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    Phosphates in Processed Foods Equals Chronic Disease Concerns


    Betty Wedman-St Louis, PhD, RD


    • Journal of Gluten Sensitivity Winter 2013 Issue


    Image Caption: Jordan phosphate mines. Image: CC--Kat Masback

    Celiac.com 07/14/2017 - Dietary phosphorus occurs naturally in foods like dairy products, animal meats and legumes. The institute of Medicine recommended dietary allowance (RDA) is 700 mg/day while the NHANES data indicates that the typical American consumes more than twice that every day.


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    Phosphorus is considered an essential nutrient but it is increasingly being added to processed foods via additives (anti-caking agents to preserve moisture and color) or as a stabilizer, leavening agent or acidifier. Since it is not required to be listed on the label, it is difficult to know how much is being added and consumed. High levels of phosphorus is now being considered an independent predictive factor in mortality and morbidity from cardiovascular, kidney, and osteoporosis disorders.

    People with celiac disease need to be considering how many processed foods they are consuming as food manufacturers continue to offer increasing numbers of gluten-free processed foods. According to Packaged Facts 2012, breads, cereals and grains comprise 53% gluten-free purchases; snack foods 44%; sweet baked goods (cookies) 30%; frozen/refrigerated meals and entrees 27%; baking mixes 26% and packaged dinner/side dishes 24%.

    Phosphates in the form of food additives contribute to the increasing health implications when not consuming a fresh foods diet. Avoiding carbonated beverages is the best way to reduce phosphorus levels in the diet. Aside from that, the person with celiac disease must pay attention to ingredient statements that may include these declarations: tricalcium phosphate, trimagnesium phosphate, disodium phosphate, dipotassium phosphate. According to current regulations, these ingredients are safe when used in good manufacturing processes but the more one consumes prepared foods, the more elevated the blood phosphorus levels can rise.

    The Institute of Food Technology in its December 2012 journal states," It has been difficult for consumers to find gluten-free alternatives that taste good and have desirable texture properties. Consequently, manufacturers are looking for different ingredient solutions that will address these problems". Phosphate additives have provided that solution without consumers being aware of the health implications.

    Yes, the food world offers a wider array of gluten-free foods than ever before but just because it states "gluten-free" on the label does not mean it is a healthy food for everyday consumption. Remember: Fresh is Best!

    Here is a guide I use to help those choosing processed foods to be wiser consumers:

    • Baked Goods: cake mixes, donuts, refrigerated dough = pyrophosphates for leavening and dough "improver".
    • Beverages: phosphoric acid in colas for acidulant, pyrophosphate in chocolate milk to suspend cocoa, pyrophosphate in buttermilk for protein dispersion, tricalcium phosphate in orange juice for fortification, tetrasodium phospahte in strawberry flavored milk to bind iron to pink color.
    • Cereals: phosphate in dry cereals to aid flow through extruder and fortification.
    • Cheese: phosphoric acid in cottage cheese to set acidification, phosphate in dips, sauces, cheese slices and baked chips for emulsifying action and surface agent.
    • Imitation Dairy Products (non-dairy products): phosphate as buffer for smooth mixing into coffee and as anti-caking agent for dry powders.
    • Egg Products: phosphate for stability and color/foam improvement.
    • Ice Cream: pyrophosphate to prevent gritty texture.
    • Meat Products: tripolyphosphate for injections into ham, corned beef, sausage, franks, bologna, roast beef for moisture and color development.
    • Nutrition Bars & Meal Replacement Drinks: phosphates for fortification and microbiological stability.
    • Potatoes: phosphate in baked potato chips to create bubbles on surface, and pyrophosphate in French fries, hash browns, potato flakes to inhibit iron induced blackening.
    • Poultry: tripolyphosphate for moisture and removal of Salmonella and Campylobacter bacterial pathogens.
    • Puddings & Cheesecakes: phosphate to develop thickened texture.
    • Seafood: tripolyphosphate in shrimp for mechanical peeling, pyrophosphate in canned tuna and crab to stabilize color and crystals, surimi ("crab/sea sticks") triphosphate and pyrophosphate as cryoprotectant to protein.

    For those not having food composition tables available, here is a comparison of common snack foods to show how phosphorus levels quickly can add up. Many food companies do not provide analysis information on phosphorus because it is not required for the nutrition label.

    • Hershey Bar with Almonds - 116 mg
    • Cola Beverage (12 oz) - 44 mg
    • M&M Peanuts (1.74 oz pkg) - 93 mg
    • Yogurt (1 cup) - 300 mg
    • Total Cereal (1 cup) General Mills - 200 mg
    • Peanuts (1 oz) - 150 mg
    • Apple, raw (1 med) - 10 mg
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  • About Me

    Betty Wedman-St Louis, PhD, RD is Assistant Professor, NY Chiropractic College, MS Clinical Nutrition Program Nutrition Assessment Course & Food Science Course.  She is author of the following books:

    • Fast and Simple Diabetes Menus, McGraw Hill Companies
    • Diabetes Meals on the Run, Contemporary Books
    • Living With Food Allergies, Contemporary Books
    • Diabetic Desserts, Contemporary Books
    • Quick & Easy Diabetes Menus Cookbook, Contemporary Books
    • American Diabetes Association Holiday Cookbook and Parties & Special Celebrations Cookbook, Prentice Hall Books

     

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    Betty Wedman-St Louis, PhD, RD
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    Betty Wedman-St Louis, PhD, RD
    Celiac.com 07/18/2016 - Dietary phosphorus occurs naturally in dairy foods, animal meats, and legumes but according to the Institute of Medicine, high levels of phosphorus can be a contributor to cardiovascular, kidney and osteoporosis disorders.
    While phosphorus is considered an essential nutrient, the increased amounts found in processed foods via additives like anti-caking agents, stabilizers and leavening agents or acidifiers does not have to be stated on the nutrition label. Individuals following a gluten-free diet need to consider the health implications of phosphates found in processed foods eaten regularly in their diet. Reducing carbonated beverages is the best way to reduce phosphorus levels in the diet. Extra attention needs to be paid to the ingredient statement on foods.
    Ingredient statements may include these declarations: tri-calcium phosphate, tri-magnesium phosphate, disodium phosphate, di-potassium phosphate. Just because the label states "natural" or "organic" does not mean it is a healthy food for daily consumption. Fresh is best!
    Here is a guide to where phosphates can be found in gluten-free processed foods:
    Baked goods- cake mixes, donuts, refrigerated dough (pyrophosphates are used for leavening and as a dough "improver") Beverages- phosphoric acid in colas (acidulant), pyrophosphate in chocolate milk to suspend cocoa, pyrophosphate in buttermilk for protein dispersion, tri-calcium phosphate in orange juice for fortification, tetra-sodium phosphate in strawberry flavored milk to bind iron to pink color Cereals- phosphate in dry cereals to aid flow through extruder, fortification of vitamins Cheese- phosphoric acid in cottage cheese to set acidification, phosphate in dips, sauces, cheese slices and baked chips for emulsifying action and surface agent Imitation Dairy Products (non-dairy products)- phosphate as buffer for smooth mixing into coffee and as anti-caking agent for dry powders Egg Products- phosphate for stability and color + foam improvement Ice Cream- pyrophosphate to prevent gritty texture Meat Products- tri-phosphate for injections into ham, corned beef, sausage, franks, bologna, roast beef for moisture Nutrition Bars & Meal Replacement Drinks- phosphates for fortification and microbiological stability Potatoes- phosphate in baked potato chips to create bubbles on the surface, pyrophosphate in French fries, hash browns, potato flakes to inhibit iron induced blackening Poultry- tri-phosphate for moisture and removal of salmonella and campylobacter pathogens Pudding & Cheesecakes- phosphate to develop thickened texture Seafood- tri-phosphate in shrimp for mechanical peeling, pyrophosphate in canned tuna and crab to stabilize color and crystals, surimi (crab/sea sticks) tri-phosphate and pyrophosphate as cryoprotectant to protein {surimi contains gluten and is not recommended for gluten-free diets] Hyperphosphate levels can contribute to muscle aches, calcification of coronary arteries and skeletal issues. Many food companies do not provide phosphorus analysis information because it is not required on the label but here is a representative sample of phosphorus levels in some commonly consumed on a gluten-free diet.
    Peanuts (1 ounce) 150 mg
    Yogurt (1 cup) 300 mg
    M&M Peanuts (1.74 oz pkg) 93 mg
    Rice Krispies Cereal (1 cup) 200 mg
    Dietary recommendations for an adult for Phosphorus is 800 to 1000 mg.

    Susan Costen Owens
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    Has gluten had other ways of affecting the immune response? We have known that gluten and proteins from milk, soy, and even spinach will form opioid peptides as they are broken down. Like other opiates, these active peptides can be addictive and would be able to skew an immune response (20).Opioids can also paradoxically activate inflammasomes in the spinal column which then may provoke, amplify, and prolong pain. (21) Other work showed us that activation at the same opioid receptors that drugs use can limit our absorption of the amino acid cysteine. This amino acid is needed by our bodies in order to provide glutathione, the primary cellular antioxidant that protects us from oxidative stress, and this is especially important to save us from neurodgeneration (22).
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    In a different context, another group of scientists discovered that PBMC's exposed to titanium salts made from oxalate caused immunotoxicity when other salts of titanium did not produce that toxic effect. That experiment tells us that oxalate does enter the type of cell that was also found to respond in celiac disease to these digests of gliadin by formation of the inflammasome (25).
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    The differences they saw in response to the gliadin digest may have required higher levels of oxalate in those cells. Do we know? If that could be the case, then it becomes possible that the response they recorded in celiac cells might also happen in those who are higher in oxalate for other reasons, but who lack the HLA risk genes that are definitional of celiac. We simply cannot tell if the risk of inflammasome activation in their experiment involved having the oxalate content of these cells also working in some kind of synergism with gluten. It is important to note that here we are talking about oxalate that this type of cell may have accumulated earlier in its life or during its time in the blood. Here we are not talking about oxalate that someone may have just eaten.
    It is possible that an inflammasome-mediated function could explain why there are so many people who don't have celiac disease discovering that removing gluten from the diet makes them feel better. The academic community and others are still having a hard time believing this story (26), and cannot understand the recent popularity of gluten free foods in the general population.
    A different reason for thinking about a possible synergism between a gluten free and a reduced oxalate diet came from a recent poll done by the Oxalate Project at www.lowoxalate.info. Those results revealed that the majority of those who reported positive effects in their autoimmune disease by reducing oxalate had been extremely high in oxalate before they reduced oxalate. Curiously, 58% of those responding to the poll said they were also gluten free, but only 16% had celiac sprue. Those who were both gluten free and low oxalate reported a 10% higher positive effect from reducing oxalate than those who were not also gluten free. That could be important.
    Many scientists still think a standard American diet will keep oxalate below 200 mgs a day, but 84% of the individuals answering that poll said that they started out with levels of oxalate over 300 mgs a day. Recent changes in eating habits for high oxalate foods may have been the result of powerful advertising that has been telling people that high oxalate foods are the healthiest foods available. Anonymous poll data has no way to be verified, and that fact keeps us from assuming that we can derive information from this poll about oxalate's role (if any) in contributing to their autoimmune condition. Even so, the poll told us that out of all respondents, 73% reported a positive effect in their autoimmune condition by reducing oxalate, but those with celiac sprue (some who had other autoimmune conditions) did much better. 88% of them reported a positive effect on their autoimmune condition. That was actually a higher percentage than what was recorded for any of the other autoimmune conditions. Does that mean that it might be important for autoinflammatory processes to be careful about both gluten and oxalate? (27) We may learn the answer to that question as more people with these issues try both dietary changes together.
    Some scientists now are generating data that they feel supports the idea that excessive activity of inflammasomes could be related to the etiology of autoimmune disease (28). The changes that the inflammasome makes to our bodies can be harsh, and in fact, some scientists studied sepsis in animals and found that just by blocking inflammasome activity by various inhibitors, they could save those animals from a certain death. The irony is that the animals were still infected, but survived anyway. That means that what had been killing them was their immunological response to infection instead of the infection itself. This type of research is still very new, but it may change some of our assumptions (29).
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    The supplement quercitin is also an inflammasome inhibitor (31). CoQ10 is another supplement that has become widely available in drug stores and health food stores because it is needed to correct a mitochondrial problem created by statin drugs. Fortunately, CoQ10 also inhibits the inflammasome, mainly by keeping the mitochondrion happier and better protected from the need to generate reactive oxygen species (32). A popular source of sulfur called MSM (methylsulfonylmethane) also was found to inhibit inflammasomes (33). So has its close cousin DMSO, a solvent that was once used as a delivery system for secretin, when it was proposed as a treatment for autism (34, 35).
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    We can hope that more investigation of other activators and other inhibitors for those with seizures might yield better success. Also, the association with ketosis may explain a previously overlooked benefit experienced by people who were exercising the discipline of fasting…the age-old tradition that comes from many cultures. These traditions are more striking when realizing that obesity can activate inflammasomes and inflammasomes are thought to be behind the roots of metabolic syndrome and diabetes (38, 39).
    Pharma does have some drugs already in its cabinet which scientists have found will inhibit inflammasomes. There are probably more such drugs in the pipeline and we may soon hear advertisements for this new class of drugs. Our Oxalate project has already begun to hear of some doctors and hospitals using the over the counter inhibitors resveratrol or coQ10 to successfully protect patients who were at risk for developing sepsis.
    More research obviously needs to be done in this area and this new frontier has become very attractive to scientists. One of the first big questions they may need to ask is whether our health care protocols in Western medicine have led to over-stimulating this arm of immunity by emphasizing killing strategies with antimicrobial therapies or other drugs that may leave crystals or other debris behind. Why might that have been a problem?
    Phagocytes are upset about cellular debris and disrupted membranes. Some scientists have been finding that our bodies may stay healthier by tolerating some infections rather than experiencing the excessive immune activity that comes from activating inflammasomes. It will take a long time for some of these scientific ideas to trickle down and begin persuading doctors to make changes in their prescribing habits for antibiotics and other antimicrobials. Some doctors and other practitioners are already finding that inflammasome inhibitors could be an appropriate adjunct therapy during antibiotics. Of course, since this is such a new scientific area to study, it may take years before proper clinical studies can be done to address all these issues.
    In the meantime, it seems wise for anyone prone to autoimmune disease to avoid triggers for inflammasomes that are easy to avoid. This would include things like being overweight, eating foods that encourage uric acid formation (and the risks known for gout). It could include situations that encourage the body to make oxalate and that could include deficiencies of B6 or thiamine, or excess use of Vitamin C. It could come from excess dietary oxalate. We also need to consider the use of drugs or supplements that are known to form crystals in blood, or Tylenol, or antifungals that punch holes in cell membranes. We need to be vigilant about our status for homocysteine. We need to be careful about our level of consumption of alcoholand our exposureto other environmental contaminants. In time, we will learn of many other triggers.
    If there is a suspicion that inflammasomes are related to a disease process that we find in our bodies, then we should at least think about using one of the over the counter and safe and well-studied inflammasome suppressors. As the research continues, we can hope that scientists studying in this area will show us more ways to dial down the frequency and the unpleasant symptoms and other consequences of autoimmune disease and autoinflammation.
    References:
    1. (http://www.aarda.org/autoimmune-information/list-of-diseases/)
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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 09/20/2016 - A surprising research report from Australia that explores non celiac gluten sensitivity (1) has given rise to a number of journalistic offerings that range between offensive and downright silly, while the reporters who wrote them appear to have somewhat compromised reading skills (3, 4). That is not to say that the research report is without problems. However, at least that report requires a close reading to identify its most troubling elements (1). Specifically, it suggests that patients who claim to feel better on a gluten free diet are either deluded or confused. The research implies that these patients may actually feel better because they have reduced their consumption of the starch in the gluten grains they are avoiding. That doesn't qualify as justification for either "fake" or "b$#@@#$$" (2, 3) as stated in the titles of the above journalistic offerings. The central thrust of the research report is that their investigations showed no evidence of benefits for patients who follow a gluten free diet due to the patients' belief that they are sensitive to gluten. These researchers could have said something indicating that a low FODMAPs diet might work better to help the person with NCGS [non celiac gluten sensitivity], as it not only eliminates gluten, but it also eliminates the associated starches, and a host of other sugars and starches that may also be contributing to their digestive symptoms. But they didn't. They said, instead, that they found ".....no evidence of specific or dose-dependent effects of gluten in patients with NCGS placed on a low FODMAPs diet" (1).
    First, let's be clear about what the acronym FODMAP means. It stands for fermentable, oligosaccharides, disaccharides, monosaccharides, and polyols. They are groups of sugars and starches that can induce or exacerbate gastrointestinal symptoms. But most of the gluten grains are made up of such starches (which are quickly turned to sugar as soon as we ingest them). The protein content is relatively small. Flours made from all forms of wheat and rye are high in FODMAPs (4). These people were not masquerading as having celiac disease. Neither were they trying to mislead anyone. They simply found that they feel better when avoiding gluten grains. So why the profanity and accusations embedded in the headlines of these articles (2, 3)?
    Avoidance of these foods will often help those with digestive problems. But this can happen for a variety of reasons. For instance, in a person with lactose intolerance, that individual has stopped or reduced production of the brush border enzymes (lactase) that are needed to break apart the two constituent sugars that form lactose (galactose and glucose) the sugar found in milk. The lactose molecule, a disaccharide (di = two and saccharide = sugar) is too large to be absorbed through the cells (enterocytes) that line the intestinal wall, and then into the bloodstream. While humans may not be able to digest these larger molecules of lactose, many of the bacteria that live in our intestines do so with little problem. These microscopic residents of our GI tracts multiply rapidly in the presence of so much available food. The enormous and growing numbers of these microbes, combined with their rapid digestion of lactose, produces considerable quantities of methane gas. The resulting symptoms we experience include gut pain, flatulence, smelly stools, and diarrhea. The low FODMAP diet excludes or limits oligosaccharides (from 3 to 6 units of simple sugars) disaccharides, and monosaccharides. It also excludes sugar alcohols and fermentable foods which can produce acids, gases and/or alcohols.
    Thus, only the gluten family of proteins should have been used to "challenge" the research subjects in this study (1) that is causing all the fuss. But that wasn't done.
    As may be very quickly ascertained from the interview with Sachin Rustgi, in the spring issue of this journal, there are many structural variations in each of the families of glutens and in specific gluten structures of each strain of each of the gluten-containing grains (5). In fact, Biesiekierski et al openly acknowledge that they purchased the refined gluten they used in their study from a different supplier than was used in a previous study, conducted by some of the same researchers, that confirmed the presence of non celiac gluten sensitivity (6). The later study used a form of gluten that may not have diverged much from the original, as the research group was able to state that the glutens from both studies were similar. However, they also acknowledged that they did not characterize the other, non-gluten components of the gluten they used, either. Thus, there are two possible confounding factors just in the gluten component used in this study. Small differences in the gluten protein structures may have been sufficient to cause the dramatically different result, or some added or missing non-gluten component of the gluten purchased may have caused the different result. We have no way of telling if, or to what extent, either of these factors may have played in the different findings. Without more careful work, neither could the Biesiekierski et al research group (1).
    It is not news to many of us who are gluten sensitive that differing families of gluten can produce differing symptoms and will sometimes elicit no symptoms at all. Some of us, including those with celiac disease, also react to corn and/or rice glutens, despite very clear medical statements that this is not part of our gluten-induced disease. So some of us have a more generalized reaction to gluten, while others are reacting only to sub-groups of gluten. Still others may cross react with similar proteins from other foods. Yet I can't help but believe that when such foods cause virtually identical digestive symptoms, there is some kind of connection to our problem with digesting and metabolizing gluten. Narrow medical definitions notwithstanding, each individual who struggles with this digestive issue must find her or his best answers through trial and error. Rigid journalists who genuflect at the altar of allopathic medicine will be unable to help us navigate this hazardous swamp. Neither will researchers with pre-conceived notions, who try to conduct dietary studies in a manner developed for pharmaceutical trials.
    For instance, Sachin Rustgi acknowledged that some biopsy-diagnosed celiacs will not react to a given strain of gluten grains while others with celiac disease will mount an immune reaction against the same strain (5). So each of us may be sensitized to different short strings of amino acids that form part of one or more of the family of gluten proteins or one or more of its sub-groups. This is wholly congruent with the science that explains and depicts selective antibody formation and activation.
    And that is only one part of the complexity here. Research that tries to formulate a strain of wheat that will not trigger gluten-induced illnesses must eliminate all sensitizing agents that each person with celiac disease may respond to with selective antibody production, while trying to retain the characteristics that produce the desired taste, smell, and nutrient content. Also, few of us with gluten issues need to be told that other foods can cause us to experience similar symptoms, or exacerbate, or vary, our symptoms. It can sometimes be a very confusing quagmire where it is difficult to identify the source of our symptoms.
    Further, Biesiekierski and colleagues overtly acknowledge that their focus on fatigue might have produced better insight into NCGS by revealing "why those who follow a GFD feel better" if they had asked their question differently (1). They also acknowledge the possibilities that gluten may only cause symptoms in combination with FODMAPs, or that FODMAPs cause gut problems which result in a gluten-induced loss of a sense of wellness. Their comments in this regard commendably reflect a willingness to look beyond the surface in this matter. I would go further, based on Scott Adams' interview of Sachin Rustgi (5) and assert that not all genetic strains of wheat gluten will elicit symptoms of celiac disease in a given individual with biopsy-proven celiac disease, never mind those with NCGS. So the researchers' failure to account for patient-to-patient variability, as is seen in celiac disease, along with specific wording of questions about symptoms are yet two more confounding factors in this study. Perhaps a mixture of several forms of gluten, bereft of contaminants, would have been a better choice for Biesiekierski's group. And other precautions in formulating their questions might have been useful. But there are many more problems with this report.
    Extensive Review by Expert Panel
    Dr. Carlo Catassi and a large group of widely recognized celiac experts published a comprehensive review of the medical literature on the topic of non-celiac gluten sensitivity in September of last year. Therein, they state that: " Lack of biomarkers is still a major limitation of clinical studies, making it difficult to differentiate NCGS from other gluten related disorders" (7). Conversely, the Australian group led by Biesiekierski, asserts in their report which was published the previous month, that "Generally, NCGS is viewed as a defined illness, much like celiac disease, where gluten is the cause and trigger for symptoms" (6). At least one of these groups is confused about whether or not non celiac gluten sensitivity is well defined and well understood.
    As a student of this literature myself, I would assert that the consensus view is that this form of gluten sensitivity is far from being either well defined or well understood. In fact, there is still a great deal that is not understood even about celiac disease. Non celiac gluten sensitivity has only recently begun to be widely recognized in circles of gastrointestinal researchers. Further, the Biesiekierski group's extensive use of celiac-related antibody tests appears to ignore the widely held view that biomarkers are one of the great impediments to understanding non celiac gluten sensitivity. I would also add that while I have often argued for the use of IgG class anti-gliadin antibodies as a marker of many cases gluten sensitivity (also see Jean Duane's article in this issue) with or without symptoms, I have also maintained that there are many cases in which these antibodies are not found, yet the patient will frequently benefit from removal of gluten from her/his diet.
    A further weakness of the Biesiekierski et al study is that each of the intervals during which the low FODMAP diet (2 weeks), the gluten-containing diet at 16 grams/day (for 1 week), the low gluten diet at 2 grams /day (for 1 week), and the whey-containing diet 16 grams/day ( for 1 week) all ran for periods of time that were just too short to produce measurable serological findings in people with celiac disease. Even the washout period of 2 weeks was a minimal duration. Also, the three days allotted for the re-challenge trial was certainly too brief to produce meaningful results. Some celiac disease researchers report that only about 50% of their research subjects, all of whom had biopsy diagnosed celiac disease, produced celiac-associated antibodies after a two week challenge: "Antibody titres increased slightly from baseline to day 14 of GC [gluten challenge] but markedly by day 28" (8). This puts the one week duration of the Biesiekierski study into perspective - it is a choice that may have been directed at a specific research result. By day 28 of the Leffler et al study, 75% of the celiac patients showed markedly increased celiac associated antibodies. Thus, a single week of gluten challenge, as was used in the Biesiekierski et al study would be unlikely to produce any measureable changes in serum antibodies, even among people with celiac disease, who should reasonably be expected to react most quickly and strongly to gluten ingestion. Those with biopsy diagnosed celiac disease form the group that is currently thought to mount a much more serious and vigorous immune reaction to gluten than that seen in those with non celiac gluten sensitivity. While I do not necessarily agree with that perspective, it is wholly unreasonable to expect a reaction from a group of NCGS patients in one quarter of the time it is seen in only 75% of celiac patients.
    This Leffler et al study (8) also indicates that these celiac patients were reporting symptoms within three days of beginning the gluten challenge. Thus, it seems especially surprising that self-diagnosed gluten sensitivity would be such a contentious issue that would incite such rancorous responses as those mentioned earlier (2, 3). Because NCGS is not well characterized or understood, allowing only one week for gluten ingestion to cause symptoms, if that is our only measurement of gluten's impact on their health, might work with about three quarters of celiac patients, if antibodies are measured after 28 days, but how can anyone say that it is appropriate for NCGS? Further, the use of tests, especially serological antibodies, takes the focus off of symptoms and undermines the patients' reports of symptoms, suggesting that their claims of gluten sensitivity are either misguided or duplicitous. Meanwhile, the ~25% of those with biopsy diagnosed celiac disease had not yet produced celiac associated serum antibodies, even after four weeks of gluten challenge.
    We do not need physicians to tell us how we feel.
    While most of the limitations to the Biesiekierski et al study were actually mentioned in their report, those journalists who formulated articles and inflammatory titles that included the terms "fake" (2) and "b$#@@#$$" (3) seem to have missed reading those parts of this report. Further, they took such statements as "These data suggest that NCGS, as currently defined, might not be a discrete entity or that this entity might be confounded by FODMAP restriction" to mean that there is no such thing as NCGS. However, those of us with reading skills above the middle-school level will recognize that Biesiekierski and colleagues qualified their statement in several important ways, suggesting that FODMAP restriction could be a confounding variable or that the current definition of NCGS may need to be adjusted, or the possibility that the gluten they used may not have been appropriate. One must wonder whether these journalists are that challenged when it comes to reading? Or are they trying to raise readership? Perhaps their ads sell according to how many hits and responses their websites garner. Thus, it may make sense to offend groups that are likely to post responses to their site, as a strategy aimed at raising their advertising revenue. I can't see what other limitation or motivation there might be to so dramatize these research findings with little regard for what the researchers actually said. On another level, I hope that the field of Journalism has not become so crass that they don't bother to exercise even a modicum of critical thought when reading reports of research results. That, after all, is their function in democratic societies. They are supposed to offer insightful commentaries on current trends in politics, science, education, law enforcement, and various other facets of our democratic cultures. It is difficult to find thoughtfulness or insight in the terms "fake" and "b$#@@#$$". It is also difficult to see such reports being published when a retrospective study I was involved in remains unpublished. Perhaps that is due to the finding that the gluten free diet had a very positive impact on the behavior and scholastic performance of many children.
    The gluten sensitive community has come a long way, but many biased journalists, physicians, and researchers continue to resist the notion that gluten is a food that harms many people.
    Sources:
    Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013 Aug;145(2):320-8.e1-3. https://ca.shine.yahoo.com/gluten-intolerance-is-fake-093131285.html http://kitchenette.jezebel.com/gluten-sensitivity-is-apparently-b$#@@#$$-1577905069 http://stanfordhospital.org/digestivehealth/nutrition/DH-Low-FODMAP-Diet-Handout.pdf Adams S. Discussion with Assistant Resident Research Professor Sachin Rustgi on the Genetic Modification of Wheat to Make it Safe for Celiacs. Jrnl Glut Sens. 2014. Spring; 13 (2): 11-13. Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD,Shepherd SJ, Muir JG, Gibson PR. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011 Mar;106(3):508-514. Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A. Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders. Nutrients. 2013 Sep 26;5(10):3839-53. Leffler D, et al. (2013) Kinetics of the histological, serological and symptomatic responses to gluten challenge in adults with coeliac disease. Gut 62(7):996–1004.

    Jefferson Adams
    Celiac.com 08/29/2017 - The popularity of gluten-free products has soared, despite little evidence that gluten-free products are beneficial for people who do not have celiac disease.
    The number and range of gluten-free products continue to grow at a rapid pace, and manufacturers are adding more all the time. The proliferation of gluten-free products is inviting the scrutiny of nutritionists, some of whom are arraigning the alarm about questionable nutrition of many gluten-free foods and snacks.
    Recent products tests show that the vast majority of gluten-free snacks tested are far saltier than their non-gluten-free alternatives, say researchers. Just how much saltier? Researchers surveyed a total of 106 products, and found that many gluten-free snacks have up to five times more salt than non-gluten-free counterparts. And only a third of these products have proper warnings on their labels, according to a separate study by health campaigners.
    The team also compared salt content for each product in a particular category to the salt content (per 100g) of a randomly chosen gluten-containing equivalent product of that category. Notable differences in salt content include:
    Schar Gluten Free Pretzels (3.0/100g), twice the salt of Sainsbury's Salted Pretzels (1.5g/100g) Mrs Crimble's Original Cheese Crackers (3.5/100g), 2.5 times the salt of Ritz Original Crackers (1.38/100g) The Snack Organisation Sweet Chilli Rice Crackers (2.6/100g), 3 times as salty as Aldi's The Foodie Market Crunchy Chilli Rice Snacks (0.84/100g) These revelations invite questions about whether health-conscious shoppers are being misled.
    Nutritionists are urging shoppers to look past clever packaging, and to not automatically assume that "gluten-free" foods are healthy.
    Full Survey Data: Actiononsalt.org

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    Jefferson Adams
    Celiac.com 06/21/2018 - Would you buy a house advertised as ‘gluten-free’? Yes, there really is such a house for sale. 
    It seems a Phoenix realtor Mike D’Elena is hoping that his trendy claim will catch the eye of a buyer hungry to avoid gluten, or, at least one with a sense of humor. D’Elena said he crafted the ads as a way to “be funny and to draw attention.” The idea, D’Elena said, is to “make it memorable.” 
    Though D’Elena’s marketing seeks to capitalizes on the gluten-free trend, he knows Celiac disease is a serious health issue for some people. “[W]e’re not here to offend anybody….this is just something we're just trying to do to draw attention and do what's best for our clients," he said. 
    Still, the signs seem to be working. D'elena had fielded six offers within a few days of listing the west Phoenix home.
    "Buying can sometimes be the most stressful thing you do in your entire life so why not have some fun with it," he said. 
    What do you think? Clever? Funny?
    Read more at Arizonafamily.com.

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    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
    Our passion is to bake the very best products while bringing happiness to our customers, each other, and all those we meet!
    We are available during normal business hours at: 1-888-533-8118 EST.
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    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
    The trials are set to begin at Australia’s University of the Sunshine Coast Clinical Trials Centre. The vaccine is designed to allow people with celiac disease to consume gluten with no adverse effects. A successful vaccine could be the beginning of the end for the gluten-free diet as the only currently viable treatment for celiac disease. That could be a massive breakthrough for people with celiac disease.
    USC’s Clinical Trials Centre Director Lucas Litewka said trial participants would receive an injection of the vaccine twice a week for seven weeks. The trials will be conducted alongside gastroenterologist Dr. James Daveson, who called the vaccine “a very exciting potential new therapy that has been undergoing clinical trials for several years now.”
    Dr. Daveson said the investigational vaccine might potentially restore gluten tolerance to people with celiac disease.The trial is open to adults between the ages of 18 and 70 who have clinically diagnosed celiac disease, and have followed a strict gluten-free diet for at least 12 months. Anyone interested in participating can go to www.joinourtrials.com.
    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.