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    Dr. Ron Hoggan, Ed.D.
    The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada.
    The Polish one is: Kozlowska, Z.E. Results of Investigation on Children with Coeliakia Treated many Years with Gluten Free Diet Psychiatria Polska 1991; 25(2): 130-134.
    The German one is: Paul, et. al. EEG-befunde Zoeliaki-kranken Kindernin Abhaengigkeit von der Ernaehrung Zeitschrift der Klinische Medizin 1985; 40: 707-709.
    The first indicates that 71% of celiac children, when newly diagnosed, demonstrate EEG abnormalities. Now please note this caution: I HAVE NO TRAINING IN THE INTERPRETATION OF EEG READINGS.
    Nonetheless, when I compare the authors descriptions of the EEG abnormalities in celiac children, and the abnormalities in children who have been diagnosed with ADD or ADHD, there are some startling similarities.
    Paul, et. al. are paraphrased by Reichelt et. al. in THE EFFECT OF GLUTEN-FREE DIET ON GLYCOPROTEIN ATTACHED URINARY PEPTIDE EXCRETION Journal of Orthomolecular Medicine 1990; 5: 223-239.
    They say: In celiac children provocation with gluten after diet causes alarmingly high frequency of EEG changes that persist up to a year (Paul et al 1985).
    I would urge (those with ADD) to be very careful to avoid contamination in (their) diets, and I would ask you to consider some alternatives to stimulant therapy (Ritalin is a brand name of the most commonly used stimulant.).
    The concept of drugging a child to facilitate learning is upsetting to me, especially when there is cause to suspect that, on the Gluten-free diet, she may improve without intervention. I know that she is falling behind now, but if her experience is similar to mine, many of my ADD type symptoms did go away during the first year. I will also forward a part of report that was forwarded to me, that showed that vitamin B-6 supplementation was as beneficial to a group of children with attention deficits, as Ritalin was. Especially in celiac disease, where vitamin deficiencies are so common, that seems a viable alternative.

    Jefferson Adams
    Celiac.com 05/08/2009 - In 1996-1997, in an effort to test a hypothesis by scientist Karl Ludvig Reichelt, Norwegian researchers began a long-term study of 23 children aged 4 to 11 from the southwestern Norwegian town of Stavanger. All of the children suffered from hyperactive disorders including ADHD. All children showed abnormal levels of peptides in their urine.
    Dr. Reichelt believed that metabolic disorders impair the effective breakdown of certain proteins in children and thereby cause mental problem, such as hyperactive disorders. Related international research has established links between protein disorder and the conditions of autism and schizophrenia.  A growing number of studies also hint that some cases of ADHD are tied to digestive disorders. Data from this Norwegian study supports the idea that ADHD may also arise from a digestive disorder.
    This study indicates that consumption of certain foods, such as milk and gluten, may contribute to ADHD in children who lack the enzyme that breaks down proteins like casein, a component of milk--which also helps in the formation of cheese.
    Interestingly, when children who lack this enzyme eat foods that require the enzyme to properly digest proteins like casein, their brains experience an opium-like effect, which might explain at least some of the spaciness and impaired attention these kids exhibit.
    According to Reichalt's theory, hyperactivity can be controlled by reducing the intake of foods that require the presence of this missing enzyme to properly break down the offending proteins.
    In the study, 22 of the 23 children were placed on strict milk-free and/or gluten-free diets. They were taken off milk products and other foods containing casein. All exhibited a rapid improvement in general well-being, including improved mental health and general behavior, improved attention-span and better learning abilities. After a year, 22 of the 23 families reported clear improvements in their child's behaviour and attention-span.
    When the kids were taken off their diets, their symptoms returned nearly immediately. Before changing their diets, most of the children were taking medications, like Ritalin, to treat their symptoms. After their diets were established, their medications were discontinued.
    By 2004, a number of the children had ceased their diets for various reasons and some have returned to medication. Still, six children remained milk-free and several had also cut out gluten, which is found in wheat, rye, barley and to some extent oats.
    Due in part to the small sample size, and limited amounts of data from comprehensive studies on the number of ADHD children who suffer from peptide-breakdown abnormalities, the study has been met with a certain resistance among the medical community, where most doctors still believe that the evidence best supports medications like Ritalin as the best way to treat the ADHD.
    Still, the results carry weight among the parents, and among the Norwegians, as hundreds of other Norwegian children with ADHD, mainly in and around Stavanger, have in recent years been put on milk-free and/or gluten-free diets to help control ADHD and related disorders.
    Agence France Presse 2008.
    Yahoo! News 2008


    Jefferson Adams
    Celiac.com 12/21/2012 - Over the past several years, researchers have made substantial progress in understanding the causes of autism, which now afflicts about 1 in 88 children. However, very little news of this progress seems to have spread into popular consciousness, much of which continues to focus on the possible role of vaccines.
    Recent discoveries indicates that one-third or more cases of autism look to be a kind of inflammatory disease, which begins well before birth.
    In the August 25th issue of the New York Times, Moises Velasquez-Manhoff has very interesting article in which he discusses the widening view among researchers that autism is, in fact, an inflammatory disease. The article is long and comprehensive, and cites numerous studies, findings and experiments.
    Inflammation is the body's natural response to certain kinds of threats. In a normal body, the immune system uses inflammation in a very precise, targeted way, before returning to a normal state.
    In autistic individuals, inflammatory signals become the dominant condition, and there is no balancing anti-inflammatory response. A state of chronic inflammation becomes normal. And the more skewed toward inflammation, the more acute the autistic symptoms.
    This inflammatory deregulation adversely impacts the brains of autistic individuals. Velasquez-Manhoff also cites a number of studies that trace these inflammatory effects back to the inflammatory responses of the mother during pregnancy.
    Among the studies cited in the article is a population-wide study from Denmark spanning two decades of births, which indicates that infection during pregnancy increases the risk of autism in the child. The study found that hospitalization for a viral infection, like the flu, during the first trimester of pregnancy triples the odds of autism. Bacterial infection, including of the urinary tract, during the second trimester increases chances by 40 percent.
    Another large Danish study, which included nearly 700,000 births over a decade, found that a mother’s rheumatoid arthritis, a degenerative disease of the joints, elevated a child’s risk of autism by 80 percent. Rates of autism in children of mothers with celiac disease were 350 percent higher than normal. Genetic studies had similar findings. Variations in genes associated with regulating the immune system also increase the risk of autism, especially when they occur in the mother.
    A mother’s diagnosis of asthma or allergies during the second trimester of pregnancy increases her child’s risk of autism. So does metabolic syndrome, a disorder associated with insulin resistance, obesity and, crucially, low-grade inflammation.
    Yet, viral and bacterials infections themselves do not seem the cause of the autism epidemic. The epidemiology doesn’t support that conclusion.
    A far more likely culprit is maternal immune dysregulation. Basically, the mother’s attempt to repel invaders, her inflammatory response, seems to be at fault. Research by Paul Patterson, an expert in neuroimmunity at Caltech, supports this idea. In his research, he introduces inflammation in pregnant mice artificially, without a live infection. This causes behavioral problems in the young. In this model, autism results from collateral damage. It’s an unintended consequence of self-defense during pregnancy.
    Since infantile autism was first described by Leo Kanner in 1943, diagnoses have risen tenfold. During that same period, viral and bacterial infections generally declined. However, overall rates of inflammatory diseases have risen sharply since then.
    As a group, these diseases include asthma, now estimated to affect 1 in 10 children, rates that have at least doubled since 1980, along with autoimmune disorders, which now afflict 1 in 20.
    Recently, William Parker at Duke University has chimed in. Some years back, he began comparing wild sewer rats with clean lab rats. The bodies of wild rats tightly controlled inflammation, but those of the lab rats did not. Parker found that the bodies of the wild rats contained high levels of parasites. Parasites are noted for limiting inflammation.
    One lesson from these rodent experiments is that fixing the maternal dysregulation will most likely prevent autism. That theory is supported by Swiss researchers, who created a lineage of mice with a genetically reinforced anti-inflammatory signal. They then inflamed the pregnant mice. The babies emerged fine, with no behavioral problems. This suggests that if inflammation is controlled during pregnancy, it won’t interfere with fetal brain development.
    Interestingly, asthma researchers are coming to similar conclusions: preventing inflammation in pregnant women will likely prevent asthma.
    Dr. Parker has introduced a more aggressive approach. He suggests that by using specially developed worms to restore “domesticated” parasites doctors can correct immune dysregulation.
    To determine if this is feasible, a trial is under way at the Montefiore Medical Center and the Albert Einstein College of Medicine. The trial is using a medicalized parasite called Trichuris suis, known as a whipworm, to treat autistic adults.
    The whipworm is native to pigs, and was first used medically to treat inflammatory bowel disease. It has shown anecdotal benefit in autistic children.
    The article suggests that the future of treating immune dysregulation, and thus preventing diseases like autism and asthma, may lie in reintroducing parasites into the human body. Stay tuned for more updates on this truly fascinating science.
    Read the full article by Moises Velasquez-Manhoff in the New York Times.

    Jefferson Adams
    Celiac.com 10/15/2013 - Most case reports suggest an association between autistic spectrum disorders (ASDs) and celiac disease (celiac disease) or positive celiac disease serologic test results, but larger studies are contradictory.
    A team of researchers recently set out to examine the association between ASDs and celiac disease according to small intestinal histopathologic findings.
    The research team included Jonas F. Ludvigsson; Abraham Reichenberg; Christina M. Hultman; and Joseph A. Murray. They are variously affiliated with the Department of Medicine, Clinical Epidemiology Unit, and the Department of Medical Epidemiology and Biostatistics at the Karolinska Institutet in Stockholm, Sweden, with the Department of Pediatrics at Orebro University Hospital, Orebro University in Orebro, Sweden, with the Division of Gastroenterology and Hepatology of the Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, with the Department of Psychosis Studies at the Institute of Psychiatry at King’s College in London, United Kingdom, and with the Department of Psychiatry at the Mount Sinai School of Medicine in New York, New York.
    For their nationwide case-control study, the researchers used 28 Swedish biopsy registers to gather data on approximately 26,995 individuals with celiac disease, which they defined as the presence of villous atrophy, Marsh stage 3.
    They found 12,304 patients with inflammation (Marsh stages 1-2), 3719 patients with normal mucosa (Marsh stage 0), but positive celiac results for IgA/IgG gliadin, endomysium, or tissue transglutaminase. They then compared these results against and results for 213,208 age- and sex-matched control subjects. The team used conditional logistic regression to estimate odds ratios (ORs) for prior ASD diagnosis according to the Swedish National Patient Register and then conducted a second analysis, using Cox proportional hazards regression to estimate hazard ratios (HRs) for future ASDs in individuals undergoing small intestinal biopsy.
    They found that previous ASD was not associated with celiac disease (OR, 0.93; 95% CI, 0.51-1.68) or inflammation (OR 1.03; 95% CI, 0.40-2.64). However, they did finds that previous ASD was associated with a sharp higher risk of having normal mucosa but positive serologic test result for celiac disease (OR, 4.57; 95% CI, 1.58-13.22).
    Once the team restricted the data to individuals without no diagnosis for ASD at the time of biopsy, they found that celiac disease (HR, 1.39; 95% CI, 1.13-1.71) and inflammation (HR, 2.01; 95% CI, 1.29-3.13) were both connected with slightly higher risks of later ASDs, compared against the HR of 3.09 (95% CI, 1.99-4.80) for later ASDs in individuals with normal mucosa but positive celiac disease serologic test results.
    Even though this study showed no connection between previous ASD and celiac disease or inflammation, it did show that individuals with normal mucosa, but positive blood screens for celiac disease, have a much higher risk of ASD.
    Source:
    JAMA Psychiatry. Published online September 25, 2013. doi:10.1001/jamapsychiatry.2013.2048

    Jefferson Adams
    Celiac.com 11/04/2016 - NIH has awarded a $3 Million grant to Dr. Betty Diamond, head of the Feinstein Institute's Center for Autoimmune and Musculoskeletal Diseases, and her colleague, Dr. Peter Gregersen, who heads the Feinstein Institute's Robert S. Boas Center for Genomics & Human Genetics, specifically to explore the relationship between a mother's autoimmunity during pregnancy and the risk of ASD in her child. Both are also researchers at the Northwell Health System's Manhasset-based R&D division.
    Doctors Diamond and Gregerson are following up their own previous studies that showed antibodies can lead to abnormal brain development and ASD symptoms.
    Also known as 'immunoglobulins,' antibodies are Y-shaped proteins produced mainly by plasma cells, white blood cells that can secrete large volumes of antibodies, and which the immune system uses to identify and neutralize pathogens including bacteria and viruses.
    The new study seeks to determine if increased levels of antibodies in pregnant women with autoimmune inflammatory disorders such as rheumatoid arthritis, lupus or celiac disease, leave these women at increased risk of having children on the autism spectrum.
    Titled "Prenatal Autoimmune and Inflammatory Risk Factors for Autism Spectrum Disorders," the new study will track 4,500 women who deliver babies at hospitals in the Northwell Health system, along with their babies, for two years.
    Participating mothers will receive a blood test during pregnancy to spot any potential autoimmune disease or diseases, and also to spot any elevations in immune activation, or in cell-signaling cytokine proteins.
    The research team will then monitor the children for signs of ASD. While researchers have already determined that autism spectrum disorders are at least partly influenced by genetics, "relatively little attention has been paid to the role of environment, and particularly the intrauterine environment," says to Gregersen.
    This research will help researchers to better understand the connections between a mother's autoimmunity levels during pregnancy, and the risk of later ASD in her child.
    Source:
    Feinstein Institute.org

    Posterboy
    Celiac.com 01/17/2017 - A diagnosis of pellagra will likely have many other disease presentations, not limited to acne, rosacea (dermatitis) skin rashes, depression, anxiety, dementia, etc., as well. Seventy-five or more years ago the symptoms of Pellagra were commonly diagnosed as separate diseases that were known to be of a common cause. Similarly celiac disease today is often referred to as the "tip of the iceberg," not only because of the large number of undiagnosed people, but also due to the vast range of symptoms and associated diseases and disorders that can be caused by untreated celiac disease. I assert that pellagra could be, in some cases, related to celiac disease, and might even cause it.
    Today Pellagra has mainly been reserved for subgroups of people like alcoholics or disadvantaged groups like the homeless, who lack good protein sources in their diet to stave it off. Quoting Niki Frost from the Pellagra Disease Blog: "Since pellagra is such a rare disease today, few people recognize it based on their symptoms alone (any of the three D's: dementia, dermatitis, and diarrhea). Pellagra patients are consequently referred to specialists in fields that are ultimately unrelated to the underlying nutritional deficiency and metabolic nature of the disease." (1)
    Dr. Heaney, Professor of Medicine at Creighton University, actually echo this fact when he says "In the United States, at least, Pellagra is a disease of the past, fortunately, and it is doubtful today that most health professionals would recognize it if a case happened to come to their attention." (2) Why is this? Because, as mentioned above, doctor's don't recognized it today unless they are a specialist, and even then, according to Nicki Frost: "specialists (are) in fields that are ultimately unrelated to the underlying nutritional deficiency and metabolic nature of the disease." (3) So the cycle repeats.
    Since these specialists might not consider people with celiac disease/Non-Celiac Gluten Sensitivity (NCGS) to be in a subgroup which is prone Pellagra, is it possible that some people are misdiagnosed? Skin conditions like acne, dermatitis, eczema, psoriasis, skin lesions, and mouth ulcers can be related to both Pellagra and celiac disease or NCGS. Some of the other signs of Pellagra, other than digestive distress, are dementia related symptoms such as depression, anxiety, brain fog, mental confusion, etc., which are also present in 40 percent of celiac patients. What if doctors haven't made the right diagnosis in some cases? Many people who might be misdiagnosed with celiac disease but who actually have Pellagra might not get better because they are not treating the right disease.
    Pellagra and its associated skin and GI problems are totally reversible with supplementation, which is one of the reasons that many foods are enriched with niacin. Glutenfree Works covers this topic well by noting a casual relationship, but not a causal relationship. They even note that a niacin deficiency itself can cause some of these symptoms. According to Glutenfree Works:
    "Intriguing animal research by Sandhur et. al. has shown that niacin deficiency itself sensitizes the intestinal mucosa of rats to gluten in wheat, barley, rye, oats and corn and induces susceptibility to gluten toxicity by means of cellular dysfunction. Human research needs to investigate this effect of niacin deficiency in human celiac disease." (4)
    But no one else seems to take note of this amazing fact. The research by Sandhur et. al. is 30+ years old, but is it possible that people are suffering from all kinds of GI problems, possibly even celiac disease, because they are ignorant of this fact?
    Around 15 years ago Prousky did follow up human research (5) that supports the idea that niacinamide can indeed treat different digestive problems. It was this initial research which I read 10+ years ago that lead me to the hypothesis that Pellagra today is might be misdiagnosed as celiac disease, because doctors are no longer able to recognize Pellagra in a clinical setting, having not seen it 75+ years.
    From Dr. Heaney's blog: "2014 marks the 100th anniversary of the war on pellagra, a war that lasted nearly 25 of those years before victory could finally be declared. You have not heard of the war on pellagra? The celebration is not on your calendar? You're not alone. Why did it take so long? Was the science so intractable, like the current "war" on cancer? No. It was politics and pigheadedness that were the obstacles." Dr. Heaney says: "Nutritional deficiency was not an accepted category of disease when Goldberger started work" on his cause/cure for Pellagra, and I must also mention that it is not looked at today in those diagnosed with celiac disease. (6)
    Let's look into this more if we can. Let's see what other expert's say about this. If we look at back issues of The International Journal of Celiac Disease we see a casual link that indicates a co-morbidity of Pellagra in celiac patients of 58%. (7) Note they the International Journal of Celiac Disease is not looking for a causal link but they only report casual association. In the article entitled "Two Exceptional Complications Revealing Celiac Pellagra" the author notes: "pellagra is essentially affecting tissues with a high rate of cell turnover, such as the digestive tract and the skin, and tissues with high energy needs, such as the brain". (8) If the symptoms are so similar, it might be easy to confuse one disease for the other.
    How is this possible? The International Journal of Celiac Disease muses on this point too. When discussing the "exceptional" and not well understood reasons why Pellagra might show up in a celiac diagnosis, they say "Little progress has been made in our knowledge of pellagra...since Goldberger discovered that nicotinamide was a preventive factor in 1926...(P)roof of this is that there have been no changes in treatment or diagnostic criteria in the last 90 years." The International Journal of Celiac Disease summarizes this case of "Exceptional complications revealing celiac disease and Pellagra illustrates...rare complication revealing celiac disease". (8)
    Since up to 58 percent of celiac patients might be co-morbid with Pellagra, could it be possible that Pellagra is the "parent disease," and the those diagnosed with celiac disease have symptoms derived from Pellagra? If we follow most normal paths for adoption it will take another 20 years (a generation) for the medical community to accept Pellagra as perhaps the proper diagnosis in some cases. So there is some evidence to suggest that medical science is, perhaps in many cases, identifying the wrong disease. If one is critically low in niacin, the 3 D's of Pellagra (Dementias, Dermatitis's, and Digestive Issues) show up.
    Take the "Niacin (Niacinamide) Challenge" and see if taking it three times a day for six months don't cause a healthy GI pattern, including a once per day bowel movement that sinks and healthy burping without bloating. Taking the niacinamide Challenge may put co-morbid cases of Pellagra, including its digestive symptoms, into remission, and provide relief for many who do not recover on a gluten-free diet alone. The number one mistake people make when taking niacinamide is they don't take it for long enough. It takes 4 to 6 months to overcome a serious deficiency of this vitamin, and for your mucus membranes (GI lining) to heal itself.
    Once you recover you can maintain your health, barring some future stress/trauma that depletes your reserves, at which time heartburn/GERD/IBS/diarrhea/constipation symptoms will return, and you will lose your ability to burp easily again. And the cycle repeats and the Pellagra symptoms come back with a vengeance.
    Read more at The Case of Mistaken Identity: How Pellagra now thought to be rare became known as Celiac Disease ? A White Paper by the Celiac Posterboy.
    References:
    https://pellagradisease.wordpress.com/  http://blogs.creighton.edu/heaney/2013/11/18/pellagra-and-the-four-ds/ https://pellagradisease.wordpress.com/ http://glutenfreeworks.com/blog/2010/06/23/niacin-vitamin-b3-deficiency-in-celiac-disease/ Prousky, Jonathan E. Is Vitamin B3 Dependency a Causal Factor in the Development of Hypochlorhydria and Achlorhydria? Journal of Orthomolecular Medicine, Vol. 16, No. 4, 4th quarter 2001, pp. 225-37. http://www.orthomolecular.org/library/jom/2001/articles/2001-v16n04-p225.shtml http://blogs.creighton.edu/heaney/2013/11/18/pellagra-and-the-four-ds/ International Journal of Celiac Disease. Celiac Disease: Intestinal, Heart and Skin Interconnections. 2015, 3(1), 28-30 doi:10.12691/ijcd-3-1-6 (http://pubs.sciepub.com/ijcd/3/1/6/) International Journal of Celiac Disease. Two Exceptional Complications Revealing Celiac Disease: Ischemic Cardiomyopathy and Pellagra. International Journal of Celiac Disease. 2015, 3(1), 31-32 doi:10.12691/ijcd-3-1-5. (http://pubs.sciepub.com/ijcd/3/1/5/)

  • 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.
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    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