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    Gluten-related Disorders: Not Black and White


    Dr. Rodney Ford M.D.


    • Journal of Gluten Sensitivity Spring 2016 Issue - Originally published April 14, 2016


    Gluten-related Disorders: Not Black and White
    Image Caption: Photo: CC--hardtopeel

    Celiac.com 04/20/2016 - I am likely to be accused of gluten heresy. That is because I propose that celiac disease and gluten sensitivity usually coexist. By this I mean that they are not mutually exclusive entities.


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    Image: Dr. Rodney FordIn other words, most people who have celiac disease are also gluten-sensitive. Many people who are gluten-sensitive are likely to develop celiac disease with continued gluten exposure (depending on their genetic markers).

    My observations show that the distinction between celiac disease and gluten-sensitivity (the gluten syndrome) is blurred. The purpose of published algorithms and decision trees are designed to separate out celiac disease from other gluten-illnesses. I suggest that this thinking is flawed.

    For example, most flow charts go something like this: (See Flow Chart 1 at left).

    People are selected for celiac-blood-tests for a number of reasons. If your blood tests are positive (and usually if you carry a DQ2/8 gene), then you get an endoscopy to confirm/deny the diagnosis. This allows you to be categorized either Yes-celiac disease or Not-celiac disease. There is no overlap. This is an "us-and-them" scenario.

    However, isolating YES-celiac disease from every other gluten problem does not take into account that people who have gluten-gut-damage may well have other manifestations of gluten-related disorders.

    Such simplistic algorithms (decision trees) strike problems at every decision point. Such as: Who should be tested? Who should be re-tested? When should these tests be done? At what age? On how much gluten? What tests should be done? What are the cut-off levels? How important is carrying the DQ2/8 genes? What about sero-negative celiac disease? How accurate are endoscopic biopsies? Who interprets the Marsh scale? How long should a gluten challenge be?

    Such simplistic algorithms (decision trees) also do not give satisfactory answers to the following questions:

    1. Why do 10% of people with celiac disease have little or no symptoms, despite having severe small bowel damage (villous atrophy)? This group is called "asymptomatic" celiac disease. Villous atrophy alone cannot account for the majority of gluten-related symptoms.
    2. Why do half of the people with celiac disease have autonomic nervous system dysfunction? This is the disturbance of the automatic nerve activity of your internal organs. This cannot be directly attributed to villous atrophy.
    3. Why do most people with celiac disease have some brain/mental upset, including the pervasive brain-fog? Many people have neurological disease from gluten but do not have established celiac disease.
    4. How can so many "extra-intestinal manifestations" of celiac disease be attributed to intestinal gut damage alone?

    I am sure that you will have witnessed strong feelings from the defenders of 'celiac-disease-is-a-stand-alone illness'. For instance, read these two opposing comments from Facebook:

    • Photo: CC--hardtopeelA. "I find it hard to believe that gluten intolerant people (or gluten avoiders) are as strict as us who have celiac disease."
    • B. "I am gluten intolerant (suspected Celiac but I refuse to eat gluten in order to be tested properly) … I am incredibly strict on what I eat."

    The world of gluten is not black and white! But there remains a tension between those who have "biopsy-proven" celiac disease, and those people who are "gluten-intolerant". However, there is a cross-over between gluten-sensitivity/intolerance and celiac disease. There is no sharp dividing line – there is lots of grey!

    I would like to see the support groups of both celiac disease and gluten sensitivity work together with a focus on their common ground. This is already happening in some countries. Both groups promote an accurate diagnosis and a strict gluten-free diet. But I call into question the accuracy of current diagnostic methodology.

    Another comment from Facebook is a good example of these blurred lines:
    "I had an endoscopy and I have some small intestine damage: increased intraepithelial lymphocytes, shortened villi and duodenitis. The gastroenterologist said I had gluten-sensitivity but because I was not celiac (wasn't Marsh stage 3a), he said that I didn't need to be quite as careful with gluten. But I know I am super sensitive - even a small piece of chocolate with gluten in it makes me sick for a few weeks. I suspect that I either didn't have enough gluten before the endoscopy, or I am in the early stages of developing it."

    This is what I conclude:

    1. Both groups (people with celiac disease, and people with gluten sensitivity/intolerance) come under the umbrella category of gluten-related disorders. The term non-celiac gluten-sensitivity (NCGS) excludes those with evidence of intestinal damage from gluten. But with time and continued gluten ingestion, some of these people will develop celiac disease. NCGS is part of the gluten-related disorders spectrum (see my book: www.glutenrelateddisorder.com).
    2. Both groups have an identical list of possible symptoms. They are both equally harmed by gluten. They are indistinguishable from each other without blood tests and/or endoscopy.
    3. For both groups, my recommendation is to be zero gluten. Avoidance of cross-contamination is crucial for everyone. Both groups can be exquisitely sensitive to gluten. Some celiacs experience no symptoms from gluten, making it more of a challenge for them to remain gluten-zero. Some gluten-sensitive people do not yet have overt symptoms but are developing an inflammatory state.
    4. Many people who are gluten-sensitive produce antibodies to gluten, AGA (anti-gliadin-antibodies). There is a large literature on this. AGA-positive people are more likely to develop gluten-illnesses. AGA tests are recommended in the Fasano paper the "spectrum of gluten related disorders", for the celiac and gluten sensitivity work-up (particularly for neurological disorders). I use them on a day-to-day basis in my Clinic, and so do many other practitioners. More wheat/gluten harmful proteins have yet to be identified. Early in the development of celiac disease, the person can have significant symptoms, and they may have elevated AGA antibodies, but they may have no evidence yet of intestinal damage. At this stage these two conditions are indistinguishable.
    5. How early can you diagnose celiac disease? Do you have to wait until there is substantial intestinal damage so that you can make the classic diagnosis with villous atrophy? Or do you keep on eating gluten until the damage has occurred? Or do you go strictly gluten zero and not know if you are gluten sensitive or have early celiac disease? The HLA gene (DQ2/DQ8) cannot be used as a casting vote. It is my recommendation to abandon gluten as early as possible and not wait until you have substantial intestinal damage, which may never heal.
    6. Not only is the gluten intolerant community (this includes celiac disease) confused about gluten-illness. Also, the medical fraternity is confused. The science and clinical issues are rapidly developing whilst most medical practitioners are still looking for the classic celiac with weight loss, malabsorption, and a bloated tummy (and are using an out-of-date simplistic algorithm). Many people request celiac tests of their GPs but are denied the test. The community is much more aware of gluten related disorder than medical practitioners.

    Yes, there are a lot of issues to think about. These gluten-illnesses are complicated to diagnose. My prediction is that increasing numbers of people will adopt a gluten zero diet. However, almost certainly it is much more than the substance gluten that is making us sick. It will take a long time to unravel all of these strings. Most people are after an easy answer, or a drug, or a vaccine. But I'm sure that it is going to become even more complicated as we learn more. These complexities do not show up in a simplistic algorithm.

    The way for an individual to solve this is to adopt a gluten-zero diet, lifelong.

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    This article is great at explaining all aspects of the connection between celiac disease and gluten sensitivity.

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    The fact that so many celiacs improve in only some areas of symptoms on a strict gluten free diet also says gluten is probably not the only thing making us sick. I am tired of doctors thinking that all celiacs feel 100% normal if they are gluten free. I still have a myriad of symptoms, some debilitating, and am extremely gluten free. After 15 years on the diet, my antigliadin antibodies, once off the charts, are at normal levels, anti endomysial the same, yet Ttg remains elevated. Something is still amiss.

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    Guest Gillian

    Posted

    Forgot to say that I also suffer with Hashimotos Thyroiditis an auto-immune condition that is also helped by a gluten-free diet.

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    I have celiac disease which is definitely an auto immune disease, and because i live in America eating wheat is usually out of the question. However, there is a restaurant near me that uses wheat farmed and processed in Europe that i eat at about once a month with no issues. My girlfriend can attest to this as well, because she has the same exact problems i do. For years i had wondered if gluten (from wheat) was the problem at all, but suspected that RoundUp or a similar toxin was the culprit. Finding out that i was in fact eating European wheat every month and not getting sick proved it to me. While i will concede that there is an extremely slight chance that some people actually have a wheat gluten allergy i would venture to say that most, if not all, people are simply sensitive to toxins in wheat from the farming and processing of it.

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    Guest Claire

    Posted

    From your mouth to primary care providers' ears. My son all but stopped growing between ages 12 and 13. He had reflux but no other GI symptoms. His antibodies weren't high enough, though, so we were told he didn't have celiac disease. Six years later, his antibodies were off the charts. Diagnosis was confirmed by endoscopic biopsy. Genetic test revealed DQ2.5 genes. What happened to clinical medicine? Please, "experts", stop giving primary care providers simplistic disease presentations and testing protocols. Yes, most celiac disease patients present with classic symptoms, but many do not. If a child stops growing well, suspect celiac disease...even if he doesn't fit the typical presentation. Please.

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    Guest Linda

    Posted

    I completely agree that many people who claim to just have sensitivity (or even other illnesses, like irritable bowel syndrome) are celiac and just need to save themselves a lot misery and money and strictly avoid gluten. Most of my family are celiac, if they admit it or not. My daughter and I have stay strictly gluten free for 25yrs and my grandchildren are gluten free. We are the only healthy people in our family, literally. My sister spends huge sums of money on her family's health, when all they need to do is avoid gluten. My Mother is slowly dying because she and her doctor won't completely keep her off gluten. She has so much diarrhea that she can not maintain nutritional levels sufficient to support her life. Yet she keeps eating gluten and saying it is ok for her to just eat "less" gluten, a little bit, she says is ok...and her doctors, even the nursing home she was in, don't even seem to have enough understanding of cooking without gluten to provide her with food. At the nursing home they just slid off her plate anything they "guessed" might have gluten in it...which translated to her having only reconstituted scrambled eggs for one breakfast I knew about, and traces of other things that had been on her plat still lingered...I am appalled at the ignorance of people in positions like doctors, nutritionists, cooks in nursing homes and hospitals... in my Mother's small town it seems most people don't even know what gluten is or they think it's just another fad diet, or they otherwise don't have a clue to how serious a gluten free diet is.

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    Guest Cherri Nelson

    Posted

    I'm so happy to read this from a doctor who lays it out as more complicated than black and white between celiac and/or gluten sensitivity. I was once warned by a physician that the longer I stayed gluten free, the more sensitive I would become. I sometimes wonder these days if I'm still dealing with gluten sensitivity or if I've become a celiac based on my reactions to smaller and smaller amounts of gluten setting a host of symptoms off, some of which are painful. And I too am not going to eat gluten to take a test that can be unreliable anyway. My sister nearly died at 6 months until diagnosed with celiac in 1948. I had never been told this was something for me to watch also. It's changed my life since for the first time in my life I no longer suffer from clinical anxiety and panic attacks. You can only guess at what it did to my self esteem. Unfortunately I was in my 60s before the discovery. I so wish there would be more research on this whole issue.

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    Guest Leslie

    Posted

    The fact that so many celiacs improve in only some areas of symptoms on a strict gluten free diet also says gluten is probably not the only thing making us sick. I am tired of doctors thinking that all celiacs feel 100% normal if they are gluten free. I still have a myriad of symptoms, some debilitating, and am extremely gluten free. After 15 years on the diet, my antigliadin antibodies, once off the charts, are at normal levels, anti endomysial the same, yet Ttg remains elevated. Something is still amiss.

    What are your thoughts on gluten and grain free eating as well as limiting toxins as much as possible (if you don't already)? I have read that other grains can mimic gluten and then our bodies start attacking them too.

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    Guest s fricker

    Posted

    If you suspect you have celiac, avoiding gluten is better than getting diagnosed. Diagnosis with this autoimmune disease will mess with your qualification for life insurance.

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    Dr. Rodney Ford M.D.
    Celiac.com 07/15/2016 - This week I have noticed many blogs/articles claiming that the only illness that can be caused by gluten is celiac disease. Yes, they state that celiac disease alone needs a gluten-free diet. I totally disagree with this distorted out-of-date viewpoint. There are tens of millions of non-celiac people who testify that gluten causes them significant harm. It is my suspicion that the wheat lobby is cranking up these anti-gluten-free messages as a way of stopping wheat sales from slumping. Why else promote such a barrage of misinformation?
    As if to counter such negative press, I got this email last week:
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    To me this is clear evidence that gluten can cause significant inflammatory damage to our nerves and brains. George was displaying ADHD behaviours, triggered by gluten. It is a pity that those who are ridiculing the gluten-free diet movement are attempting to deny children like George the knowledge of healing on a gluten free diet.
    Evidence points to the nervous system as the prime site of gluten damage. This theory is attractive because it gives a unifying answer that explains the following conundrums:
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    I got mad and grumpy
    I would also like to tell you about Nick. When he was 8 years old he wrote his story down for me:
    "My name is Nick and I am eight and a half years old. I had a problem when I had gluten, so my mum found Doctor Ford to help me. He helped me get off gluten. When I tasted the first chocolate biscuit it tasted weird but now I'm getting used to it. I had troubles when I was on gluten. Every day I got mad with myself and sometimes with others. I didn't want to be mad. I was grumpy." I had dizzy spells
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    I am off gluten and I have more energy
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    Mum
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    Written in the spirit of cooperation and knowledge sharing. You can read many more patient stories in my book "Gluten-Related Disorder: Sick? Tired? Grumpy?" http://www.GlutenRelatedDisorder.com 

    Susan Costen Owens
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    Another trigger for the inflammasome is homocysteine (14). The pathway to recycle homocysteine back to methionine is called remethylation, and this process requires both methylcobalamin and the folic acid cycle. Others on internet groups have brought attention to polymorphisms in one of the relevant enzymes, called MTHFR. This system is also tied to the process of making sulfate, taurine and glutathione, because homocysteine can be routed that direction when the body is trying to resolve oxidative stress. Many of these steps require B6, and heme is also needed to direct homocysteine towards transsulfuration. The issue of excess homocysteine may prove to be more important to our non-professional phagocytic cells that are found lining our blood vessels, because these same vessels can also take up oxalate, creating a condition of vascular swelling called livedo reticularis (15). Issues with both homocysteine and oxalate have been associated with atherosclerosis (16).
    Did your child's pediatrician recommend giving your child Tylenol before his immunizations to make him more comfortable about his body's reaction to his shots? Scientists have now found that Tylenol not only depletes our body's ability to deal with the oxidative stress from immunization, but it also turns on the inflammasome (17). The inflammasome will skew immune defense away from Th2 adaptive immunity, and that is unfortunate, in this case, because the process of developing a Th2 response was the whole point of giving a child a vaccine. Our vaccines are designed to contain adjuvants that skew the immune response in the Th2 direction (18) but some adjuvants may not be working as expected (19).
    Researchers sometimes look for the evidence that someone has developed antibodies before they will call an immunization a success. That test will ordinarily not be ordered by a pediatrician, but instead, a child will simply later be given, by default, a booster shot. Is there any chance the recommendation of Tylenol or other inflammasome activators could have impaired the antibody response in some children? Certainly, the new research on inflammasomes might suggest that in children who fail to make antibodies after a vaccine, a look at what is happening with innate immunity could be in order before assuming that these systems are working normally. Are doctors testing antibody titres or doing other immune testing in children with celiac sprue? This may be more important if such a child has developed another autoimmune condition.
    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).
    Why is that important? The formation of glutathione can calm down a mitochondrion that is upset enough for it to be generating reactive oxygen species (ROS). Unfortunately, scientists recently learned that the ROS produced by a mitochondrion under such stress will also trigger the inflammasome. Having adequate glutathione is especially important when our bodies are coping with the demands of immune activity, as during illness or after immunization. Unfortunately, oxalate at those times may compete with glutathione for entry into the mitochondrion at the mitochondrial dicarboxylate carrier (23).
    Until very recently, we did not know that partially digested pieces formed from gliadin could trigger the formation of the inflammasome. This occurred more in peripheral blood mononuclear cells (PBMCs) from people with celiac sprue compared to healthy donors (24). The people who did this research may not have known that people with celiac tend to be higher in oxalate than other people, and they also may not have known that oxalate by itself has been found to trigger the formation of the inflammasome. People with celiac may need to be careful about avoiding both triggers for inflammasome formation.
    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).
    The well-studied vulnerability of individuals with celiac to antibody mediated effects of gliadin came from the adaptive arm of our immunity. The HLA type is definitely known to be relevant there, but it would not be relevant to an issue of cell-mediated immunity. That is why it is a puzzle that the authors of this study did not control for oxalate by matching the control and celiac subjects for the oxalate content of their cells.
    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).
    What interventions have scientists found that will suppress inflammasome activity? The good news is that a lot of their research has involved supplements that anyone can buy in a health food store, and some people were already using them for different reasons. One of those items is resveratrol. When it was first studied, it seemed to have been made out of red wine, mostly, but our project has discovered that commercially, the usual product is made from an herb called Japanese knotwood, which is known to be high in oxalate (30). The Oxalate Project has not yet tested the oxalate content of commercially available brands of resveratrol to see how much oxalate ends up in a capsule, but that testing is on its agenda.
    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).
    Another exciting inhibitor is 3-hydroxybutyrate, which is one of the two ketones (along with acetoacetate) that our bodies make in ketosis (36). Ketosis occurs when the body is not getting enough energy from carbohydrate, and it switches into a mode of burning fat, and that produces these ketones. Some people will try to induce this switch in metabolism on purpose, like those dealing with seizures who find the seizures are controlled with a ketogenic diet. If the change that this ketogenic diet accomplished was due to down regulation of inflammasome activity, that might bring new hope or strategies to mind for individuals where this diet treatment by itself failed. Such individuals may have had a different environmental component that was still activating inflammasomes in spite of their use of the use of the ketogenic diet. This mechanism may point to yet another reason that obesity, which may have come from excess consumption of carbohydrate, has been linked with inflammasome activation (37).
    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.
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    Dr. Rodney Ford M.D.
    How Early Can You Diagnose Celiac Disease?
    Celiac.com 10/12/2016 - How early can you diagnose celiac disease? This is a most challenging question for everyone: children, parents, pediatricians, gastroenterologists and many other health professionals. This is because, like so many other diseases, celiac disease is a progressive condition that slowly creeps up on you. In addition, there is disagreement about what constitutes a definitive diagnosis of celiac disease. What if the small bowel biopsy result is at odds to the blood test results?
    It is my opinion that the fundamental diagnostic requirements for celiac disease remain unresolved. This makes early diagnosis problematic!
    Do you keep waiting (whilst suffering from symptoms) for classic gut damage to be visible in a bowel biopsy before adopting a gluten-free diet? Or do you recognize the early onset of celiac disease and go gluten-free prior to this gut damage occurring? Will you be accused of "masking" celiac disease if you are an early gluten-free adopter?
    Currently, most guideline protocols require a definitive diagnosis of celiac disease by demonstrating small bowel tissue damage. This is achieved by performing and upper gastrointestinal endoscopy, taking a tissue biopsy of the mucous lining of the small bowel, and then showing specific tissue damage (villus atrophy) under the microscope: this is the small bowel biopsy procedure.
    However there is significant controversy about the accuracy and necessity of a small bowel biopsy test. We will have a close look at the difficulties and shortcomings of these tests. But first, let's look at these diagnostic problems in relation to Francesca.
    Meet Francesca who is highly at risk of celiac disease
    So how early could we diagnose Francesca's celiac disease? She has just turned 3-years-old. Her mother has celiac disease, diagnosed over 10 years ago. So mum bought Francesca for my opinion because she had started to have some loose bowel motions (runny poops), although sometimes she did have hard bowel motions, which were difficult to pass. She also had a big distended tummy, was getting more cranky, and a bit more tired. Because of mother's celiac disease, Francesca was already consuming a smaller amount of gluten, although she was eating at least one slice of normal wheat gluten bread each day. Her mother's question was: "Has Francesca now developed celiac disease?" This problem confronts me most days in the Clinic.
    How should I investigate and manage her illness?
    What blood tests should I request? How do I interpret her results? Should I organize a small bowel biopsy? Do we look for early evidence of gluten problems, or do we wait for end stage celiac damage? Should she go on a gluten-free diet now? Should we be concerned about "masking" celiac disease? Francesca's blood tests show:
    She does carry the HLA gene DQ2: this makes her a likely candidate for developing celiac disease. The tissue-damage antibodies were normal: the tTG (tissue Trans-Glutaminase) levels were low normal, but the IgG-DGP (Diamidated Gliadin Peptide) levels were borderline (18 units, with a normal range 0-20). Her EMA (Endomesial Antibody) was negative: the borderline DGP is very suspicious and evidence of early celiac disease. IgG-AGA (Anti-Gliadin-Antibody) level was moderately raised: showing that she has developed an immune response to gluten. She has not had an endoscopy: with her tissue damage antibodies at low levels, the likelihood of abnormal tissue histology is very low. My opinion
    In my opinion, this child is at extreme risk of developing celiac disease. I would like to see her on a strict gluten zero. However, it is now up to her parents to decide whether they will wait until she actually develops gut damage, or do something now to prevent her getting a serious disease.
    What would you do if she were your child? Well her parents decided to place her gluten-free and they saw a big change for the better in just a few weeks. Her bowels become normal, her energy levels improved and she is now a happy girl.
    So what is her diagnosis? I call her early celiac disease. Others would say she has non-celiac gluten-sensitivity. Some would claim that I am unwarranted to suggest a gluten-free diet until she has a positive biopsy and they accuse me of "masking" celiac disease by treating her symptoms.
    Why let Francesca unnecessarily suffer whilst waiting for her to get progressively sicker until we can get a tissue diagnosis?
    Written in the spirit of cooperation and knowledge sharing. You can read many more patient stories in my book "Gluten-Related Disorder: Sick? Tired? Grumpy?" (www.GlutenRelatedDisorder.com).

  • Recent Articles

    Jefferson Adams
    Can a Gluten-Free Diet Normalize Vitamin D Levels for Celiac Patients?
    Celiac.com 08/16/2018 - What is the significance of vitamin D serum levels in adult celiac patients? A pair of researchers recently set out to assess the value and significance of 25(OH) and 1,25(OH) vitamin D serum levels in adult celiac patients through a comprehensive review of medical literature.
    Researchers included F Zingone and C Ciacci are affiliated with the Gastroenterology Unit, Department of Surgery, Oncology and Gastroenterology, University of Padua, Padua, Italy; and the Celiac Center, AOU San Giovanni di Dio e Ruggi di Aragona, University of Salerno, Department of Medicine and Surgery, Salerno, Italy. 
    Within the wide spectrum of symptoms and alteration of systems that characterizes celiac disease, several studies indicate a low-level of vitamin D, therefore recent guidelines suggest its evaluation at the time of diagnosis. This review examines the data from existing studies in which vitamin D has been assessed in celiac patients. 
    Our review indicates that most of the studies on vitamin D in adult celiac disease report a 25 (OH) vitamin D deficiency at diagnosis that disappears when the patient goes on a gluten-free diet, independently of any supplementation. Instead, the researchers found that levels of calcitriol, the active 1,25 (OH) form of vitamin D, fell within the normal range at the time of celiac diagnosis. 
    Basically, their study strongly suggests that people with celiac disease can recover normal vitamin D levels through a gluten-free diet, without requiring any supplementation.
    Source:
    Dig Liver Dis. 2018 Aug;50(8):757-760. doi: 10.1016/j.dld.2018.04.005. Epub 2018 Apr 13.  

    Jefferson Adams
    Could Gluten-Free Food Be Hurting Your Dog?
    Celiac.com 08/15/2018 - Grain-free food has been linked to heart disease in dogs. A canine cardiovascular disease that has historically been seen in just a few breeds is becoming more common in other breeds, and one possible culprit is grain-free dog food. 
    The disease in question is called canine dilated cardiomyopathy (DCM), and often results in congestive heart failure. DCM is historically common in large dogs such as Great Danes, Newfoundlands, Irish Wolfhounds, Saint Bernards and Doberman Pinschers, though it is also affects some Cocker Spaniels.  Numerous cases of DCM have been reported in smaller dogs, whose primary source of nutrition was food containing peas, lentils, other legume seeds or potatoes as main ingredients. These reported atypical DCM cases included Golden and Labrador Retrievers, a Whippet, a Shih Tzu, a Bulldog and Miniature Schnauzers, as well as mixed breeds. 
    As a result, the U.S. Food and Drug Administration's Center for Veterinary Medicine, along with a group of veterinary diagnostic laboratories, is investigating the possible link between DCM and pet foods containing seeds or potatoes as main ingredients. The good news is that in cases where the dog suffers no genetic component, and the disease is caught early, simple veterinary treatment and dietary change may improve heart function.
    According to Nutritional Outlook, an industry publication for makers of dietary supplements and healthy foods and beverages, there is a growing market for “free from” foods for dogs, especially gluten-free and grain-free formulations. In 2017, about one in five dog foods launched was gluten-free. So, do dogs really need to eat grain-free or gluten-free food? Probably not, according to PetMD, which notes that many pet owners are simply projecting their own food biases when choosing dog food.
    Genetically, dogs are well adapted to easily digest grains and other carbohydrates. Also, beef and dairy remain the most common allergens for dogs, so even dogs with allergies are unlikely to need to need grain-free food. 
    So, the take away here seems to be that most dogs don’t need grain-free or gluten-free food, and that it might actually be bad for the dog, not good, as the owner might imagine.
    Stay tuned for more on the FDA’s investigation and any findings they make.
    Read more at Bizjournals.com
     

    Jefferson Adams
    Did You Miss the Gluten-Free Fireworks This Past Fourth of July?
    Celiac.com 08/14/2018 - Occasionally, Celiac.com learns of an amusing gluten-free story after the fact. Such is the case of the “Gluten-Free Fireworks.” 
    We recently learned about a funny little event that happened leading up to Fourth of July celebrations in the town of Springdale in Northwest Arkansas. It seems that a sign advertising "Gluten Free Fireworks" popped up near a fireworks stand on interstate 49 in Springdale. 
    In case you missed the recent dose of Fourth of July humor, in an effort to attract customers and provide a bit of holiday levity, Pinnacle Fireworks put up a sign advertising "gluten-free fireworks.” 
    The small company is owned by Adam Keeley and his father. "A lot of the people that come in want to crack a joke right along with you," Keeley said. "Every now and then, you will get someone that comes in and says so fireworks are supposed to be gluten-free right? Have I been buying fireworks that have gluten? So then I say no, no they are gluten-free. It's just a little fun."
    Keeley said that their stand saw a steady flow of customers in the week leading up to the Fourth. In addition to selling “gluten-free” fireworks, each fireworks package sold by Pinnacle features a QR code. The code can be scanned with a smartphone. The link leads to a video showing what the fireworks look like.
    We at Celiac.com hope you and your family had a safe, enjoyable, and, yes, gluten-free Fourth of July. Stay tuned for more on gluten-free fireworks and other zany, tongue-in-cheek stories.
    Read more at kark.com
     

    Jefferson Adams
    Stress-Related Disorders Associated with Higher Risk for Autoimmune Disease
    Celiac.com 08/13/2018 - It’s not uncommon for people to have psychiatric reactions to stressful life events, and these reactions may trigger some immune dysfunction. Researchers don’t yet know whether such reactions increase overall risk of autoimmune disease.
    Are psychiatric reactions induced by trauma or other life stressors associated with subsequent risk of autoimmune disease? Are stress-related disorders significantly associated with risk of subsequent autoimmune disease?
    A team of researchers recently set out to determine whether there is an association between stress-related disorders and subsequent autoimmune disease. The research team included Huan Song, MD, PhD; Fang Fang, MD, PhD; Gunnar Tomasson, MD, PhD; Filip K. Arnberg, PhD; David Mataix-Cols, PhD; Lorena Fernández de la Cruz, PhD; Catarina Almqvist, MD, PhD; Katja Fall, MD, PhD; Unnur A. Valdimarsdóttir, PhD.
    They are variously affiliated with the Center of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; the Department of Epidemiology and Biostatistics, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; the Department of Rheumatology, University Hospital, Reykjavík, Iceland; the Centre for Rheumatology Research, University Hospital, Reykjavík, Iceland; the National Centre for Disaster Psychiatry, Department of Neuroscience, Psychiatry, Uppsala University, Uppsala, Sweden; the Stress Research Institute, Stockholm University, Stockholm, Sweden; the Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; the Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden; the Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden; the Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden; the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; and the Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
    The team conducted a Swedish register-based retrospective cohort study that included 106, 464 patients with stress-related disorders, 1,064 ,640 matched unexposed individuals, and 126 ,652 full siblings to determine whether a clinical diagnosis of stress-related disorders was significantly associated with an increased risk of autoimmune disease.
    The team identified stress-related disorder and autoimmune diseases using the National Patient Register. They used Cox model to estimate hazard ratios (HRs) with 95% CIs of 41 autoimmune diseases beyond 1 year after the diagnosis of stress-related disorders, controlling for multiple risk factors.
    The data showed that being diagnosed with a stress-related disorder, such as post-traumatic stress disorder, acute stress reaction, adjustment disorder, and other stress reactions, was significantly associated with an increased risk of autoimmune disease, compared with matched unexposed individuals. The team is calling for further studies to better understand the associations and the underlying factors.
    Source:
    JAMA. 2018;319(23):2388-2400. doi:10.1001/jama.2018.7028  

    Jefferson Adams
    Gluten-Free Bacon-Wrapped Chicken Breasts
    Celiac.com 08/11/2018 - Need a quick, easy, reliable gluten-free dish that will satisfy everyone and leave the cook with plenty of time to relax? This recipe is sure to do the trick. Best of all, it's super easy. Just grab some chicken breasts, season them, hit them with a sprig of rosemary, wrap some bacon around them, and chuck them on the grill and call it dinner. Okay, you can add some rice and veggies.
    Ingredients:
    4 skinless, boneless chicken breast halves 4 thick slices bacon 4 teaspoons garlic powder 4 small sprigs fresh rosemary salt and pepper to taste Directions:
    Heat an outdoor grill to medium-high heat, and lightly oil the grate.
    Sprinkle 1 teaspoon garlic powder on a chicken breast and season with salt and pepper. 
    Place a rosemary sprig on each chicken breast. 
    Wrap the bacon around the chicken and the rosemary. 
    Hold bacon in place with a toothpick or extra rosemary stem.
    Cook the chicken breasts until no longer pink in the center and the juices run clear, about 8 minutes per side. 
    Keep an eye out for any grill flare ups from the bacon grease. 
    Remove the toothpicks and serve with steamed rice and your favorite vegetables for a winning meal.