• Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Member Statistics

    77,239
    Total Members
    3,093
    Most Online
    Kinz
    Newest Member
    Kinz
    Joined
  • 0

    Grain Industry Funds Study That Says White Bread Not So Bad


    Jefferson Adams


    • Consumption of wheat is plummeting, and that has the people who grow wheat wondering what to do.


    Image Caption: Grain industry study touts benefits of bread. Photo: CC--Kevin Dooley

    Celiac.com 10/03/2017 - As people eat less processed foods, and more people adopt a gluten-free diet, manufacturers are selling less and less refined wheat flour, less bread, rolls, and cereals.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Consumption of wheat is plummeting, and that has the people who grow wheat wondering what to do.

    Well, one thing wheat growers can do is hire researchers to study the problem in such a way that the logical conclusion is that foods made from refined grains, such as breads, rolls, and cereals, aren’t really that bad after all.

    And that seems to be what happened with a recent study funded by the Grain Foods Foundation, an industry group.

    Unsurprisingly, perhaps, the studypublished last month in the journal Nutrients, calls things like breads, rolls, tortillas, and ready-to-eat cereals "meaningful contributors" of nutrients like thiamin, folate, iron, zinc, and niacin.

    The study notes that such foods are also low in added sugars and fats, which is not the case with many grain foods like baked goods.

    Rather than being independent, both authors of the study work for PR companies that help other companies, including major food and beverage companies, communicate the benefits of their products.

    While it’s true that many refined grain foods provide these nutrients, there are many other sources.

    For example, foods like white beans, lentils, spinach, dark chocolate, and tofu provide iron, while oysters, beef, baked beans, yogurt, and chickpeas provide zinc.

    Is bread bad for people? Mostly not. People with celiac disease need to eat gluten-free, and should probably make an extra effort to eat foods that are nutrient dense. For most folks bread is fine, but as with many foods, not all breads are equal. Look for whole-grain breads that are nutrient dense. Watch out for the added sugar, salt, and fat that come with many processed foods.

    And don’t be swayed by industry-funded studies that tell you to eat more of the product they are peddling.

    Read more at: Healthline.com

    0


    User Feedback

    Recommended Comments

    Guest AWOL cast iron stomach

    Posted

    "And don't be swayed by industry-funded studies that tell you to eat more of the product they are peddling."Agreed, always good to know where that funding comes from.

    Share this comment


    Link to comment
    Share on other sites
    Guest Gail Ferraiolo

    Posted

    No matter what bread you eat it all has chemicals added since 1952, I myself fall into that category, it's not the wheat that is the problem it's the chemicals that are added and pesticides! Nobody in my family had celiac it is not in our genes! Wake up America if the food and drug Administration keeps people sick they make a fortune! If you can't read the ingredients then don't eat it!

    Share this comment


    Link to comment
    Share on other sites

    In 2009 grain gluten caused an immunological reaction that resulted in "leaky gut syndrome". LGS has a continuing array of problems with food ingestion. Here is the latest "poison" thrown into our foods. It caused GI disturbances & tachycardia. Cooking oils go through an insane amount of processing with chemical solvents (hexane for one), steamers, neutralizers, de-waxers, bleach and deodorizers! The only safe oil that I have found is 1st Cold Pressed olive & coconut oils and only those brands that have undergone testing. Many companies blend other oils together which are often NOT always reflected in the labeling. With the incidence of climbing GI Cancers in young people, I urge those reading this comment to consider how the processing agents and extreme heat necessary for extracting oils from seeds and plants might be affecting your body.

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • Popular Contributors

  • Ads by Google:

  • Who's Online   14 Members, 0 Anonymous, 1,024 Guests (See full list)

  • Related Articles

    Sayer Ji
    This article originally appeared in the Winter 2009 edition of Journal of Gluten Sensitivity.
    Celiac.com 07/17/2009 - 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 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 (celiac disease) was once considered an extremely rare affliction, limited to individuals of European origin.  Today, however, a growing number of studies indicate that celiac disease is found throughout the US at a rate of up to 1 in every 133 persons, which is several orders of magnitude higher than previously estimated.   
    These findings have led researchers to visualize celiac disease 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 celiac disease 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 celiac disease and wheat consumption among non-celiac disease populations.
    First let us address the traditional view of celiac disease 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 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 is sufficient to account for all the proteins in our body. Despite initial expectations, the HGP revealed that there are only 30,000-35,000 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 itself 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 DNA code, 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 celiac disease is that the genetic susceptibility locus, HLA DQ, does not determine the exact clinical outcome of the disease. Instead of being the cause, if the HLA genes are activated, they are 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 celiac disease 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 celiac disease 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 may actually have an advantage over the apparently unafflicted 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. celiac disease 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 glycoprotein 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 Metabolic 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 leaf) than that from which our body sustained itself for millions of years: dicotyledonous (two-leaf).  The preponderance of scientific evidence points to a human origin in the tropical rain forests 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 (3 genomes 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 glycoprotein 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.
    Wheat Gliadin Creates Immune Mediated Damage To The Intestines
    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.
     
    Wheat Gliadin Creates Intestinal Permeability
    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.  
     
    Wheat Gliadin Has Pharmacological Properties
    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, gl idorphin 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 civilisation (and may also have contributed to the long delay in recognising their pharmacological properties).”
     
    Wheat Lectin (Wga) Damages Our Tissue
    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.   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.
     
    Wheat Peptides Exhibit Molecular Mimicry
    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.  
     
    Wheat Contains High Levels Of Excito-Toxins
    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’s, Huntington’s disease, and other nervous disorders such as Epilepsy, Attention Deficit Disorder and Migraines.  

    Conclusion
    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.

    Jefferson Adams
    Celiac.com 02/24/2017 - Have wheat and gluten changed over time? Is the wheat we consume today substantially different to the wheat we ate fifty or one-hundred years ago? These are interesting questions that have invited a good deal of speculation, but so far, at least, no good answers.
    Dr. Chris Miller, a former faculty member at Kansas State University in Grain Science and Industry, now the director of wheat quality research at Heartland Plant Innovations, is working on a project that could allow people with celiac disease to safely consume wheat. As part of that project, Dr. Miller is studying different wheat varieties from the Kansas State University breeding program.
    So far, he has examined 50 Hard Red Winter wheat lines, which include current commercial varieties, older varieties once common, but rarely planted today, and wild relatives of wheat.
    "With these different varieties we can get a broad understanding of how genetics change over time, or if they have changed through our breeding selection," Miller says.
    Miller and his colleagues started by characterizing the varieties' traits from the field all the way through their protein characterization, their genetic makeup (which involves the plants' genotypes), end-product testing (which examines the plants' milling and baking qualities), and health and nutrition attributes.
    Eventually, they hope to have good data on all of the wheat varieties in the study. This is exploratory research, says Aaron Harries, Vice President of Research and Operations at Kansas Wheat, "We're not sure what we are going to find."
    They hope their preliminary research data will help them toward their main goal of helping people with celiac disease be able to consume wheat products without any digestion problems.
    "This is a study that's focused for the good of all human health. We're doing research here that they aren't doing anywhere else," Jordan Hildebrand, program assistant at Kansas Wheat, said. "The fact that Kansas wheat farmers took the initiative to fund the research showed their foresight and their desire to deliver a wholesome product for everyone who wants to have their bread and eat it too."
    Stay tuned for developments on this and related stories.
    Source:
    Midwestproducer.com

    Jefferson Adams
    Celiac.com 04/20/2017 - More people than ever are following a gluten-free diet, but does the diet carry health risks that could cause harm in the long run? That's a very possible scenario, according to a report published in the journal Epidemiology.
    The report presents strong data to suggest that numerous gluten-free food staples contain high levels of toxic metals, which means that many gluten-free eaters could face higher risks for cancer and other chronic illnesses.
    Moreover, the US studies both reveal that people who follow a gluten-free diet have twice as much arsenic in their urine as those who eat a non-gluten-free diet. They also have 70 per cent more mercury in their blood, along with high levels of other toxic metals, such as lead and cadmium. Clearly the report invites further study to determine if these potentially negative effects are merely statistical, or if they are actually represented in corresponding numbers of gluten-free dieters.
    So, look for more study to see if people eating gluten-free are actually having higher rates of cancer and other toxic metal-related disorders.
    Meantime, you may be able to mitigate negative effects of a gluten-free diet by choosing products with lower levels of toxic metals. California-grown rice, for example seems to have lower levels compared to Chinese rice.
    If you follow a gluten-free diet for medical reasons, keep an eye out for symptoms related to toxic metal exposure, and consult a doctor if you think you are experiencing such symptoms.
    Read more at: Celiac.com.
    Does a Gluten-free Diet Mean Higher Arsenic and Mercury Levels? Read more at The Daily Mail.



    Jefferson Adams
    Celiac.com 08/21/2017 - Can a tiny Virginia start-up change the world with a cheap, reliable devise to test food for gluten on the fly?
    With their startup called Altede, Ed and Anna Champion, together with business partner Briana Petruzzi, hope to build quick, cheap tests for all sorts of food allergens. Their first target is gluten. Altede is looking to develop a test that is reliable, sensitive to FDA levels of 20ppm gluten, costs less than $5 and could be performed within a couple of minutes while sitting at a restaurant table.
    The Altede team doesn't expect anyone to test everything they eat. But those with severe gluten intolerance might find peace of mind in a pinch.
    "We really want to keep the cost low. We think that's going to be critical," says Ed Champion. "You know, $15 and you're not going to do it. It's going to be too painful. But $3 or $5…what's your afternoon worth?"
    Altede has developed an antibody that they grow inside of and later extract from mice, a technique also used by pregnancy test manufacturers. The antibody is specially engineered to latch onto protein molecules inside gluten. A user like Anna Champion would carry the kit, which is about the size of a pack of M&M's. When she comes across a food she wants to eat but suspects may make her sick, she puts a pea-sized sample into a liquid container that comes inside the pouch.
    She would shake it up and then dip the test strip.
    The liquid would creep along the paper, passing a stripe of the antibodies Altede designed. If gluten is present, the antibodies will latch on to the proteins, accumulate on the paper and produce a visible pink line.
    So far, their prototype device can detect small amounts of gluten. The prototype looks and operates just like a pregnancy test. But the test currently takes hours, instead of minutes.
    Ed Champion says that tweaks to the chemistry will provide quicker results, though there are still a number of technical challenges to overcome. But after two years of development, Champion says the team is getting close.
    To help the, prepare their portable gluten tester for a product launch, Altede recently enrolled in the first cohort of RAMP, Roanoke's business accelerator, and received a $50,000 grant from the state's Commonwealth Research Commercialization Fund.
    Once the company can quickly and reliably test for gluten, it will use the same technology to build tests for a number of different food allergens.
    Champion has invested more than $30,000 in the venture to date. He supplies the business knowledge for the company, while Anna Champion, a Virginia Tech researcher, and Petruzzi, a Ph.D. student, are the scientific brains behind the operation.
    Stay tuned for updates on Altede and their efforts to build a better gluten test.

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.