• Join our community!

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

  • Ads by Google:
     




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

    Ads by Google:



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

  • Member Statistics

    81,118
    Total Members
    4,125
    Most Online
    Julia Williams
    Newest Member
    Julia Williams
    Joined
  • 0

    Celiac Diease and Other Autoimmune Diseases Equals Low Inflammatory Diet


    Betty Wedman-St Louis, PhD, RD


    • Journal of Gluten Sensitivity Autumn 2014 Issue


    Celiac.com 08/29/2016 - In 2005 the National Institute of Health indicated more than 23 million Americans suffered from autoimmune disease. Today the projection is 30 million who experience extreme fatigue, muscle and joint pain, muscle weakness, sleeplessness, weight loss or gain, and memory problems as symptoms of autoimmune disorders.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Celiac disease has gotten the most attention in antibody research, but the current data on cross-reactivity of antibodies is allowing a better understanding of gluten sensitivity. Antigen reactivity to alpha-gliadin can trigger immune attacks on many individuals beyond those with positive DQ 2, DQ 8 and TTG test results.

    Gluten ataxia has been identified not only in people with celiac disease, but also in autism, lupus and multiple sclerosis. The lack of muscle control for movement, speech, eye coordination and swallowing can now be assessed in most autoimmune disorders.

    Gliadin reacts with foods and human tissue antigens causing symptoms beyond the gastro-intestinal tract. A low inflammatory diet customized to each person through testing for cross-reactivity or elimination diet protocols is needed to restore a state of health and well-being (for a copy of Low Inflammatory Diet & Elimination Diets check the author's website at the end of this article).

    According to Aristo Vojdani, PhD, professor of neuroimmunology at Carrick Institute and Chief Science Advisor for Cyrex Labs, about 50 percent gluten-sensitive individuals are also sensitive to dairy proteins (cow's milk, casein, whey) and sensitivity to oats depends on the variety of the grain and not just contamination from the milling process.

    In the author's personal experience, a gluten-free diet has many limitations. The reactivity between alpha gliadin and corn, millet, oats, rice and dairy has been denounced as invalid by gastroenterologists and celiac disease researchers. While at a medical school in Missouri, biopsies did not show improvement in villous atropy until all alpha gliadin sources and corn, millet, rice and oats were removed from the diet.

    Intestinal permeability or leaky gut allows antigens into the blood stream including food proteins, pathogens, and toxic chemicals which can cause inflammation. Continuous antigen exposure to tissues and organs is a factor in developing autoimmune disorders. Symptoms develop silently in the gut, joints and endocrine glands for several years. Tissue destruction with T and B lymphocyte reactions are a warning that autoimmune issues are developing during the next 5 to 10 year period until immunosuppressive drugs like corticosteroids are needed.

    To reduce the triggers to autoimmune diseases early, nutrition and lifestyle habits need adjusting.

    A Gluten-free Diet may seem easier today than 10 years ago, but current regulations in many countries allow up to 20 ppm gluten to be labeled "gluten-free". Many gliadin and cross -reactive proteins are most likely still available to create inflammatory symptoms.

    Assessing Viral Activity is key to managing autoimmune disease symptoms. Viral panels for EBV, Lyme, Bartonella, Mycoplasma, Chlamydia, CMV are available. Nutrition management of viral load is critical for the person with celiac disease and other autoimmune diseases.

    Reducing Toxic Chemicals is just as important as omitting gluten. Plastics like bisphenol A, heavy metals, pesticide residues, solvents all create inflammation. Water filtration devices that remove fluoride, heavy metals and pathogens plus stainless steel water bottles could reduce the body burden of chemicals that influence digestive function, joint movement, and immune well-being.


    0


    User Feedback

    Recommended Comments

    Guest Julie Morris

    Posted

    Very interesting and helpful information. I just wish there was someone who understands these problems that you can talk to. I have allergic and sensitivities to many things now, wheat and then eggs then it really escalated after my strokes and when I say yet again eating many foods and a great many medications. I'm looked at with disbelief or as if I'm exaggerating which is really upsetting on top of really struggling to deal with what I don't fully understand, like how to manage with what seems like my body has gone against me . Thanks for this.

    Share this comment


    Link to comment
    Share on other sites

    So interested in knowing where to start with testing for myself. Diagnosed at 33 with degenerative disc disease, 40 with celiac, 42 with Chiari I Malformation, and battling muscle and joint pain with a very active job. I can keep going in my job but would LOVE to keep going with a little less pain!

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

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

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

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

    ×   Your previous content has been restored.   Clear editor

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


  • Ads by Google:

  • 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

     

  • Popular Contributors

  • Who's Online   16 Members, 0 Anonymous, 320 Guests (See full list)

  • Related Articles

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 12/08/2015 - Is the rate of food sensitivity and allergy growing? Or are we just more concerned about it because children experience anaphylactic crisis, sometimes even dying from exposure to peanuts, strawberries, and all the other foods that most of us think of as harmless? Even if the rates are growing, what is the cause? And should we, in the gluten sensitive community, be concerned about developing such allergies? After all, celiac patients were often told that there was no greater risk of developing IgE food allergies among those with celiac disease than is experienced by the general population (1, 2). I was certainly told this, on more than one occasion, by apparently well qualified medical practitioners. Yet, more recent research is showing that those with any autoimmune disease, including celiac disease, have a much greater risk of developing such allergies (3). Unfortunately, we still have more questions than answers. Nonetheless, the issue really does warrant exploration, especially among those who are gluten sensitive. Further, since the numbers of those with non-celiac gluten sensitivity remain controversial, we can also look at the issue from another perspective.
    For instance, a study of childhood IgE allergy frequency, at a center in Texas devoted to treating allergies and similar ailments, the investigators looked at antibody reactions to cow's milk, eggs, fish, peanuts, sesame, shellfish, soy, tree nuts, and wheat. They reported that the rate of all of these allergies combined had almost tripled (from 3% to 8%) in only five years (4). That is a startling rate of increase. If this finding can be applied more broadly, it should be alarming.
    However, another research group at Cornell University in Ithaca, New York, reported that childhood emergency department visits for food allergy reactions remained stable over a nine year period, while adult visits for food allergy reactions declined over this same time period (5). The central thrust of their report appears to be that we have an improving understanding of how to manage our own and our children's allergic reactions, so emergency room visits are becoming, relatively less frequent. This may simply signal that allergies are becoming so common that, as a culture, we are becoming better versed in how to avoid or manage mild allergic manifestations.
    Yet another group of investigators in Australia state that there has been a "dramatic rise in the prevalence of IgE-mediated food allergy over recent decades, particularly among infants and young children " (6). They go on to suggest that this increase may be due to "the composition, richness and balance of the microbiota that colonize the human gut during early infancy" (6). They further assert that IgE food allergies are connected to an impaired barrier function of epithelial cells that line the intestinal wall, in combination with immune dysregulation (6).
    Still others assert that the increase in allergies may be tied to climate change via several factors including "variability of aeroallergens, food allergens and insect-based allergic venoms" (7).
    Martin Blazer, M.D., in his book titled Missing Microbes argues that overuse of antibiotics may be at the root of both the increase in food allergies, as well as the increasing prevalence of celiac disease, through disrupting the gut microbiome and selection for antibiotic-resistant strains of microbes (8).
    Some or all of the foregoing theories may well have a legitimate influence on our growing rates of allergies. As I see it, however, the various theories postulated to explain these increasing rates have left out one powerful dietary trend that has also accompanied these increases in IgE food allergy prevalence. For instance, compromised intestinal barrier function is a well documented feature of gluten grain consumption, although it is greatest in the context of celiac disease. The increased release of zonulin, triggered by eating gluten grains, may also be a critical factor in the development and persistence of the disease process, especially in cases of celiac disease, type 1 diabetes, rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, systemic lupus erythematosus, and about one quarter of cases of multiple sclerosis (9, 10).
    In the gut, gluten triggers increased release of zonulin, which weakens the junction between the epithelial cells that form the intestinal walls, and usually provide a protective barrier where these cells connect (11). The "gap" between these cells, caused by increased zonulin release, allows undigested proteins and peptides to bypass the cells that usually transport digested particles from the intestine to the bloodstream. Partly digested proteins, small peptides, also move through these epithelial cells, following the same path that fully digested food particles follow. However, according to Dr. Fasano, those are usually so degraded that they don't trigger antibody production (9). Thus, the leaky gut that has long been associated with celiac disease, and is often seen as a characteristic of, but not restricted to this ailment, is a critical stage in the development of this illness. This leakiness is, as most readers will know, reversed by a gluten-free diet.
    We are now seeing, in the peer reviewed medical literature, a wide range of ailments being identified as manifestations of undigested food proteins being "leaked" into the circulatory system. Further, there is a dose-dependent relationship between increasing gut permeability and increased gluten consumption, both in celiac disease and in other forms of autoimmunity (12). If this dose-dependent relationship also applies to many of those with other sensitivities, at admittedly lower levels of permeability (13), and if that is the dynamic that underlies much of the increasing trend of IgE food allergies, we should be seeing the rates of these allergies continue to rise in the general population. And, if we continue with our gluten gluttony, who can say how many ailments are associated with gluten consumption and increased zonulin release?
    It is also possible, perhaps even probable, that some of us experience increased zonulin release into the bloodstream, rather than into the intestinal lumen. If so, those peoples' epithelial linings of lungs, nasal passages, and blood brain barriers, may be more compromised than those individuals who primarily experience a leaky gut. By weakening these other barriers, they may invite other ailments that are less obviously triggered by gluten and other food proteins.
    Dr. Alessio Fasano has stated that new understandings of zonulin's role in autoimmunity, inflammation, and some cancers, "suggests that the autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by reestablishing [sic] the intestinal barrier function" (9). An animal study showed that AT1001, an experimental drug that blocks the action of zonulin, protected against autoimmune attack on pancreatic islet cells (9) which produce insulin. A human study of twenty-one subjects, reported similar findings (14).
    While it is true that intestinal infections have also been shown to induce zonulin release in the gut, the issue of microbes may not be as large a factor as it at first appears. When bacteria colonize our intestines, there are three possible outcomes: First, the infection may run rampant and kill us, thus solving the problem in a most undesirable manner. Second, and much more likely, we may take antibiotics and deplete or eliminate these infectious agents in our intestines. Third, and most likely, a combination of our immune systems, other microbes resident in our gut, antibiotics, and other, possibly unknown factors, may quickly or slowly bring the infectious agent under control. By reducing its numbers sufficiently that it won't pose a serious threat to our well being, and the harmful impact of these microbes has been muted.
    The second and third possibilities will be both the most common and most desirable. Also, as soon as the microbe in question is under control, zonulin release should be diminished to a point where it is either a minor factor in triggering continued zonulin release or, because it has been eradicated, the microbe will become irrelevant to zonulin release. On the other hand, for as long as we consume gluten, zonulin continues to be released, thus disrupting tight junctions in the intestinal, pulmonary, sinus, and other mucosal membranes, permitting allergens to reach our circulatory systems, ultimately giving rise to the growing prevalence of dangerous allergies that may sometimes manifest in anaphylactic reactions.
    The most important issue here seems to be the impact of gluten consumption on zonulin release, along with its impact on several protective barriers in the body, weakening them at the previously tight junctions between their cells. These include the blood brain barrier, which usually protects the brain from impurities and antibodies in the blood. It also includes the mucosa that line the lungs and nasal passages that protect us from airborne toxins and microbes. When that barrier is compromised, small particles from the air that we breathe will reach our circulation and trigger immune reactions...also known as allergies.
    Perhaps the most important barrier is in the digestive tract. It is made up of several variants of mucosa that protect the tissues of the gastrointestinal tract from toxins and the unwanted particles in our foods and beverages (well, most of them anyway). This, it seems to me, is the crux of our growing crisis with environmental allergies and the elevated zonulin levels that sometimes accompany them. And we can't even begin to combat this dynamic without first understanding it better.
    In the meantime, adding AT1001 to gluten-containing flours might be useful. Conversely, the media voices that are selling the idea that a gluten-free diet is an expensive fad might soon see research that reveals the gluten-free diet as an excellent prophylactic against developing IgE allergies, a variety of cancers, autoimmunity, some psychiatric illnesses, and many neurological diseases. In the interim, we can only use our own best judgement and decide for ourselves. Would the dietary products of gluten grains really be that great a loss to the palate? Is it a reasonable trade-off to risk falling prey to all of the potential consequences that come to us through elevated release of zonulin?
    More compellingly, perhaps, Professor Loren Cordain's assertion that humans have not had enough time to become fully adapted to eating cereal grains, especially as a dominant portion of our diet (15), appears to gain considerable support from the discovery and characterization of zonulin. Further, although some European, Asian, and northern African genes may have had as much as 15,000 years to adapt to this food source, most of the world's inhabitants have had a much shorter time to adapt. These are periods that are most appropriately measured in centuries and decades. The assumption that gluten grains can be safely consumed by all humans, because we have been eating them for "thousands of years" is unlikely to be true for most of the world's current population, and may represent a Eurocentric perspective.
    Sources:
    Csorba S, Jezerniczky J, Ilyés I, Nagy B, Dvorácsek E, Szabó B. Immunoglobulin E in the sera of infants and children. Acta Paediatr Acad Sci Hung. 1976;17(3):207-14. Greco L, De Seta L, D'Adamo G, Baldassarre C, Mayer M, Siani P, Lojodice D. Atopy and coeliac disease: bias or true relation? Acta Paediatr Scand. 1990 Jun-Jul;79(6-7):670-4. Fraser K, Robertson L. Chronic urticaria and autoimmunity. Skin Therapy Lett. 2013 Nov-Dec;18(7):5-9. Amin AJ, Davis CM. Changes in prevalence and characteristics of IgE-mediated food allergies in children referred to a tertiary care center in 2003 and 2008. Allergy Asthma Proc. 2012 Jan-Feb;33(1):95-101. Clark S, Espinola JA, Rudders SA, Banerji A, Camargo CA. Favorable trends in the frequency of U.S. emergency department visits for food allergy, 2001-2009. Allergy Asthma Proc. 2013 Sep-Oct;34(5):439-45. Molloy J, Allen K, Collier F, Tang ML, Ward AC, Vuillermin P. The potential link between gut microbiota and IgE-mediated food allergy in early life. Int J Environ Res Public Health. 2013 Dec 16;10(12):7235-56. Bielory L(1), Lyons K, Goldberg R. Climate change and allergic disease. Curr Allergy Asthma Rep. 2012 Dec;12(6):485-94. Blazer M. Missing Microbes. Harper Collins, Toronto, Canada, 2014. Fasano A. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev. 2011 Jan;91(1):151-75. Yacyshyn B, Meddings J, Sadowski D, Bowen-Yacyshyn MB. Multiple sclerosis patients have peripheral blood CD45RO+ B cells and increased intestinal permeability. Dig Dis Sci. 1996 Dec;41(12):2493-8. Tripathi A, Lammers KM, Goldblum S, Shea-Donohue T, Netzel-Arnett S, Buzza MS, Antalis TM, Vogel SN, Zhao A, Yang S, Arrietta MC, Meddings JB, Fasano A. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2. Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16799-804. Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8. Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A,Thakar M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006 Apr;41(4):408-19. Paterson BM, Lammers KM, Arrieta MC, Fasano A, Meddings JB. The safety, tolerance, pharmacokinetic and pharmacodynamic effects of single doses of AT-1001 in coeliac disease subjects: a proof of concept study. Aliment Pharmacol Ther. 2007 Sep 1;26(5):757-66. Cordain L. Cereal Grains: Humanity's Double-Edged Sword. in Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73

    Betty Wedman-St Louis, PhD, RD
    Celiac.com 04/12/2016 - Vitamin B12 is a group of cobalt containing compounds described by Alan R. Gaby, M.D. in Nutritional Medicine called cobalamins. Methylcobalamin is the coenzyme form of B12 that is critical for human health. Hydroxocobalamin is a more stable form of B12 but it first needs to be converted to an active form before use in metabolism.
    Vitamin B12 is important in DNA synthesis, red blood cell formation, homocysteine metabolism and the production of S-adenosylmethionine (SAMe). Adequate B12 is essential for proper neurological and immune function.
    The importance of Vitamin B12 in health and anemia management began during the Depression era when animal protein foods were limited in the American diet. Three physicians who reversed pernicious anemia in dogs were awarded the 1934 Nobel Prize for medicine. Dr. George Hoyt Whipple and two other physicians fed the dogs and humans 1/2 pound of fresh liver per day as a means to control anemia.
    Animal proteins—meat, poultry, fish, eggs—are the sources of Vitamin B12 for humans. Plants do not need or produce B12. How B12 gets into your blood is a complex dance of stomach acids and intrinsic factors that starts with pepsin in the stomach splitting off the B12 from the protein compound. The intrinsic factor made by the parietal cells of the stomach attaches to the B12 to be shuttled to the ileum where receptors pull it into the blood.
    Once in the blood, B12 is picked up by transcobalamin to be carried to cells throughout the body. Any excess is stored in the liver or excreted in the urine.
    If inadequate intrinsic factor is available—loss from aging or proton pump inhibitor use—B12 deficiency symptoms such as macrocytic anemia, neurological disorders and psychiatric symptoms (memory loss, depression, confusion, paranoia) may occur. Severe B12 deficiency can result in intestinal damage, hyper-pigmentation of the skin, hypotension, and immune dysfunction.
    The Institute of Medicine indicates that only 2 to 4 mcg Vitamin B12 is needed daily. The average American diet contains 5-15 mcg per day according to NHANES studies. Vegetarians and infants breastfed by vegan mothers are at greatest risk of developing B12 deficiency.
    Other factors increase the risk of developing Vitamin B12 insufficiency. Achlorydria secondary to gastritic, gastric bypass surgery, and ileal resection for Crohn’s disease need assessment due to malabsorption. Apathy abounds throughout the medical community despite the 2009 Centers for Disease Control and Prevention statistics indicating 1 out of every 31 people over 50 being B12 deficient. With increasing numbers of gastric bypass patients and Crohn’s resections, this deficiency could be significantly higher.
    Adverse symptoms can first be noted with the CBC test indicating large RBC or macrocytosis—a folate and B12 deficiency. Other symptoms may include balance problems, numb hands and feet, leg pains, early onset dementia, pre-Parkinson’s-like disease, infertility and depression.
    Many physicians are poorly educated on Vitamin B12 importance since it is a vitamin and easy to treat. Treatment with methylcobalamin injections with few definitive ways to test efficacy seems to be a primary factor. A complete medical history assessing for gut inflammation, celiac disease, GERD, recent nitric oxide use in surgery, and genetic factors like MTHFR should trigger a closer look at B12 adequacy even with a normal homocysteine (HCY) plasma test. High levels of B12 on standard blood analysis usually indicates poor absorption and not intoxification of Vitamin B12. Elevated B12 results >800pg/ml frequently indicate PPI use or low stomach acid malabsorption. Lab results <350pg/ml may still be inadequate for a patient with celiac disease, gluten enteropathy or gastric bypass surgery, so supplementation should be considered.
    Medications matter when considering Vitamin B12 status. Below are common drugs that impair absorption:
    Antacids- maalox, MOM, Mylanta, Tums Histamine blockers- Zantac, Tagamet, Axid, Pepcid Proton Pump Inhibitors- Prevacid, Prilosec, Nexium,. Omeprazole, Acidhex Colchicine Questran Metformin, Glucophage Celexa, Effexor, Elavil, Nardil, Paxil, Prozac, Zoloft, Wellbutrin Ativan, Librium, Valium, Xanax Viagra, Cialis, Levitra Compazine, Haldol, Risperdal, Tegretal Vitamin B12 supplementation is probably the safest medical treatment available. Many people need B12 injections to show improvement in their symptoms. Effectiveness of injections depends more on frequency of administration than on amount given with each injection. Those who improve with injections rarely improve with oral or sublingual products no matter how large the dose because the routes of administration are not capable of achieving high enough absorption levels.
    Treatment with Vitamin B12 needs to be continued for life. Until more research on efficacy and safety of oral B12 is available, intramuscular daily or weekly injections should be considered a standard of care, especially in celiac disease and those with gastric bypass surgery.
    A 20 page handout on Digestive Wellness is available for $15 from Dr. Betty Wedman-St Louis, 17920 Gulf Blvd, Ste 606, St. Petersburg, FL 33708. It includes information on how GMO foods destroy health which will be covered in a future article.

    Sarah  Curcio
    Celiac.com 05/24/2016 - How many of us have suffered from cross contamination? Most celiacs have felt the side effects of getting gluten in their food. If it is not your own kitchen, utensils, pots or pans it can be a bit nerve racking. It is not only extremely unpleasant, but unhealthy to our intestines as well. It can cause damage that can be very detrimental in the long run.
    This is exactly why the gluten-free label is particularly important. This gives celiacs a sense of safety, like a security blanket. However, how is that labeling decided upon? What certifications are really used? What standards are considered to ensure that it is 20 parts per million (ppm) or even less? Just think about the danger that can occur if something has to be recalled. For example, let's take a look at General Mills Cheerios versus Udi's Gluten-Free Foods.
    Now, Udi's is certified by the Gluten Free Certification Organization (GFCO), which is an industry program of the Gluten Intolerance Group (GIG.) Whereas Cheerios, takes the oats, used to make the cereal, and puts it through a proprietary, mechanical system. This is supposed to remove any cross-contamination from wheat, barley or rye, according to General Mills. How safe is this for individuals with celiac disease? This is why standards are very vital.
    Now, the GFCO requires that all finished products' ingredients, using their logo, contain 10ppm or even less of gluten. It requires a stringent review process, in order to gain approval. Plus, barley-based ingredients are absolutely not allowed, under any circumstances.
    Then, you look at Cheerios and the differences are as plain as day. Recently, there was a major recall of 1.8 million boxes due to an error where a gluten ingredient was accidentally added. General Mills issued a recall of some Original Cheerios and Honey Nut Cheerios cereal because some boxes were labeled as gluten-free but actually contained wheat.
    This is absolutely not safe for the celiac community. This improper labeling can be dangerous and there are no certifications or review processes like the GFCO. The thought of becoming ill from the cross-contamination is not on any celiac's to do list. Having certified oats versus regular oats is safer that simply having the wheat washed out. The oat fields are way too close to the wheat fields.
    In the end, which would you rather purchase? There is Certified Gluten Free Foods versus just gluten-free foods. Think about your villi because they really should be up and not down!
    References:
    Udi's Gluten Free - FAQs. Retrieved from: http://udisglutenfree.com/faq/ Gluten Intolerance Group - The Gluten-Free Certification Organization. Retrieved from http://www.gfco.org/ CNBC - General Mills recalls 1.8M Cheerios boxes for allergens. Retrieved from http://www.glutenfreeliving.com/gluten-free-foods/diet/gluten-free-cheerios/ Gluten Free Living - Gluten-Free Cheerios. Retrieved from http://www.cnbc.com/2015/10/05/general-mills-recalls-cheerios-for-allergen-issue.html

    Betty Wedman-St Louis, PhD, RD
    Celiac.com 06/16/2016 - Do you realize that metabolic and emotional stress, hormonal imbalance and food sensitivities all impact digestion? Many individuals believe that once they stop eating gluten, digestive disorders will disappear. Nothing could be further from the truth as we take a closer look at gastroenterology and the link between the gut and brain.
    The adult gut has between 10 trillion and 100 trillion bacteria that make up the microbiome or surface of the intestines. The goal for digestive wellness is to be sure that there are more GOOD bacteria than BAD bacteria in the microbiome. Food choices, antibiotic use and lifestyle play an important part in creating that balance. Endocrine disrupting chemicals in plastics, along with artificial sweeteners all influence the bacteria or microbiome levels.
    The bacteria content of the gut begins at birth. A vaginal delivery results in a microbiome from the mother while a cesarean section produces a microbiome from everyone who handles the infant. Gut bacteria levels are also influenced by breast feeding versus the use of infant formula.
    Diets deficient in fruits and vegetables mean less antioxidants are consumed so free radicals can destroy digestive and immune function. In addition, fruits and vegetables provide fiber for bacteria to grow on. Current research from the Journal of Clinical Nutrition indicates high fiber diets yield more bacteroides bacteria growth that helps control body weight. Low fiber diets result in more firmicute bacteria which produces weight gain and can lead to obesity.
    Microbiological safety in fresh produce continues to gain prominence in the media. Fresh cut, RTE (ready to eat) produce in convenient packages leads the way in food safety recalls. Fruits and vegetables are prone to microbial contamination from irrigation water, soil, fertilizers, insects, animal feces and field workers during pre-harvest processing. After harvest, the washing and sanitation procedures lack oversight. Remember to wash all raw fruits and vegetables to minimize food poisoning potential.
    Listeria monocytogenes is one of the leading causes of death from food borne illness. It is found in raw milk, cheese, and packaged deli meats. Flu-like symptoms can last days to weeks, and in pregnant women listeria infection can lead to miscarriage.
    Noroviruses make the news regularly, especially on cruise ships. Common food sources include raw produce and shellfish such as clams, mussels, scallops and oysters. Symptoms begin as early s 12 hours after ingestion and the malaise disappears 3 to 4 days later.
    Salmonella continues to plague many with chills, nausea, joint pain and headaches beginning 12 hours post ingestion. Eggs, poultry and raw produce are major sources of salmonella.
    Probiotics are an important addition to the celiac diet for balancing the bacteria levels in the GI tract. They should be taken WITH food to reduce the degradation in an acid stomach. Research has shown that urinary tract and vaginal infections have an improved management rate when lactobacillus and bifidobacterium multi-species probiotics are used.
    Probiotics are live bacteria which have been shown to reduce inflammation in the gastrointestinal tract. They also reduce intestinal permeability and influence serotonin and melatonin production in the gut.
    So since the human gut contains 10 times more bacteria than all the human cells in our body, keeping a healthy balance of bacteria in the gut is critical for digestive wellness.

    Susan Costen Owens
    Celiac.com 07/29/2016 - Celiac is an autoimmune condition, and along with other autoimmune diseases, scientists are beginning to have a larger context for understanding what could be contributing to its immune dysregulation. In the last decades we've seen diseases becoming prevalent now that look very different from the diseases of our ancestors. The American Autoimmune and Related Diseases Association lists 159 autoimmune diseases on their website (1), but most of these diseases are very new.
    In recent years, scientists began to identify and explore a new complex that was identified within our cells and belongs to our immunological line of defense. This new player is part of innate immunity, which is also called cell-mediated immunity. This is our body's rapid responder, and its approach to immunity is more like hand to hand combat. Its role is surveillance, and it uses generalized markers to identify something as an enemy and something the immune system needs to defeat. It looks for evidence of infection from bacteria, fungi, viruses and parasites but it also analyzes cellular debris. It is looking for any sort of danger signal that conveys the message that life is not normal as it ought to be (2). This analysis can even include looking for changes in pH (3).
    The innate branch of the immune system is dependent on cells that are called phagocytes, and these cells like to engulf small pieces of things they encounter, in a process called phagocytosis. Often these cells will be breaking down those pieces it engulfs and then will returning the nutrition it contained back into the extracellular space. After fragments from outside are internalized, cells needed a way to decide if what was engulfed should lead to a stepped up immune response. That's why it is not surprising that scientists recently discovered a whole network of molecules internal to these cells that form a complex called an inflammasome. There are various types of inflammasome that cover different biological niches (4).
    What this means is that, in response to what is deemed an enemy, a phagocytic cell will gather together a distinctive list of parts to assemble into an inflammasome, and then that inflammasome will produce specific cytokines called IL-1 beta and IL-18. These chemical messengers can then go and recruit more help.
    In contrast, antibody mediated immunity is more like having an air defense. The antibodies made by this part of our immune system function more like missiles that are sent out to find a designated target.
    Vaccines are designed for the antibody side of the immune response. Future recognition of a previous invader involves selecting a piece of protein, called a peptide, that is large enough to recognize. This side of our immune response forms a memory of that peptide so that in the future, our cells will use that memory to recognize that we have seen that germ before. If the germ is recognized from a previous infection, then the immune system can respond very quickly and with more hands on deck. The piece of the intruder's identity that will be remembered is determined by our HLA type, and that is determined by a section of DNA on our sixth chromosome. The vulnerability to celiac disease is defined by the genes that are behind the formation of HLA-DQ2 and/or HLA-DQ8.
    Scientists have known for many years that these two branches of immunity compete with each other and need to stay in balance. The chemical immune messengers called cytokines will shift our immune response between a dominance of cell mediated or antibody-mediated immunity. Until very recently, all the attention in celiac was on the antibody mediated branch whose major decision-makers are T cells, but even T cells can form inflammasomes (5).
    Scientists are now studying the innate immune response to gluten. Our innate immunity relies on a specialized call type called a phagocyte. Cells of this type of include monocytes, macrophages, neutrophils, granuloctyes, mast cells, dendritic cells, osteoclasts and even migroglial cells in the brain. Phagocytic cells will incorporate debris that comes close to them into a vesicle, and that is a sort of bubble with liquid and other contents inside. This vesicle is taken into the cell through a process called endocytosis. After that, this type of cell will quickly process the contents of that vesicle probably much faster than other cell types. This competence is likely why this type of cell is given the job of surveillance for invaders. It is also is useful as a tool for recycling things from the outside that they take in. Scientists prefer to call this set of cells the professional phagocytic cells. Other cell types can be enlisted for the job of phagocytosis but they don't have that role as their main purpose. That is why this different set is called the non-professional phagocytic cells and they may also form inflammasomes but may need more stimulation. (6).
    Scientists in the last decade have done experiments to learn how inflammasomes work. These intracellular immune complexes are assembled often in response to exposures to a type of molecule called a lipopolysaccharide that can be detected after engulfing the cell membranes of invading organisms. There are many other triggers, all recognized by their ability to tell us when something inside us is not as it should be. ATP, our body's energy molecule, when it is identified as coming in from the outside, can be a trigger for the inflammasome. Engulfing this sort of molecule suggests to our phagocytes that cell death events may have occurred in the environment of that cell (7). Some of our cells have been found to extrude nucleotides in self-defense, because leftovers from that kind of event may tell the inflammasome machinery that the cell is encountering a dangerous situation (8).
    This system recognizes that certain pathogens create holes in cell walls, so when a phagocyte encounters evidence of damaged membranes with holes in them, that alone can trigger a cell danger response that enlists inflammasomes. That means two popularly used medicines that kill fungus by inserting holes in their cells, Nystatin and Amphotericin B, have by themselves been found to create this danger signal even when there is no infectious agent. Doctors and lay people need to know that many signs that are usually associated with an infection, including fever, can occur when there is nothing infectious involved (9). Another inflammasome trigger is excess alcohol which can be very damaging when it triggers inflammasomes in the nervous system. (10) Another concern is environmental contaminates like asbestos and silica which have been studied the most when they are inhaled. (11)
    Crystals of uric acid associated with gout or other cell debris can also trigger the inflammasome, as can crystals of oxalate, which may be important to celiac disease since scientists have found higher levels of oxalate in celiac sprue. These crystals must reach a critical concentration to generate this cell danger mechanism in phagocytic cells (12). In the past, nobody really was aware that oxalate could have a major effect on the immune system outside of what it does in the kidneys.
    Scientists for so many years thought the kidney alone contained cells that oxalate could influence. That's why other cell types were not studied. At least now, we realize this narrow focus had been based on some premature conclusions. We should have known to look more broadly because there was so much evidence from Primary Hyperoxaluria, a genetic disorder where a defective liver produces oxalate that travels to the whole body, creating a condition called oxalosis. That's how we know that oxalate goes all over the body. For the longest time, nobody was measuring oxalate outside of kidney disease, even though there were a few exceptions, like in people after bariatric surgery, and in celiac sprue and in cystic fibrosis, and eventually, in autism (13).
    Because there already was a literature about oxalate in celiac sprue, when our project began, we started informing the public about these links on our website, www.lowoxalate.info. More recently we have written a series of articles about oxalate in this journal, discussing the science, and also practical issues about how to reduce oxalate while on a gluten free diet. That was working with knowledge we had then, but now we know that this issue of inflammasomes has been a part of the story we didn't know, but it holds great promise of possibly addressing why there could be complications in celiac sprue that do not resolve by merely going gluten free.
    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.
    References:
    1. (http://www.aarda.org/autoimmune-information/list-of-diseases/)
    2. Doria A, Zen M, Bettio S, Gatto M, Bassi N, Nalotto L, Ghirardello A, Iaccarino L, Punzi L. Autoinflammation and autoimmunity: bridging the divide. Autoimmun Rev. 2012 Nov;12(1):22-30. doi: 10.1016/j.autrev.2012.07.018. Epub 2012 Aug 2. Review. PubMed PMID: 22878274.
    3. Rajamäki K, Nordström T, Nurmi K, Åkerman KE, Kovanen PT, Öörni K, Eklund KK. Extracellular acidosis is a novel danger signal alerting innate immunity via the NLRP3 inflammasome. J Biol Chem. 2013 May 10;288(19):13410-9. doi: 10.1074/jbc.M112.426254. Epub 2013 Mar 25. PubMed PMID: 23530046; PubMed Central PMCID: PMC3650379.
    4. Kummer JA, Broekhuizen R, Everett H, Agostini L, Kuijk L, Martinon F, van Bruggen R, Tschopp J. Inflammasome components NALP 1 and 3 show distinct but separate expression profiles in human tissues suggesting a site-specific role in the inflammatory response. J Histochem Cytochem. 2007 May;55(5):443-52. Epub 2006 Dec 12. PubMed PMID: 17164409.
    5. Arbore G, West EE, Spolski R, Robertson AA, Klos A, Rheinheimer C, Dutow P, Woodruff TM, Yu ZX, O'Neill LA, Coll RC, Sher A, Leonard WJ, Köhl J, Monk P, Cooper MA, Arno M, Afzali B, Lachmann HJ, Cope AP, Mayer-Barber KD, Kemper C. T helper 1 immunity requires complement-driven NLRP3 inflammasome activity in CD4⺠T cells. Science. 2016 Jun 17;352(6292):aad1210. doi: 10.1126/science.aad1210. PubMed PMID: 27313051.
    6. Paoletti, R.; Notario, A.; Ricevuti, G., eds. (1997). Phagocytes: Biology, Physiology, Pathology, and Pharmacotherapeutics. New York: The New York Academy of Sciences. ISBN 1-57331-102-2.
    7. Kim JJ, Jo EK. NLRP3 inflammasome and host protection against bacterial infection. J Korean Med Sci. 2013 Oct;28(10):1415-23. doi: 10.3346/jkms.2013.28.10.1415. Epub 2013 Sep 25. Review. PubMed PMID: 24133343; PubMed Central PMCID: PMC3792593.
    8. Coutinho-Silva R, Ojcius DM. Role of extracellular nucleotides in the immune response against intracellular bacteria and protozoan parasites. Microbes Infect. 2012 Nov;14(14):1271-7. doi: 10.1016/j.micinf.2012.05.009. Epub 2012 May 23. Review. PubMed PMID: 22634346; PubMed Central PMCID: PMC4110109.
    9. McDonald B, Pittman K, Menezes GB, Hirota SA, Slaba I, Waterhouse CC, Beck PL, Muruve DA, Kubes P. Intravascular danger signals guide neutrophils to sites of sterile inflammation. Science. 2010 Oct 15;330(6002):362-6. doi: 10.1126/science.1195491. Erratum in: Science. 2011 Mar 25;331(6024):1517. PubMed PMID: 20947763.
    10. Lippai D, Bala S, Petrasek J, Csak T, Levin I, Kurt-Jones EA, Szabo G. Alcohol-induced IL-1β in the brain is mediated by NLRP3/ASC inflammasome activation that amplifies neuroinflammation. J Leukoc Biol. 2013
    Jul;94(1):171-82. doi: 10.1189/jlb.1212659. Epub 2013 Apr 26. PubMed PMID: 23625200; PubMed Central PMCID: PMC3685015.
    11. Dostert C, Pétrilli V, Van Bruggen R, Steele C, Mossman BT, Tschopp J. Innate immune activation through Nalp3 inflammasome sensing of asbestos and silica.Science. 2008 May 2;320(5876):674-7. doi:
    10.1126/science.1156995. Epub 2008 Apr 10. PubMed PMID: 18403674; PubMed Central PMCID: PMC2396588.
    12. Petrasek J, Iracheta-Vellve A, Saha B, Satishchandran A, Kodys K, Fitzgerald KA, Kurt-Jones EA, Szabo G. Metabolic danger signals, uric acid and ATP, mediate inflammatory cross-talk between hepatocytes and immune cells in alcoholic liver disease. J Leukoc Biol. 2015 Aug;98(2):249-56. doi: 10.1189/jlb.3AB1214-590R. Epub 2015 May 1. PubMed PMID: 25934928; PubMed Central PMCID: PMC4501673.
    13. Owens SC. What is the Relationship Between Oxalate and Celiac Disease?. Journal of Gluten Sensitivity. Spring 2015; 14(2):1-11.
    14. Xi H, Zhang Y, Xu Y, Yang WY, Jiang X, Sha X, Cheng X, Wang J, Qin X, Yu J, Ji Y, Yang X, Wang H. Caspase-1 Inflammasome Activation Mediates Homocysteine-Induced Pyrop-Apoptosis in Endothelial Cells. Circ Res. 2016 May 13;118(10):1525-39. doi: 10.1161/CIRCRESAHA.116.308501. Epub 2016 Mar 22. PubMed PMID: 27006445; PubMed Central PMCID: PMC4867131.
    15. Shih HA, Kao DM, Elenitsas R, Leyden JJ. Livedo reticularis, ulcers, and peripheral gangrene: cutaneous manifestations of primary hyperoxaluria. Arch Dermatol. 2000 Oct;136(10):1272-4. PMID: 11030785.
    16. Faure V, Dou L, Sabatier F, Cerini C, Sampol J, Berland Y, Brunet P, Dignat-George F. Elevation of circulating endothelial microparticles in patients with chronic renal failure. J Thromb Haemost. 2006 Mar;4(3):566-73. Epub 2005 Dec 23. PubMed PMID: 16405517.
    17. Jaeschke H, Williams celiac disease, Ramachandran A, Bajt ML. Acetaminophen hepatotoxicity and repair: the role of sterile inflammation and innate immunity. Liver Int. 2012 Jan;32(1):8-20. doi: 10.1111/j.1478-3231.2011.02501.x. Epub 2011 Mar 14. Review. PubMed PMID: 21745276; PubMed Central PMCID: PMC3586825.
    18. Quandt D, Rothe K, Baerwald C, Rossol M. GPRC6A mediates Alum-induced Nlrp3 inflammasome activation but limits Th2 type antibody responses. Sci Rep. 2015 Nov 25;5:16719. doi: 10.1038/srep16719. PubMed PMID: 26602597; PubMed Central PMCID: PMC4658484.
    19. Franchi L, Núñez G. The Nlrp3 inflammasome is critical for aluminium hydroxide-mediated IL-1beta secretion but dispensable for adjuvant activity. Eur J Immunol. 2008 Aug;38(8):2085-9. doi: 10.1002/eji.200838549. PubMed PMID: 18624356; PubMed Central PMCID: PMC2759997.
    20. Trivedi MS, Shah JS, Al-Mughairy S, Hodgson NW, Simms B, Trooskens GA, Van Criekinge W, Deth RC. Food-derived opioid peptides inhibit cysteine uptake with redox and epigenetic consequences. J Nutr Biochem. 2014 Oct;25(10):1011-8. doi: 10.1016/j.jnutbio.2014.05.004. Epub 2014 Jun 6. PubMed PMID: 25018147; PubMed Central PMCID: PMC4157943.
    21. Grace PM, Strand KA, Galer EL, Urban DJ, Wang X, Baratta MV, Fabisiak TJ, Anderson ND, Cheng K, Greene LI, Berkelhammer D, Zhang Y, Ellis AL, Yin HH, Campeau S, Rice KC, Roth BL, Maier SF, Watkins LR. Morphine paradoxically prolongs neuropathic pain in rats by amplifying spinal NLRP3 inflammasome activation. Proc Natl Acad Sci U S A. 2016 Jun 14;113(24):E3441-50. doi:
    10.1073/pnas.1602070113. Epub 2016 May 31. PubMed PMID: 27247388; PubMed Central PMCID: PMC4914184.
    22. Johnson WM, Wilson-Delfosse AL, Mieyal JJ. Nutrients. Dysregulation of glutathione homeostasis in neurodegenerative diseases.2012 Oct 9;4(10):1399-440. doi: 10.3390/nu4101399. Review.PMID:23201762
    23. Chen Z, Lash LH. Evidence for mitochondrial uptake of glutathione by dicarboxylate and 2-oxoglutarate carriers. J Pharmacol Exp Ther. 1998 May;285(2):608-18. PubMed PMID: 9580605.
    24. Palová-Jelínková L, Dáňová K, Drašarová H, DvoÅ™ák M, Funda DP, Fundová P, Kotrbová-Kozak A, ÄŒerná M, Kamanová J, Martin SF, Freudenberg M, TuÄková L. Pepsin digest of wheat gliadin fraction increases production of IL-1β via TLR4/MyD88/TRIF/MAPK/NF-κB signaling pathway and an NLRP3 inflammasome activation. PLoS One. 2013 Apr 29;8(4):e62426. doi: 10.1371/journal.pone.0062426. Print 2013. PubMed PMID: 23658628; PubMed Central PMCID: PMC3639175.
    25. Di Giampaolo L, Di Gioacchino M, Ponti J, Sabbioni E, Castellani ML, Reale M, Toto E, Verna N, Conti P, Paganelli R, Boscolo P. "In vitro" comparative immune effects of different titanium compounds. Int J Immunopathol Pharmacol. 2004 May-Aug;17(2 Suppl):115-22. PubMed PMID: 15345202.
    26. Rakhimova M, Esslinger B, Schulze-Krebs A, Hahn EG, Schuppan D, Dieterich W. In vitro differentiation of human monocytes into dendritic cells by peptic-tryptic digest of gliadin is independent of genetic predisposition and the presence of celiac disease. J Clin Immunol. 2009 Jan;29(1):29-37. doi: 10.1007/s10875-008-9228-x. Epub 2008 Aug 12. PubMed PMID: 18696220.
    27. Owens SC, de La Garza P. Autoimmunity Survey. [Other]. Palo Alto, California, USA: Survey Monkey, Inc.; 2016 March. Available from: www.surveymonkey.com.
    28. Shaw PJ, McDermott MF, Kanneganti TD. Inflammasomes and autoimmunity. Trends Mol Med. 2011 Feb;17(2):57-64. doi: 10.1016/j.molmed.2010.11.001. Epub 2010 Dec 14. Review. PubMed PMID: 21163704; PubMed Central PMCID: PMC3057120.
    29. Sui DM, Xie Q, Yi WJ, Gupta S, Yu XY, Li JB, Wang J, Wang JF, Deng XM. Resveratrol Protects against Sepsis-Associated Encephalopathy and Inhibits the NLRP3/IL-1β Axis in Microglia. Mediators Inflamm. 2016;2016:1045657. doi: 10.1155/2016/1045657. Epub 2016 Jan 26. PubMed PMID: 26924896; PubMed Central PMCID: PMC4746398.
    30. Chen H, Tuck T, Ji X, Zhou X, Kelly G, Cuerrier A, Zhang J. Quality assessment of Japanese knotweed (Fallopia japonica) grown on Prince Edward Island as a source of resveratrol. J Agric Food Chem. 2013 Jul 3;61(26):6383-92. doi: 10.1021/jf4019239. Epub 2013 Jun 19. PubMed PMID: 23742076.
    31. Hu QH, Zhang X, Pan Y, Li YC, Kong LD. Allopurinol, quercetin and rutin ameliorate renal NLRP3 inflammasome activation and lipid accumulation in fructose-fed rats. Biochem Pharmacol. 2012 Jul 1;84(1):113-25. doi: 10.1016/j.bcp.2012.03.005. Epub 2012 Mar 16. PubMed PMID: 22426011.
    32. Cordero MD, Alcocer-Gómez E, Culic O, Carrión AM, de Miguel M, Díaz-Parrado E, Pérez-Villegas EM, Bullón P, Battino M, Sánchez-Alcazar JA. NLRP3 inflammasome is activated in fibromyalgia: the effect of coenzyme Q10. Antioxid Redox Signal. 2014 Mar 10;20(8):1169-80. doi: 10.1089/ars.2013.5198. Epub 2013 Sep 19. PubMed PMID: 23886272; PubMed Central PMCID: PMC3934515.
    33. Ahn H, Kim J, Lee MJ, Kim YJ, Cho YW, Lee GS. Methylsulfonylmethane inhibits NLRP3 inflammasome activation. Cytokine. 2015 Feb;71(2):223-31. doi: 10.1016/j.cyto.2014.11.001. Epub 2014 Nov 21. PubMed PMID: 25461402.
    34. Ahn H, Kim J, Jeung EB, Lee GS. Dimethyl sulfoxide inhibits NLRP3 inflammasome activation. Immunobiology. 2014 Apr;219(4):315-22. doi: 10.1016/j.imbio.2013.11.003. Epub 2013 Nov 22. PubMed PMID: 24380723.
    35. Lamson DW, Plaza SM. Transdermal secretin for autism - a case report. Altern Med Rev. 2001 Jun;6(3):311-3. PubMed PMID: 11410075.
    36. Netea MG, Joosten LA. Inflammasome inhibition: putting out the fire. Cell Metab. 2015 Apr 7;21(4):513-4. doi: 10.1016/j.cmet.2015.03.012. PubMed PMID: 25863243.
    37. Shao BZ, Xu ZQ, Han BZ, Su DF, Liu C. NLRP3 inflammasome and its inhibitors: a review. Front Pharmacol. 2015 Nov 5;6:262. doi: 10.3389/fphar.2015.00262. eCollection 2015. Review. PubMed PMID: 26594174; PubMed Central PMCID: PMC4633676.
    38. Jin C, Flavell RA. Innate sensors of pathogen and stress: linking inflammation to obesity. J Allergy Clin Immunol. 2013 Aug;132(2):287-94. doi: 10.1016/j.jaci.2013.06.022. Review. PubMed PMID: 23905917.
    39. Lee HM, Kim JJ, Kim HJ, Shong M, Ku BJ, Jo EK. Upregulated NLRP3 inflammasome activation in patients with type 2 diabetes. Diabetes. 2013 Jan;62(1):194-204. doi: 10.2337/db12-0420. Epub 2012 Oct 18. PubMed PMID: 23086037; PubMed Central PMCID: PMC3526026.

    Jefferson Adams
    Celiac.com 03/18/2017 - Do you have an autoimmune disease? Does someone you know? Did you know that the numbers regarding autoimmune rates are all over the place, and that incomplete or wrong information can result in delayed or missed diagnoses? Want to help researchers create a database that will help them understand exactly how many people are living with autoimmune conditions?
    Then behold the latest project from ARI, a 501c(3) nonprofit, with a mission "to create a hub for research, statistics, and patient data on all autoimmune illnesses." The project seeks to provide data that will help researchers nail down some basic answers about the numbers of people who live with one or more autoimmune conditions. The ARI website says that the company "operate a national database for patients who suffer from any autoimmune disease."
    ARI's mission is to "reduce the time of diagnosis, support research, compute prevalence statistics, and establish autoimmune disease as a major class of disease so that it receives the awareness of the public, the attention of healthcare providers, and the appropriate funding needed to improve upon existing treatment protocols and disease management strategies."
    This is one reason why Aaron Abend, the founder and president of ARI, decided to create the Autoimmune Registry after his mother was misdiagnosed for 10 years because, based on incorrect statistical data, "doctors thought Sjogren's syndrome was a rare disease with only 37,000 cases in the U.S." Today, researchers agree there are probably 3 million cases in the U.S., so not so rare at all.
    Researchers currently estimate that anywhere from 9 million to 50 million people in the United States have an autoimmune disease. That's quite a wide range. Pinpointing the actual prevalence is part of what ARI will try to do. So, they are reaching out directly to patients to information about diseases like rheumatoid arthritis (RA), lupus, psoriasis, diabetes, Crohn's, celiac disease, Sjogren's syndrome, multiple sclerosis (MS), and many others fall under the autoimmune umbrella.
    The registry is easy to join. It is free to sign up and consists of a simple survey that people with autoimmune diseases answer.
    The information that people provide to ARI remains secure. The data may be used to compile statistics and qualify them for research opportunities, but no identifying information will be shared without permission.
    The hope is that the registry can help researchers connect with people and the data. You can view the registry here.

    Jim Swayze
    Celiac.com 09/08/2017 - For for the overwhelming majority of our time here on this planet we've all followed a paleo, or hunter-gatherer, diet. This is not a way of eating invented by the latest Hollywood guru – though truth be told there are now plenty of stars who eat this way. It's common sense, really, if you're able to unlearn a good portion of the dietary wisdom we've been force-fed over the last generation or two.
    Paleo means little more than, in the words of Ray Audette, what you could find to eat if you were "naked with a sharp stick.” And the foods you'd find would have to be, at least in theory (though usually not in practice), edible raw. So what foods would have been available to our ancestors?
    Meat, for sure. There are no known hunter gatherer populations who were vegetarian/vegan. Animal protein is vital to human health. Why then do we hear about healthy vegetarian diets? Because they are healthy as compared to the modern Western diet, with its ubiquitous high fructose corn syrup, artificial fats and sweeteners, and high-glycemic carbohydrates.
    Ok, so animal protein. What else could have been found by our ancestral hunter-gatherers? Fruit and true vegetables, in season.
    That's basically it: meat, fruit, vegetables. And of course, plenty of good, cold water.
    What did we not eat then? Grains in any form, gluten-free or not. Legumes, which are extremely toxic raw and have to be soaked and cooked in order to be edible. (Hint: peanuts are legumes!) New world foods like chocolate, coffee. The list goes on and you should have the hang of it by now. Again, the standard: foods edible raw that would have been available to our ancestors.
    Question: Would dairy have been available to our ancestors? The answer is clearly no, other than in the form of human breastmilk for the first few months or years of life. Bovine milk, meant for calf populations, is not a natural human food.
    Sound overly restrictive? Let me tell you today's menu: For breakfast, three eggs over easy with bacon and a glass of fresh-squeezed orange juice. Lunch was tuna on romaine lettuce with sliced almonds and a vinaigrette with iced green tea to drink. And dinner, a mere five minutes away, is grassfed flank steak lettuce-wrap tacos with roasted hatch green chile guacamole. And a nice glass of New Zealand Sauvignon Blanc.
    Give paleo a try. It's the ultimate gluten-free way of eating.

  • Recent Articles

    Christina Kantzavelos
    Celiac.com 07/20/2018 - During my Vipassana retreat, I wasn’t left with much to eat during breakfast, at least in terms of gluten free options. Even with gluten free bread, the toasters weren’t separated to prevent cross contamination. All of my other options were full of sugar (cereals, fruits), which I try to avoid, especially for breakfast. I had to come up with something that did not have sugar, was tasty, salty, and gave me some form of protein. After about four days of mixing and matching, I was finally able to come up with the strangest concoction, that may not look the prettiest, but sure tastes delicious. Actually, if you squint your eyes just enough, it tastes like buttery popcorn. I now can’t stop eating it as a snack at home, and would like to share it with others who are looking for a yummy nutritious snack. 
    Ingredients:
    4 Rice cakes ⅓ cup of Olive oil  Mineral salt ½ cup Nutritional Yeast ⅓ cup of Sunflower Seeds  Intriguing list, right?...
    Directions (1.5 Servings):
    Crunch up the rice into small bite size pieces.  Throw a liberal amount of nutritional yeast onto the pieces, until you see more yellow than white.  Add salt to taste. For my POTS brothers and sisters, throw it on (we need an excess amount of salt to maintain a healthy BP).  Add olive oil  Liberally sprinkle sunflower seeds. This is what adds the protein and crunch, so the more, the tastier.  Buen Provecho, y Buen Camino! 

    Jefferson Adams
    Celiac.com 07/19/2018 - Maintaining a gluten-free diet can be an on-going challenge, especially when you factor in all the hidden or obscure gluten that can trip you up. In many cases, foods that are naturally gluten-free end up contain added gluten. Sometimes this can slip by us, and that when the suffering begins. To avoid suffering needlessly, be sure to keep a sharp eye on labels, and beware of added or hidden gluten, even in food labeled gluten-free.  Use Celiac.com's SAFE Gluten-Free Food List and UNSAFE Gluten-free Food List as a guide.
    Also, beware of these common mistakes that can ruin your gluten-free diet. Watch out for:
    Watch out for naturally gluten-free foods like rice and soy, that use gluten-based ingredients in processing. For example, many rice and soy beverages are made using barley enzymes, which can cause immune reactions in people with celiac disease. Be careful of bad advice from food store employees, who may be misinformed themselves. For example, many folks mistakenly believe that wheat-based grains like spelt or kamut are safe for celiacs. Be careful when taking advice. Beware of cross-contamination between food store bins selling raw flours and grains, often via the food scoops. Be careful to avoid wheat-bread crumbs in butter, jams, toaster, counter surface, etc. Watch out for hidden gluten in prescription drugs. Ask your pharmacist for help about anything you’re not sure about, or suspect might contain unwanted gluten. Watch out for hidden gluten in lotions, conditioners, shampoos, deodorants, creams and cosmetics, (primarily for those with dermatitis herpetaformis). Be mindful of stamps, envelopes or other gummed labels, as these can often contain wheat paste. Use a sponge to moisten such surfaces. Be careful about hidden gluten in toothpaste and mouthwash. Be careful about common cereal ingredients, such as malt flavoring, or other non-gluten-free ingredient. Be extra careful when considering packaged mixes and sauces, including soy sauce, fish sauce, catsup, mustard, mayonnaise, etc., as many of these can contain wheat or wheat by-product in their manufacture. Be especially careful about gravy mixes, packets & canned soups. Even some brands of rice paper can contain gluten, so be careful. Lastly, watch out for foods like ice cream and yogurt, which are often gluten-free, but can also often contain added ingredients that can make them unsuitable for anyone on a gluten-free diet. Eating Out? If you eat out, consider that many restaurants use a shared grill or shared cooking oil for regular and gluten-free foods, so be careful. Also, watch for flour in otherwise gluten-free spices, as per above. Ask questions, and stay vigilant.

    Jefferson Adams
    Celiac.com 07/18/2018 - Despite many studies on immune development in children, there still isn’t much good data on how a mother’s diet during pregnancy and infancy influences a child’s immune development.  A team of researchers recently set out to assess whether changes in maternal or infant diet might influence the risk of allergies or autoimmune disease.
    The team included Vanessa Garcia-Larsen, Despo Ierodiakonou, Katharine Jarrold, Sergio Cunha,  Jennifer Chivinge, Zoe Robinson, Natalie Geoghegan, Alisha Ruparelia, Pooja Devani, Marialena Trivella, Jo Leonardi-Bee, and Robert J. Boyle.
    They are variously associated with the Department of Undiagnosed Celiac Disease More Common in Women and Girls International Health, Johns Hopkins School of Public Health, Baltimore, Maryland, United States of America; the Respiratory Epidemiology, Occupational Medicine and Public Health, National Heart and Lung Institute, Imperial College London, London, United Kingdom; the Section of Paediatrics, Department of Medicine, Imperial College London, London, United Kingdom; the Centre for Statistics in Medicine, University of Oxford, Oxford, United Kingdom; the Division of Epidemiology and Public Health, University of Nottingham, Nottingham, United Kingdom; the Centre of Evidence Based Dermatology, University of Nottingham, Nottingham, United Kingdom; and Stanford University in the USA.
    Team members searched MEDLINE, Excerpta Medica dataBASE (EMBASE), Web of Science, Central Register of Controlled Trials (CENTRAL), and Literatura Latino Americana em Ciências da Saúde (LILACS) for observational studies conducted between January 1946 and July 2013, and interventional studies conducted through December 2017, that evaluated the relationship between diet during pregnancy, lactation, or the first year of life, and future risk of allergic or autoimmune disease. 
    They then selected studies, extracted data, and assessed bias risk. They evaluated data using the Grading of Recommendations Assessment, Development and Evaluation (GRADE). They found 260 original studies, covering 964,143 participants, of milk feeding, including 1 intervention trial of breastfeeding promotion, and 173 original studies, covering 542,672 participants, of other maternal or infant dietary exposures, including 80 trials of 26 maternal, 32 infant, or 22 combined interventions. 
    They found a high bias risk in nearly half of the more than 250 milk feeding studies and in about one-quarter of studies of other dietary exposures. Evidence from 19 intervention trials suggests that oral supplementation with probiotics during late pregnancy and lactation may reduce risk of eczema. 44 cases per 1,000; 95% CI 20–64), and 6 trials, suggest that fish oil supplementation during pregnancy and lactation may reduce risk of allergic sensitization to egg. GRADE certainty of these findings was moderate. 
    The team found less evidence, and low GRADE certainty, for claims that breastfeeding reduces eczema risk during infancy, that longer exclusive breastfeeding is associated with reduced type 1 diabetes mellitus, and that probiotics reduce risk of infants developing allergies to cow’s milk. 
    They found no evidence that dietary exposure to other factors, including prebiotic supplements, maternal allergenic food avoidance, and vitamin, mineral, fruit, and vegetable intake, influence risk of allergic or autoimmune disease. 
    Overall, the team’s findings support a connection between the mother’s diet and risk of immune-mediated diseases in the child. Maternal probiotic and fish oil supplementation may reduce risk of eczema and allergic sensitization to food, respectively.
    Stay tuned for more on diet during pregnancy and its role in celiac disease.
    Source:
    PLoS Med. 2018 Feb; 15(2): e1002507. doi:  10.1371/journal.pmed.1002507

    Jefferson Adams
    Celiac.com 07/17/2018 - What can fat soluble vitamin levels in newly diagnosed children tell us about celiac disease? A team of researchers recently assessed fat soluble vitamin levels in children diagnosed with newly celiac disease to determine whether vitamin levels needed to be assessed routinely in these patients during diagnosis.
    The researchers evaluated the symptoms of celiac patients in a newly diagnosed pediatric group and evaluated their fat soluble vitamin levels and intestinal biopsies, and then compared their vitamin levels with those of a healthy control group.
    The research team included Yavuz Tokgöz, Semiha Terlemez and Aslıhan Karul. They are variously affiliated with the Department of Pediatric Gastroenterology, Hepatology and Nutrition, the Department of Pediatrics, and the Department of Biochemistry at Adnan Menderes University Medical Faculty in Aydın, Turkey.
    The team evaluated 27 female, 25 male celiac patients, and an evenly divided group of 50 healthy control subjects. Patients averaged 9 years, and weighed 16.2 kg. The most common symptom in celiac patients was growth retardation, which was seen in 61.5%, with  abdominal pain next at 51.9%, and diarrhea, seen in 11.5%. Histological examination showed nearly half of the patients at grade Marsh 3B. 
    Vitamin A and vitamin D levels for celiac patients were significantly lower than the control group. Vitamin A and vitamin D deficiencies were significantly more common compared to healthy subjects. Nearly all of the celiac patients showed vitamin D insufficiency, while nearly 62% showed vitamin D deficiency. Nearly 33% of celiac patients showed vitamin A deficiency. 
    The team saw no deficiencies in vitamin E or vitamin K1 among celiac patients. In the healthy control group, vitamin D deficiency was seen in 2 (4%) patients, vitamin D insufficiency was determined in 9 (18%) patients. The team found normal levels of all other vitamins in the healthy group.
    Children with newly diagnosed celiac disease showed significantly reduced levels of vitamin D and A. The team recommends screening of vitamin A and D levels during diagnosis of these patients.
    Source:
    BMC Pediatrics

    Jefferson Adams
    Celiac.com 07/16/2018 - Did weak public oversight leave Arizonans ripe for Theranos’ faulty blood tests scam? Scandal-plagued blood-testing company Theranos deceived Arizona officials and patients by selling unproven, unreliable products that produced faulty medical results, according to a new book by Wall Street Journal reporter, whose in-depth, comprehensive investigation of the company uncovered deceit, abuse, and potential fraud.
    Moreover, Arizona government officials facilitated the deception by providing weak regulatory oversight that essentially left patients as guinea pigs, said the book’s author, investigative reporter John Carreyrou. 
    In the newly released "Bad Blood: Secrets and Lies in a Silicon Valley Startup," Carreyrou documents how Theranos and its upstart founder, Elizabeth Holmes, used overblown marketing claims and questionable sales tactics to push faulty products that resulted in consistently faulty blood tests results. Flawed results included tests for celiac disease and numerous other serious, and potentially life-threatening, conditions.
    According to Carreyrou, Theranos’ lies and deceit made Arizonans into guinea pigs in what amounted to a "big, unauthorized medical experiment.” Even though founder Elizabeth Holmes and Theranos duped numerous people, including seemingly savvy investors, Carreyrou points out that there were public facts available to elected officials back then, like a complete lack of clinical data on the company's testing and no approvals from the Food and Drug Administration for any of its tests.
    SEC recently charged the now disgraced Holmes with what it called a 'years-long fraud.’ The company’s value has plummeted, and it is now nearly worthless, and facing dozens, and possibly hundreds of lawsuits from angry investors. Meantime, Theranos will pay Arizona consumers $4.65 million under a consumer-fraud settlement Arizona Attorney General Mark Brnovich negotiated with the embattled blood-testing company.
    Both investors and Arizona officials, “could have picked up on those things or asked more questions or kicked the tires more," Carreyrou said. Unlike other states, such as New York, Arizona lacks robust laboratory oversight that would likely have prevented Theranos from operating in those places, he added.
    Stay tuned for more new on how the Theranos fraud story plays out.
    Read more at azcentral.com.