheat and amaranth, may help us roll back the hands of biological and cultural time, to a time of clarity, health and vitality that many of us have never known before. When one eliminates wheat and fills the void left by its absence with fruits, vegetables, high quality meats and foods consistent with our biological needs we may begin to feel a sense of vitality that many would find hard to imagine. If wheat really is more like a drug than a food, anesthetizing us to its ill effects on our body, it will be difficult for us to understand its grasp upon us unless and until we eliminate it from our diet. I encourage everyone to see celiac disease not as a condition alien to our own. Rather, the celiac gives us a glimpse of how profoundly wheat may distort and disfigure our health if we continue to expose ourselves to its ill effects. I hope this article will provide inspiration for non-celiacs to try a wheat free diet and judge for themselves if it is really worth eliminating.

SOURCE: http://www.greenmedinfo.com/page/dark-side-wheat-new-perspectives-celiac-disease-wheat-intolerance-sayer-ji
2017-06-07 07:41:04 UTC
While it is clear that wheat lectin has potential to do harm, it must be emphasized that the type of harm it does is harder to diagnose than in classically defined wheat/gluten allergies and celiac disease. In other words, confirmation of intolerance will not be found in antibody, allergy or intestinal biopsy testing because the damage it does is direct, and not necessarily immune-mediated, or only secondarily so.

This diagnostic "invisibility" is why lectin consumption is rarely linked to the ailments that afflict those who consume them. While lectins are not the sole or primary cause of a wide range of disorders, they are a major factor in sustaining or reinforcing injuries or diseases once they are initiated and/or established in the body.

In the case of wheat lectin (WGA) this is due to the fact that it binds to, interacts and disrupts a basic component found within all neural, connective and epithelial tissue, namely, n-acetyl-glucosamine. Once WGA makes it through a compromised mucosa and/or digestive lining, for instance, it can exert systemic effects which easily become overlooked as being caused by consuming wheat.

So Why Do Plants Like Wheat Produce Lectins?

Nature engineers, within all species, a set of defenses against predation, though not all are as obvious as the thorns on a rose or the horns on a rhinoceros. Plants do not have the cell-mediated immunity of higher life forms, like ants, nor do they have the antibody driven, secondary immune systems of vertebrates with jaws.

They must rely on a much simpler, innate immunity. It is for this reason that seeds of the grass family, e.g. rice, wheat, spelt, rye, have exceptionally high levels of defensive glycoproteins known as lectins. In a previous article we explored this in greater depth:

Wheat lectin is Nature's ingenious solution for protecting the wheat plant from the entire gamut of its natural enemies. Fungi have cell walls composed of a polymer of N-Acetylglucosamine. The cellular walls of bacteria are made from a layered structure called the peptidoglycan, a biopolymer of N-Acetyl-glucosamine. N-Acetylglucosamine is the basic unit of the biopolymer chitin, which forms the outer coverings of insects and crustaceans (shrimp, crab, etc.). All animals, including worms, fish, birds and humans, use N-Acetyglucosamine as a foundational substance for building the various tissues in their bodies, including the bones. The production of cartilage, tendons, and joints depend on the structural integrity of N-Acetylglucosamine. The mucous known as the glycocalyx, or literally, "sugar coat" is secreted in humans by the epithelial cells which line all the mucous membranes, from nasal cavities to the top to the bottom of the alimentary tube, as well as the protective and slippery lining of our blood vessels. The glycocalyx is composed largely of N-Acetylglucosamine and N-Acetylneuraminic acid (also known as sialic acid), with carbohydrate end of N-Acetylneuraminic acid of this protective glycoprotein forming the terminal sugar that is exposed to the contents of both the gut and the arterial lumen (opening). WGA's unique binding specificity to these exact two glycoproteins is not accidental. Nature has designed WGA perfectly to attach to, disrupt, and gain entry through these mucosal surfaces.

The Omnipresence of Chitin-Binding Lectin in the Western Diet

While eliminating wheat from the diet is an excellent and necessary step for improving health, it may not be alone sufficient, especially in those with serious health challenges. There are other lectins in the Western diet that have properties similar to wheat lectin (WGA), namely, "chitin-binding lectins." Remember, "chitins" are long polymers of n-acetyl-glucosamine, the primary binding target of wheat lectin. Wheat lectin and "chitin-binding lectin" therefore share functional similarities. These chitin-binding lectin containing foods are:

1) Potato [view abstract]

2) Tomato [view abstract]

3) Barley [view abstract]

4) Rye [view abstract]

5) Rice [view abstract]

Yes, you are seeing correctly: potato and rice, which are two of the most commonly used ingredients in "gluten and wheat free" products, are on the list of foods which contain a lectin structurally and functionally similar to wheat lectin.

While the "nightshade" (potato and tomato) connection with inflammation has been known about for quite some time anecdotally, rice has rarely been considered problematic and has become something of a poster child for the wheat/gluten free industry which often substitutes it for gluten-containing ingredients.

The discovery that chitin-binding lectin is broadly distributed throughout cereal grasses sheds light on how the grain-free diet produces health results superior to that of eliminating wheat and gluten containing grains alone.
How These Lectins Explain Our Dependence on NSAIDs and Glucosamine

Because many tissues within humans are comprised of n-acetyl-glucosame (a chitin-like substance) the consumption of seemingly innocuous foods such as listed above could result in a wide range of adverse effects (see WGA Research). The fact that so many Americans consume at least two or three of the above foods (plus wheat) daily may explain, for one, why degenerative joint disease (i.e. osteoarthritis) is the rule and not the exception in Western societies. This should explain the connection further:

One way to gauge just how pervasive the adverse effects of these foods are among Western populations is the popularity of the dietary supplement glucosamine. In the USA, a quarter billion dollars’ worth of glucosamine is sold annually.The main source of glucosamine on the market is from the N-Acetylglucosamine rich chitin exoskelotons of crustaceans, like shrimp and crab. Glucosamine is used for reducing pain and inflammation. We do not have a dietary deficiency of the pulverized shells of dead sea critters, just as our use of NSAIDs is not caused by a deficiency of these synthetic chemicals in our diet. When we consume glucosamine supplements, the chitin-binding lectins in our foods, instead of binding to our tissues, bind to the pulverized chitin in the glucosamine supplements, sparing us from their full impact. Many millions of Americans who have greatly reduced their pain and suffering by ingesting glucosamine and NSAIDs may be better served by removing chitin-binding lectin containing foods (the underlying cause of their malaise) from their diets. This would result in even greater relief from pain and inflammation along with far less dependency on palliative supplements and medicines alike.

The connection between these chitin-binding lectins and NSAID/Glucosamine dependency has now been explained, but this is only the tip of the "lectin" iceberg. I believe that an in-depth investigation into wheat lectin/chitin-binding lectin will reveal that these "invisible thorns" are a rather dominant contributing factor to morbidity and mortality in Westernized societies, and largely go unnoticed because they do not require immune mediation (and therefore may not be diagnosable through antibody testing) in order to inflict damage.

SOURCE: http://www.greenmedinfo.com/blog/rice-potato-tomato-may-be-inflammatory-wheat


OMG, just say NO to wheat/rye/barley, potato, tomato and rice! Are oats OK ??????

2017-06-07 13:57:36 UTC
The Judge
2017-06-07 15:48:51 UTC
This leaves humanity almost nothing to eat!
2017-06-07 16:39:44 UTC
Post by The Judge
This leaves humanity almost nothing to eat!

2017-06-08 19:18:39 UTC
Post by Taka
OMG, just say NO to wheat/rye/barley, potato, tomato and rice! Are oats OK ??????
Well there is this:

Gastroenterology. 2017 Apr 18. pii: S0016-5085(17)35474-4. doi:
10.1053/j.gastro.2017.04.009. [Epub ahead of print]

Safety of Adding Oats to a Gluten-free Diet for Patients with Celiac Disease:
Systematic Review and Meta-analysis of Clinical and Observational Studies.

Pinto-Sánchez MI(1), Causada-Calo N(1), Bercik P(1), Ford AC(2), Murray JA(3),
Armstrong D(1), Semrad C(4), Kupfer SS(4), Alaedini A(5), Moayyedi P(1), Leffler
DA(6), Verdú EF(7), Green P(5).

Author information:


Patients with celiac disease should maintain a gluten-free
diet (GFD), excluding wheat, rye, and barley. Oats might increase the nutritional
value of a GFD, but their including is controversial. We performed a systematic
review and meta-analysis to evaluate the safety of oats as part of a GFD in
patients with celiac disease.

We searched the Cochrane Central Register of Controlled Trials, MEDLINE,
and EMBASE databases for clinical trials and observational studies of the effects
of including oats in GFD of patients with celiac disease. The studies reported
patients' symptoms, results from serology tests, and findings from histologic
analyses. We used the GRADE approach to assess the quality of evidence.
RESULTS: We identified 433 studies; 28 were eligible for analysis. Of these, 6
were randomized and 2 were not-randomized controlled trials comprising a total of
661 patients-the remaining studies were observational. All randomized controlled
trials used pure/uncontaminated oats. Oat consumption for 12 months did not
affect symptoms (standardized mean difference: reduction in symptom scores in
patients who did and did not consumed oats, -0.22; 95% CI: -0.56 to 0.13; P=.22),
histologic scores (relative risk for histologic findings in patients who consumed
oats, 0.24; 95% CI, 0.01 to 4.8; P=.35), intraepithelial lymphocyte counts
(standardized mean difference: 0.21; 95% CI, reduction of 1.44 to increase in
1.86), or results from serologic tests. Subgroup analyses of adults vs children
did not reveal differences. The overall quality of evidence was low.

In a systematic review and meta-analysis, we found no evidence that
addition of oats to a GFD affects symptoms, histology, immunity, or serologic
features of patients with celiac disease. However, there were few studies for
many endpoints, as well as limited geographic distribution and low quality of
evidence. Rigorous double-blind, placebo-controlled, randomized controlled
trials, using commonly available oats sourced from different regions, are needed.


DOI: 10.1053/j.gastro.2017.04.009
PMID: 2843188
2017-06-10 16:42:36 UTC
Our modern-day gluten is not the same gluten that your grandparents ate. In order to create ever fluffier pastries and hardier wheat, scientists developed new hybrid strains of wheat that contain entirely new forms of gluten not found in any of the original plants, and this is what makes our muffins and bagels bigger and fluffier. Scientists were also able to deaminate gluten which allows it to be dissolved into liquids and other products that didn’t previously contain gluten, like lunch meat and shampoo. These two factors mean that we are not only eating a different kind of gluten than our ancestors ate, we are eating and being exposed to way more of it.

MORE: http://www.amymyersmd.com/2017/02/3-important-reasons-give-gluten-autoimmune-disease/


They f*cked up our food chain with seed oils and grains, i.e. Omega-6 + gluten .... Taka
2017-06-10 16:49:12 UTC
Rye is one of the three gluten grains. It contains a protein called secalin, which is a form of gluten. Therefore, any food containing rye as an ingredient is most definitely not safe on the gluten-free diet.

If you see mention of rye (or its Latin name, secale) on a label, you should steer clear of that product.

Triticale is a hybrid of rye and wheat, and contains gluten, so avoid any products containing triticale, too.

SOURCE: https://www.verywell.com/is-rye-gluten-free-562370

While oats do not contain the form of gluten that can not be used by people who are sensitive to the gluten in wheat, barley, and rye, it is often processed on the same equipment as is wheat so it is important to look for oatmeal that is labeled gluten-free.

SOURCE: https://saramoulton.com/2013/01/grains-which-grains-contain-gluten/
2017-07-01 01:53:43 UTC


Oh my......
2017-08-07 05:34:29 UTC
Post by Taka
"I had a man and a woman, my parents, eating pretty much the same traditional diet and reacting to it very differently: while my Dad practiced calorie restriction and was blessed with genes that tolerated gluten very well, my Mom was most probably hypothyroid in the second half of her life and gluten sensitive, which brought about obesity and diabetes. These eventually shortened her life."

SOURCE: http://ispeatright.blogspot.jp/p/ray-peat-forum-postings.html
2017-08-12 06:58:45 UTC
Is gluten the new Candida?

Celiac disease and non-celiac gluten sensitivity are very different things. The former has a large, visible, well-understood scientific foundation that is lacking in the latter.

Much of the therapeutics I was taught as part of my pharmacy degree is now of historical interest only. New evidence emerges, and clinical practice change. New treatments replace old ones – sometimes because they’re demonstrably better, and sometimes because marketing trumps evidence. The same changes occurs in the over-the-counter section of the pharmacy, but it’s here marketing seems to completely dominate. There continues to be no lack of interest in vitamin supplements, despite a growing body of evidence that suggests either no benefit, or possible harm, with many products. Yet it’s the perception that these products are beneficial seem to be seem to continue to drive sales. Nowhere is this more apparent than in areas where it’s felt medical needs are not being met. I covered one aspect a few weeks ago in a post on IgG food intolerance blood tests which are clinically useless but sold widely. The diagnosis of celiac disease came up in the comments, which merits a more thorough discussion: particularly, the growing fears over gluten consumption. It reminds me of another dietary fad that seems to have peaked and faded: the fear of Candida.

It wasn’t until I left pharmacy school and started speaking with real patients that I learned we are all filled with Candida – yeast. Most chronic diseases could be traced back to Candida, I was told. And it wasn’t just the customers who believed it. One particular pharmacy sold several different kits that purported to eliminate yeast in the body. But these didn’t contain antifungal drugs – most were combinations of laxative and purgatives, combined with psyllium and bentonite clay, all promising to sponge up toxins and Candida and restore you to an Enhanced State of Wellness™. There was a strict diet to be followed, too: No sugar, no bread – anything it was thought the yeast would consume. While you can still find these kits for sale, the enthusiasm for them seems to have waned. Whether consumers have caught on that these kits are useless, or have abandoned them because they don’t actually treat any underlying medical issues, isn’t clear.

The trend (which admittedly is hard to quantify) seems to have shifted, now that there’s a new dietary orthodoxy to question. Yeast is out. The real enemy is gluten: consume it at your own risk. There’s a growing demand for gluten labeling, and food producers are bringing out an expanding array of gluten-free (GF) foods. This is fantastic news for those with celiac disease, an immune reaction to gluten, where total gluten avoidance is essential. Only in the past decade or so has the true prevalence of celiac disease has become clear: about 1 in 100 have the disease. With the more frequent diagnosis of celiac disease, the awareness of gluten, and the harm it can cause to some, has soared. But going gluten free isn’t just for those with celiac disease. Tennis star Novak Djokovic doesn’t have celiac disease, but went on a GF diet. Headlines like “Djokovic switched to gluten-free diet, now he’s unstoppable on court” followed. Among children, there’s the pervasive but unfounded linkage of gluten consumption with autism, popularized by Jenny McCarthy and others. Even in the absence of any undesirable symptoms, gluten is being perceived as something to be avoided.

What’s been lost in an enthusiasm for gluten avoidance, is the fact that there are some people who do experience undesirable symptoms from gluten consumption, but don’t have celiac disease. It’s this group that was the focus of a recent paper in the Annals of Internal Medicine: “Nonceliac Gluten Sensitivity: Sense or Sensibility?” It’s behind a paywall, but I’ll try to summarize the paper in the context of what we know, and what we don’t know, about celiac disease and possible non-celiac gluten sensitivity.
Celiac disease

Celiac disease (CD) is an autoimmune disease, not an allergy or intolerance. The disease manifests with inflammation and injury to the bowel lining when gluten is consumed. It can cause gastrointestinal scarring and villous atrophy – resulting in permanent damage. While it normally presents with gastrointestinal symptoms, symptoms can also manifest as conditions like skin rash.The disease has been described as protean, which is appropriate. A 2001 survey of patients with confirmed celiac disease indicated patients reported symptomatic disease an average of 11 years before a diagnosis was reached. A similar survey of pediatric patients suggested a similar trend: Multiple physicians and other diagnoses. By manifesting in so many different ways, it cannot be diagnosed based on symptoms alone. So why is it so difficult to identify? It isn’t – but you need to look for it.

The immunologic response in celiac disease is a reaction to gliadin, a protein found in wheat, barley and rye. A highly effective test is now widely available. Blood is tested for IgA antibody human recombinant tissue transglutaminase (IgA-tTGA) or endomysium (IgA-EMA). These tests are both highly sensitive (90%–96%) and specific (>95%) for celiac disease. Positive results are followed by biopsy, necessary to establish a diagnosis. That diagnosis is confirmed by evaluating the effectiveness of a gluten-free diet on reported symptoms. (The full diagnostic workup is nicely summarized in the AGA Institute Medical Position Statement on the Diagnosis and Management of Celiac Disease.) Given the availability of a sensitive and specific test for celiac disease, there has been some discussion on whether widespread and routine screening for celiac disease should occur. The evidence and risk/benefit currently suggests screening in the absence of any symptoms is still unwarranted.
Non-celiac gluten sensitivity

We have a sensitive and specific test for celiac disease, so diagnosis should be straightforward, right? If you have celiac disease, you must avoid gluten for life. But what about those that test negative for celiac disease, but have symptoms from eating gluten-containing foods? There are at least five possible scenarios:

You could be IgA deficient, in which case there’s a false negative. Other laboratory tests may be done, and compared with the biopsy.
You may already be on a gluten-free diet, which will cause a false negative result.
It could simply be a false negative laboratory test result (no laboratory test is 100% sensitive and specific).
There may be some form of subclinical CD present (not yet established as fact, but plausible).
It may not be celiac disease, and other causes need to be evaluated.

It’s this last category, deemed non-celiac gluten sensitivity (NCGS) which is the subject of the recent Annals paper. Despite the identification of NCGS over 30 years ago, it’s only recently that interest seems to have exploded – I count about 336,000 Google results, but only 10 results in PubMed. Remarkably, the Annals paper points out that the public awareness of NCGS exceeds that of celiac disease [PDF].

So how do we distinguish between the CD and NCGS, objectively? Here the Annals paper includes a nice table which summarizes the challenge:

It is the protean nature of CD that makes NCGS seem so prevalent. As there’s a myriad of non-specific symptoms that could signal true CD, any any of these symptoms can also be attributed to NCGS. So what high-quality evidence exists to establish NCGS is real? Not a lot, yet. The Annals paper identifies only a single placeb0-controlled rechallenge trial, which concluded that NCGS “may exist”. There is a lack of systematic research, but lots of opinions. A recent essay [PDF] from Sapone et al in Biomed Central used a consensus-based approach to evaluate NCGS and other gluten-related disorders. It concludes by labeling gluten “toxic”, declaring celiac disease an “epidemic”, and suggesting that the prevalence of gluten sensitivity will continue to increase, supposedly because of a lack of adaptive response to deliberate changes bred into wheat strains.

But is that accurate? There are no accurate prevalence estimate for NCGS – because there are no objective signs or symptoms that can be evaluated. Given the magnification of fears of gluten among the general population, I suspect prevalence will increase simply because of perceived health concerns and rank fearmongering over gluten: nocebo effects, where an inert substances causes negative symptoms. From a scientific perspective a few possible mechanisms that have been postulated for NCGS, none of which have been established yet:

a stress response, rather than an immune response, which is unlikely given the varied manifestations of NCGS
an IgE-mediated reaction to wheat flour, possibly to another chemical compound it contains
starch malabsorption
opioid-like effects of gluten on the colon (opioid receptors in the gastrointestinal tract are the reason narcotics cause constipation)
some degree of low-grade inflammation, possibly signalling some sort of subclinical CD, presenting in a way that cannot be diagnosed with the current tests

Conclusion: Gluten sensitivity is not well-supported

The idea that gluten sensitivity is real and widespread goes far beyond the current scientific evidence, and the well-established facts of celiac disease. Time will tell if gluten avoidance follows the path of Candida, and other dietary fears and fads that preceded it. But it doesn’t need to. Given the protean nature of CD, symptoms cannot be dismissed as nocebo effects: A CD diagnosis needs to be ruled out before NCGS is even contemplated. Going gluten-free in the absence of a proper medical evaluation may not be directly harmful, but it complicates a diagnosis. Moreover, it can be expensive, and difficult to maintain 100% avoidance – essential with CD, but not established as necessary with NCGS. Besides, who really wants to cut out all gluten-containing products if they don’t need to? Until better diagnostic criteria are established, the N of 1 trial is probably the most science-based (if impractical) approach: single-blind challenges to measure for subjective or objective symptoms. Our challenge in dealing with dietary fads as health professionals is to recognize that some of our patients are suffering, and evaluate them in a science based way: without dismissing the symptoms, and without advocating dietary transformations that may be unnecessary.

Di Sabatino A, & Corazza GR (2012). Nonceliac gluten sensitivity: sense or sensibility? Annals of internal medicine, 156 (4), 309-11 PMID: 22351716

SOURCE: https://sciencebasedmedicine.org/is-gluten-the-new-candida/