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    Great Specialty Company Owner Arrested for Selling Contaminated Gluten Free Bread


    Destiny Stone

    Celiac.com 02/04/2010 - Paul Seelig, the owner of the GreatSpecialty Products bread company in Durham, North Carolina, has beenarrested and is facing felony charges for intentionally deceivingconsumers by selling bread which he promoted as gluten free, whenevidence shows it was not.


    The North Carolina Department ofAgriculture and Consumer Services began investigating Seelig aftercomplaints flooded in regarding his breads that were sold at theNorth Carolina State Fair. An estimated 25 people have currentlyfiled complaints against Seelig. Customers complained of reactions tohis bread products ranging from rashes to vomiting & diarrhea.


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    State agriculture officials sentsamples of Seelig's bread to a laboratory at the University ofNebraska (FDA facility), where test results confirmed the presence ofgluten in his products. Tests of Seelig's products showed that his“gluten free” breads actually contained more than 5,000 parts ofgluten per million; and for a product to be considered gluten free itmust be less than 20 parts per million. However, Seelig still refusesto cooperate with authorities and provide information about where hisbreads come from. Therefor, a Judge ruled that Seelig cannot sellanymore products until he cooperates with investigators.

    Seelig claims his breads have beenrigorously tested for gluten. According to his website-which was shutdown following a court order - it took two years of testing to makehis gluten free bread. He also claims that if there was really glutenin his products, hundreds of complaints would have been filed againsthim.

    Investigators say that Seelig is lyingabout his products, and at this point has not provided any evidenceto prove otherwise. In fact, the investigation revealed informationthat Seelig's company, was buying gluten containing bread productsfrom Tribecca Oven Company and repackaging the bread with gluten freelabels. Additionally, according to Brian Long of the agriculturedepartment, Seelig's company is run out of his house on Cardinal LakeDrive in Durham, North Carolina.

    Seelig is not new to the court system.In 2001, he spent 4 months in Nebraska prison for several counts offraud. For his current trial, Seelig has been using various stallingmethods in an attempt to delay his trial date, including, claimsthat he has H1N1, was quarantined due to staph infection, had cancertreatment and even a heart attack. Contrary to previous Judge rulings, recent reports indicate that thehearing has now been moved to 2/24/2010, and bail is set at $100,000due to his high flight risk.

    Sources:



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  • Related Articles

    Dr. Ron Hoggan, Ed.D.
    January 9, 1999 post by Ron Hoggan to the Celiac Listserv:
    Im posting this response to the list as this information may not be common knowledge in the celiac community, and perhaps it should be. There are a number of reports, regarding celiac patients, of coexisting intolerance to milk proteins. One recent report was of an investigation for cross reacting antibodies. They found none, but a number of these patients displayed antibodies against gliadin and parallel anticasein antibodies (1). Another group has indicated that 36% to 48% of celiac patients demonstrate antibody reactions to milk proteins (2), although there are some reports that the frequency of such sensitivities reduce with treatment of a gluten-free diet (3), although the latter publication reported a higher initial frequency of reactions to milk proteins. There is another report of one celiac patient thought to have refractory sprue who recovered with the additional dietary exclusion of egg, chicken, and tuna (4). The patient became very ill before the possibility of immune reactions to other dietary proteins was considered. These reports suggest to me that we need to be vigilant about the possibility of additional food sensitivities. Before leaping to the use of steroids, further antibody testing seems prudent. The therapeutic use of systemic steroids carries the potential for some very dangerous side effects. Dietary exclusion of allergenic proteins, on the other hand, is just an inconvenience, one that most of us are already well versed in. ELISA or similar testing ought to be done prior to beginning steroids, as such drugs may be unnecessary, or they may compromise the accuracy of such testing.
    Sources:
    Paranos S, et al. Lack of cross-reactivity between casein and gliadin in sera from coeliac disease patients. Int Arch Allergy Immunol. 1998 Oct;117(2):152-4. Volta U, et al. Antibodies to dietary antigens in coeliac disease. Scand J Gastroenterol. 1986 Oct;21(8):935-40. Scott H, et al. Immune response patterns in coeliac disease. Serum antibodies to dietary antigens measured by an enzyme linked immunosorbent assay (ELISA). Clin Exp Immunol. 1984 Jul;57(1):25-32. Baker AL, et al. Refractory sprue: recovery after removal of nongluten Dietary proteins. Ann Intern Med. 1978 Oct;89(4):505-8.

    Sayer Ji
    Approximately 70% of all American calories come from a combination of the following four foods: wheat, dairy, soy and corn - assuming, that is, we exclude calories from sugar.
    Were it true that these four foods were health promoting, whole-wheat-bread-munching, soy-milk-guzzling, cheese-nibbling, corn-chip having Americans would probably be experiencing exemplary health among the world's nations. To the contrary, despite the massive amount of calories ingested from these purported "health foods," we are perhaps the most malnourished and sickest people on the planet today. The average American adult is on 12 prescribed medications, demonstrating just how diseased, or for that matter, brainwashed and manipulated, we are.
    How could this be? After all, doesn't the USDA Food Pyramid emphasize whole grains like wheat above all other food categories, and isn’t dairy so indispensible to our health that it is afforded a category all of its own? 
    Unfortunately these “authoritative” recommendations go  much further in serving the special interests of the industries that produce these commodities than in serving the biological needs of those who are told it would be beneficial to consume them.  After all, grains themselves have only been consumed for 500 generations – that is, only since the transition out of the Paleolithic into the Neolithic era approximately 10,000 years ago.  Since the advent of homo sapiens 2.5 million years ago our bodies have survived on a hunter and gatherer diet, where foods were consumed in whole form, and raw!  Corn, Soy and Cow's Milk have only just been introduced into our diet, and therefore are “experimental” food sources which given the presence of toxic lectins, endocrine disruptors, anti-nutrients, enzyme inhibitors, indigestible gluey proteins, etc, don’t appear to make much biological sense to consume in large quantities - and perhaps, as is my belief, given their deleterious effects on health, they should not be consumed at all.
    Even if our belief system doesn’t allow for the concept of evolution, or that our present existence is borne on vast stretches of biological time, we need only consider the undeniable fact that these four “health foods” are also sources for industrial adhesives, in order to see how big a problem they present.
    For one, wheat flour is used to make glues for book binding and wall-papering, as well as being the key ingredient for paper mache mortar. Sticky soy protein has replaced the need for formaldehyde based adhesives for making plywood, and is used to make plastic, composite and many other things you probably wouldn’t consider eating. The whitish protein known as casein in cow's milk is the active ingredient in Elmer's glue and has been used for paint since ancient times. Finally, corn gluten is used as a glue to hold cardboard boxes together. Eating glue doesn't sound too appetizing does it?  Indeed, when you consider what these sticky glycoproteins will do to the delicate microvilli inside our intestines, a scenario, nightmarish in proportions, unfolds. 
    All nutrients are absorbed in the intestine through the microvilli. These finger-like projections from off the surface of the intestine amplify the surface area of absorption in the intestine to the area the size of a tennis court. When coated with undigested or partially digested glue (glycoproteins), not only is the absorption of nutrients reduced leading to malabsorption and consequently malnourishment, but the villi themselves become damaged/dessicated/ inflammed and begin to undergo atrophy - at times even breaking off.  The damage to the intestinal membrane caused by these glues ultimately leads to perforation of the one cell thick intestinal wall, often leading to "leaky gut syndrome": a condition where undigested proteins and plant toxins called lectins enter the bloodstream wreaking havoc on the immune system. A massive amount of research (which is given little to no attention both in the mass media and allopathic medicine) indicates that diseases as varied as fibromyalgia, diabetes, autism, cancer, arthritis, crohn's, chronic fatigue, artheroscerosis, and many others, are directly influenced by the immune mediated responses wheat, dairy, soy and corn can provoke.
    Of all four suspect foods Wheat, whose omnipresence in the S.A.D or Standard American Diet indicates something of an obsession, may be the primary culprit.  According to Clinical Pathologist Carolyn Pierini the wheat lectin called "gliadin" is known to to participate in activating NF kappa beta proteins which are involved in every acute and chronic inflammatory disorder including neurodegenerative disease, inflammatory bowel disease, infectious and autoimmune diseases.
    In support of this indictment of Wheat’s credibility as a “health food,” Glucosamine – the blockbuster supplement for arthritis and joint problems – has been shown to bind to and deactivate the lectin in wheat that causes inflammation. It may just turn out to be true that millions of Americans who are finding relief with Glucosamine would benefit more directly from removing the wheat (and related allergens) from their diets rather than popping a multitude of natural and synthetic pills to cancel one of Wheat’s main toxic actions. Not only would they be freed up from taking supplements like Glucosamine, but many would also be able to avoid taking dangerous Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) like Tylenol, Aspirin and Ibuprofen, which are known to cause tens of thousands of cases of liver damage, internal hemorrhaging and stomach bleeding each and every year.
    One might wonder:  “How is it that if America's favorite sources of calories: Wheat and Dairy, are so obviously pro-inflammatory, immunosuppressive, and generally toxic, why would anyone eat them?”  ANSWER: They are powerful forms of socially sanctioned self-medication.
    Wheat and Dairy contain gliadorphin and gluten exorphins, and casomorphin, respectively.  These partially digested proteins known as peptides act on the opioid receptors in the brain, generating a temporary euphoria or analgesic effect that has been clinically documented and measured in great detail.  The Institute of Pharmacology and Toxicology in Magdeburg, Germany has shown that a Casein (cow's milk protein) derivative has 1000 times greater antinociceptive activity (pain inhibition) than morphine. Not only do these morphine like substances create a painkilling "high," but they can invoke serious addictive/obsessive behavior, learning disabilities, autism, inability to focus, and other serious physical and mental handicaps. 
    As the glues destroy the delicate surface of our intestines, we for the life of us can't understand why we are so drawn to consume these "comfort foods", heaping "drug soaked" helping after helping.  Many of us struggle to shake ourselves out of our wheat and dairy induced stupor with stimulants like coffee, caffeinated soda and chocolate, creating a viscous “self-medicating” cycle of sedation and stimulation.
    As if this were not enough, Wheat, Dairy, and Soy also happen to have some of the highest naturally occurring concentrations of Glutamic Acid, which is the natural equivalent of monosodium glutamate. This excitotoxin gives these foods great "flavor" (or what the Japanese call umami) but can cause the neurons to fire to the point of death.  It is no wonder that with all these drug-like qualities most Americans consume wheat and dairy in each and every meal of their day, for each and every day of their lives.
    Whether you now believe that removing Wheat, Dairy, Soy and Corn from your diet is a good idea, or still need convincing, it doesn’t hurt to take the “elimination diet” challenge. The real test is to eliminate these suspect foods for at least 2 weeks, see how you feel, and then if you aren’t feeling like you have made significant improvements in your health, reintroduce them and see what happens.  Trust in your feelings, listen to your body, and you will move closer to what is healthy for you.
    This article owes much of its content and insight to the work of John Symes whose ground-breaking research on the dangers of wheat, dairy, corn and soy have been a great eye opener to me, and a continual source of inspiration in my goal of educating myself and others.


    Jefferson Adams
    Celiac.com 09/30/2013 - The negative impact of celiac disease on the sexual health of celiac sufferers is one of the great undiscussed aspects of the disease, according to Phil Zimbardo, a prominent psychologist and professor emeritus at Stanford University in California.
    “No one talks about the sex part in celiac disease,” Zimbardo says, no one tells people that celiac disease can destroy their sex drive and challenge "their very manhood." This and other of Zimbardo's views on celiac disease and its impact on sexual health can be found in an excellent article by Lisa Fitterman in Allergicliving.com.
    For Zimbardo, life before his celiac diagnosis was a dark place. As his body suffered the effects of celiac disease, Zimbardo grew so depressed that he lost all interest in sex and intimacy. This, in turn, had a negative impact upon Zimbardo's marriage.
    This negative impact of celiac disease on sexual health is not unique to men. Many woman with celiac disease see their own sex lives suffer.
    In the case of Alice Bast, founder and president of the National Foundation for Celiac Awareness (NFCA), celiac disease had a number of adverse effects on her health and well-being.
    Bast acknowledges to Fetterman that symptoms of undiagnosed celiac disease pushed sex far from her mind, and that her libido did not make a miraculous return upon diagnosis and going gluten-free. Even after she was diagnosed, her physical recovery was slow, due to chronic malnourishment that contributed to multiple miscarriages and a stillbirth. In fact, when it came to sex, Bast says that the return of her sexual health came slowly, almost imperceptibly, until she realized that she was enjoying intimacy again after years of avoiding it.
    Echoing Bast's experience, Zimbardo points out that, "as a psychologist, I’m always analyzing behavior and I just couldn’t understand what has happening to me until I was diagnosed.”
    Once he was diagnosed, however, Zimbardo cut gluten from his diet and started taking anti-inflammatories and probiotics to regrow his gut flora. It took a full year for his gut to heal and for his full health and vigor to return, but now he is healthy, both physically and sexually.
    For Zimbardo, and many others, giving up the gluten is the key to returning to good health, and healthy sexual activity. Giving up gluten was "nothing short of transformative.” Now, he says he "can’t wait to be 80."
    There is a great deal of anecdotal information to suggest that celiac disease can have adverse impacts on sexual health, yet very little actual data exists. It will be interesting to see if and when researchers begin to look for answers. 

    Jefferson Adams
    Celiac.com 11/01/2013 - Dairy and gluten contain "opioid peptides," that belong to the same family as opium. Dairy products contain small amounts of casomorphin, while gluten contains small amounts of gluten exorphin, and gliadorphin/gluteomorphin.
    When peptides from either gluten or casein react with opiate receptors in the brain, they produce effects similar to opiate drugs, such as heroin and morphine, albeit on a much more subtle level.
    These receptors influence the part of the brain involved with speech and auditory integration, which means this part of the brain can cause addiction to foods, spacing out or having foggy brain, migraines/headaches, sleepiness, chronic fatigue, aggressive behavior, moodiness, anxiety, depression, and high tolerance to pain.
    Little research exists on the potentially addictive qualities of gluten and dairy. However, there is plenty of research to back up how a gluten-free and casein-free diet can help improve those who suffer from ADHD, depression, anxiety, OCD, schizophrenia and Autism Spectrum Disorders.
    Many people first beginning a gluten-free and casein-free diet experience withdrawal symptoms, many experience powerful cravings. People can get cranky and irritable, and even pick fights and throw tantrums.
    How do you know if you might be sensitive to gluten or casein?
    Signs that you might be having a reaction to gluten or casein include abnormal bowel movements, either constipated or poorly formed; headaches; aggressive behavior, such as biting, hitting, pushing; inability to focus at school; erratic sleep or rising early -- before 6 a.m.
    Also, if your diet is heavily wheat and dairy based, as many are, it can take up to three weeks to fully be rid of gluten and casein with no reactions.
    If you think you or your child might have an allergy to gluten or casein, you should consider visiting a doctor for an IgG food allergy blood panel to see if that really is the problem. Blood tests are not 100 percent conclusive, but still a good measure.
    If you're still not sure, then ditch all the gluten and dairy in the house, and try a 30-day elimination diet should help return to normal.
    Source:
    Chicagoparent.com

  • Recent Articles

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

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

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

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

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