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    Hippies Weren't the Only Ones Tripping in the Sixties


    Dr. Ron Hoggan, Ed.D.
    Image Caption: New insights into celiac disease and schizophrenia

    This article originally appeared in the Winter 2010 edition of Journal of Gluten Sensitivity.


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    Celiac.com 10/06/2010 - Do you know where LSD comes from? It is made from gluten grains.  In 1938 Albert Hofmann, a Swiss chemist, discovered LSD, having refined it from a mold that grows on grains.  However, it was not until 1943 that he discovered its psycho-active properties.  In his own words Hofmann states: “I synthesized the diethylamide of Iysergic acid with the intention of obtaining an analeptic.” The expectation of such a drug was based on its source—ergot—which grows on gluten grains and causes ergotism, also known as ergotoxicosis, ergot poisoning, holy fire, and Saint Anthony’s Fire. 

    This poisonous mold has long been known to infect gluten grains.  It was to prevent the development of these molds that the Romans invented central heating systems.  They stored their grains on the lowest floor of residences and other buildings that were centrally heated and well ventilated.  Their fears of ergot were based on the powerful and bizarre symptoms that developed in people who ate grains that had become moldy with ergot.  Some afflicted individuals began to hallucinate, often becoming so mentally disturbed that they injured or killed themselves.  Others experienced loss of blood circulation to their extremities which became gangrenous.  Their digits and limbs sometimes fell off before these people died.  Some experienced a combination of these two sets of symptoms.  Animals sometimes display similar symptoms after consuming moldy grains. 

    Familiar with the vaso-constricting nature of ergot, Dr. Hofmann was trying to develop a stimulant drug that, in combination with another drug refined from ergot, could be used to halt hemorrhaging following childbirth.  Hofmann experienced an accidental dosing of LSD.  Here are some of his comments from his laboratory notes:

    • Last Friday, April 16, 1943, I was forced to stop my work in the laboratory in the middle of the afternoon and to go home, as I was seized by a peculiar restlessness associated with a sensation of mild dizziness.  On arriving home, I lay down and sank into a kind of drunkenness which was not unpleasant and which was characterized by extreme activity of imagination.  As I lay in a dazed condition with my eyes closed (I experienced daylight as disagreeably bright) there surged upon me an uninterrupted stream of fantastic images of extraordinary plasticity and vividness and accompanied by an intense, kaleidoscope-like play of colors.  This condition gradually passed off after about two hours. From http://www.psychedelic-library.org/hofmann.htm.
    Several days later Dr. Hofmann intentionally ingested 250 µg of LSD which he hypothesized would be a threshold dose.  Here is what he said about his second ingestion:
    • April 19, 1943: Preparation of an 0.5% aqueous solution of d-lysergic acid diethylamide tartrate.
    • 4:20 P.M.: 0.5 cc (0.25 mg LSD) ingested orally.  The solution is tasteless.
    • 4:50 P.M.: no trace of any effect. 
    • 5:00 P.M.: slight dizziness, unrest, difficulty in concentration, visual disturbances, marked desire to laugh...
    • At this point the laboratory notes are discontinued: The last words were written only with great difficulty.  I asked my laboratory assistant to accompany me home as I believed that I should have a repetition of the disturbance of the previous Friday.  While we were cycling home, however, it became clear that the symptoms were much stronger than the first time.  I had great difficulty in speaking coherently, my field of vision swayed before me, and objects appeared distorted like images in curved mirrors.  I had the impression of being unable to move from the spot, although my assistant told me afterwards that we had cycled at a good pace.  http://www.psychedelic-library.org/hofmann.htm
    The difficulty Hofmann experienced with speaking coherently is reminiscent of a 1988 case report from Massachusetts General Hospital in which a patient was admitted for investigation of bowel complaints.  While in the hospital he became unable to speak coherently.  Eventually diagnosed with celiac disease, he was placed on a gluten free diet.  After several months on the diet, his speech was fully returned.  But I’m getting ahead of myself.  We were talking about Hofmann’s discovery. 

    LSD arrived in the USA in 1948 and was used to gain a better understanding of the schizophrenic experience:

    • In psychiatry, the use of LSD by students was an accepted practice; it was viewed as a teaching tool in an attempt to enable the psychiatrist to subjectively understand schizophrenia.  http://en.wikipedia.org/wiki/History_of_LSD
    These students who tried LSD apparently failed to consider that the connection between the symptoms of LSD ingestion and schizophrenia might be due to a common source—psycho-active peptides from gluten grains. 

    About a decade after LSD had crossed the Atlantic, and from a very different research perspective, Dr. Curtis Dohan began investigating the possibility that gluten grains might be a factor in schizophrenia.  He had found that people with celiac disease and those with schizophrenia both excrete increased quantities of specific groups of indoles in their urine.  Some such indoles are known to be psychoactive and some psychoactive alkaloids also contain such indoles. 

    Having learned about this connection between celiac disease and schizophrenia, Dr. Dohan then undertook a study in which he examined hospital admission rates for schizophrenia both during periods of plenty and during World War II grain shortages.  He found that there was, indeed, a reduction in admissions during grain shortages, which normalized when ample grains became available again. 

    Dohan’s next step, along with several colleagues, was to design and conduct a single-blind cross-over study of schizophrenic patients in a locked ward.  They found that symptoms of schizophrenia abated on a gluten-free, dairy-free diet.  These same patients relapsed on re-introduction of these foods.  These data were published in The British Journal of Psychiatry in 1969.  Dohan’s findings were replicated and published in the January1976 issue of Science by Man Mohan Singh and Stanley Kay.

    Three years later, Christine Zioudrou and her colleagues demonstrated the presence of psychoactive peptides in the incomplete digests of gluten grains, including some with morphine-like properties, which they named “exorphins”.  Subsequent research by Fukudome and Yoshikawa has shown that there are five separate sequences from gluten grains that have psycho-active properties.  They named these exorphins A4, A5, B4, B5, and C. 

    At some point in this process, Dohan may have learned about the pseudo-hallucinations sometimes reported in celiac patients.  The primary difference between the schizophrenic’s hallucinations and those associated with celiac disease is that the celiac patient can exercise conscious control to stop them.  The schizophrenic appears unable to do this. 

    As he continued to accumulate more such data, Dohan went on to publish 16 more papers and letters over the next twenty years demonstrating an impressive body of evidence to support his suspicion that psychoactive peptides from gluten and possibly dairy proteins had a powerful impact on many cases of schizophrenia.  Yet, to an even greater extent than today, most people simply could not believe that such supposedly healthful foods as gluten grains and dairy products could be causing illness.  It was probably this paradigm that helped lead to subsequent publications and a period of dormancy in this area of research. 

    Several reports of very small numbers of schizophrenic patients, chronic patients, which Dohan had specifically identified as unlikely to respond to the diet, showed no benefit from a gluten-free diet.  Other studies were improved through double-blinding but weakened by extremely limited dietary control, permitting visitors to bring food to patients participating in that study, essentially abrogating the value of the entire study.  Some researchers ignored Dohan’s assertions that celiac disease could serve as a model for studying schizophrenia.  They chose, instead, to produce data that discredited the possibility that schizophrenia is identical to celiac disease by showing that most schizophrenic patients do not show signs of malabsorption.  Other work, conducted in the same vein, showed that celiac antibodies are not found in most schizophrenic patients. 

    Despite all the powerful evidence compiled by Dohan and others, this wave of studies and letters discredited Dohan’s work by contradicting notions that Dohan had never voiced.  For instance, he never expressed the notion that schizophrenia was celiac disease.  He simply asserted that there were compelling similarities and a small but significant overlap between schizophrenia and celiac disease, suggesting the need to explore gluten as a possible contributing factor in schizophrenia.  Considerable data support that notion but Dohan’s vigorous and persistent pursuit of this important discovery was soon depicted as a personal quest.  For instance, in a private email with one of Dohan’s contemporaries, Dohan was repeatedly called “unscientific.” Yet, fifteen years later, this same researcher has since participated in a published study that supports Dohan’s hypothesis. 

    Fortunately for all of us, the last dozen years have seen a resurgence of interest in the gluten hypothesis regarding schizophrenia, beginning with a case report by De Santis et al.  They described a patient with schizophrenia and a SPECT scan showing abnormal blood flow patterns in the brain typical of schizophrenia.  This patient developed symptoms of celiac disease and was placed on a gluten free diet.  Not only did this patient’s celiac symptoms disappear, her/his symptoms of schizophrenia disappeared and blood flow patterns in her brain normalized.  The gluten-free diet was the only plausible explanation for these changes.  

    A list of reports suggest important reasons to investigate the impact of gluten on our brains.  For instance, Dr. Knivsburg reported the discovery of two cases of celiac disease and one of milk protein sensitivity among 15 dyslexic children.  That is a huge increased incidence over the general population.  Similarly, Dr. Kozlowska found that almost 70% of celiac children have ADHD that normalizes on a gluten-free diet.  The Massachusetts General Hospital case study mentioned earlier reported celiac-associated aphasia that resolved on a gluten free diet.  Dr. Hu and colleagues report a laundry list of cognitive impairments in association with celiac disease including amnesia, acalculia, confusion, and personality changes.  Many of these disabilities wax and wane according to the gluten content of the diet. 

    However, the notion of gluten-driven cognitive deficits, including learning disabilities, and behavioral abnormalities in association with non-celiac gluten sensitivity, has only recently gotten some research attention.  For instance, Alexandra Blair of The TimesOnline in the United Kingdom reported on an informal study conducted at a small school for dyslexic children in Northumberland.  They got some startlingly positive improvements in students’ performance after placing them on a gluten free diet.  Dr. Marios Hadjivassiliou et al.  at the Royal Hallamshire Hospital in Sheffield, U.K.  have repeatedly reported that a majority of patients with neurological disease of unknown origin are also gluten sensitive while only about one third of these patients have celiac disease. 

    Kalaydjian et al.  reviewed the medical literature to about 2005 and called for large, controlled studies of the connection between gluten and schizophrenia because it is clear that some schizophrenic patients benefit enormously from a gluten free diet.  Similarly, earlier this year, Kraft et al.  reported on a schizophrenic patient who was diagnosed at seventeen years of age.  Fifty three years later, at her doctor’s suggestion, she undertook a ketogenic diet to lose weight.  Not only did she lose weight, she also lost all signs and symptoms of schizophrenia. 

    As 2009 comes to a close, two more publications have made this year into something of a turning point for this research.  Cascella et al.  state that “Our results confirm the existence of a subgroup of patients with antibody characteristics associated with the presence of a specific immune response to gluten.”

    Similarly, Samaroo et al.  report that their findings “….  indicate that the anti-gliadin immune response in schizophrenia has a different antigenic specificity from that in celiac disease…” they go on to assert that the genetic HLA markers for celiac disease were not found in the schizophrenic patients they studied. 

    At the most basic level, we know that gluten causes increased intestinal permeability among a wide range of genetically susceptible individuals.  We also know that substances from moldy grains will cause schizophrenic symptoms in any of us.  It is not a great leap to suggest that, in the context of gluten-induced increased intestinal permeability, similarities in hallucinations, altered brain perfusion, and a range of cognitive deficits found in schizophrenia, celiac disease, and gluten sensitivity might all be rooted in the commonest food in our diets from which hallucinogenic drugs can be produced. 

    Institutional nutrition and food programs for the needy and/or homeless include large proportions of inexpensive gluten-laden foods.  Such diets, often provided charitably for those at the lowest socio-economic strata, are at least self-defeating.  Further, such foods are often consumed at this economic level despite visible molds growing on them.  I have heard stories of homeless persons scavenging through dumpsters located at or near bakeries.  There can be little doubt that such eating practices perpetuate the very psychiatric conditions that have reduced many of these people to a state of homelessness. 

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    Guest Barbara Greene

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    Are there any epidemiological studies comparing numbers of diagnosed schizophrenics in countries where wheat is not the predominant grain consumed with those in countries where wheat is the predominant grain?

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    Guest ralph Kuon

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    I like it a lot, makes a lot of sense, I have a wife and two children with celiac disease and it prevails in the majority of mother's side relatives; they who now try gluten free diets are doing much better than those who not.

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    Guest Crystal

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    From personal experience, ADHD symptoms, are significantly reduced when a gluten free or reduced lifestyle is achieved.

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    Guest Christine Toms

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    Excellent! My family has had the courage to do something about it and the results are outstanding. I encourage other people to do likewise. Don't give up, it's worth it.

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    Are there any epidemiological studies comparing numbers of diagnosed schizophrenics in countries where wheat is not the predominant grain consumed with those in countries where wheat is the predominant grain?

    In developing countries it resides after a shorter length of time, that is to say countries that still have a rich farm economy of fruits and such??

     

    At least India maybe, they have a lot of curry in their diet and one of the effects is anti depressives from kava?

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    Just say no to the body of Christ.

    The blood being the water....

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    Guest Ron Hoggan

    Posted

    Are there any epidemiological studies comparing numbers of diagnosed schizophrenics in countries where wheat is not the predominant grain consumed with those in countries where wheat is the predominant grain?

    Not that I know of, but there are several studies by Dohan that look at WW II grain shortages and admission rates for schizophrenia. He also reports on populations where gluten is rarely eaten and shows that schizophrenia is rare.

     

     

    1. Dohan FC.Wheat "consumption" and hospital admissions for schizophrenia during World War II. A preliminary report. Am J Clin Nutr. 1966 Jan;18(1):7-10.

     

     

    2. Dohan FC, Harper EH, Clark MH, Rodrigue RB, Zigas V. Is schizophrenia rare if grain is rare? Biol Psychiatry. 1984 Mar;19(3):385-99.

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    Schizophrenia runs in my family. When my 20 year old daughter began showing paranoid behavior, a friend knowledgeable about celiac disease persuaded me to have her evaluated by a nurse who is a specialist in celiac. After 2 weeks on a gluten-free and dairy-free diet, her mental symptoms have disappeared and she seems to be her "old" self. The change was dramatic. I wouldn't have believed it if I hadn't seen this personally. I got tested, and I have the gluten antibodies and genes. A gluten-free trial takes little effort, but could be a literal life-saver.

     

    Thanks for the excellent informational article.

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    I was diagnosed with Adult ADHD when I was 32 after complaining to my doctor (whom had me on antidepressants for years) that I was not depressed and I didn't like the numb feeling that the antidepressants gave me. A different Doctor put me on Dexedrine for 7 years, to no avail. I would always get very angry at the littlest things (like road rage angry), at things that never made sense. My wife and kids were terrified of me, and we were on the verge of a divorce. I stopped eating all carbs to loose weight after new years 2012. Being completely carb free was to hard and just went gluten free (this is completely random at this time, and for no other reason then to loose weight). 6 weeks later on Valentines Day, we celebrate as a family, and we were going to order a gluten free pizza, but they were all out of gluten free crust. So, we went with the regular crust (What a mistake that was). I had the worst meltdown I had ever had, I have only vague memories of it, but my wife filled me in and it was not pretty (There was a lot of screaming and throwing things). Over the course of about a year and a lot of trial and error, for us, it turns out that we cannot eat Wheat. Every time I eat Wheat all my ADHD symptoms return and I feel drunk, and I act the way you would expect a stereotypical 42-year-old Alcoholic would act like (I know now that Wheat was the cause of 90% of all my family problems). I still don't know what to call it when people ask. My doctor says that he has never heard of anything like it, so I call it Gluten Ataxia (after a lot of my own research). I don't think people would respond to well if I called it Wheat induced schizophrenia. After about 2 months of a Gluten Free diet I stopped all my medication and have been medication free for 3+ years now.

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    Guest Ron Hoggan

    Posted

    Are there any epidemiological studies comparing numbers of diagnosed schizophrenics in countries where wheat is not the predominant grain consumed with those in countries where wheat is the predominant grain?

    Yes. Just search the publications by Curtis Dohan in the 1960's to 1980's. I don't remember the title of the study, but he did publish one that makes that comparison.

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    Guest Ron Hoggan

    Posted

    Schizophrenia runs in my family. When my 20 year old daughter began showing paranoid behavior, a friend knowledgeable about celiac disease persuaded me to have her evaluated by a nurse who is a specialist in celiac. After 2 weeks on a gluten-free and dairy-free diet, her mental symptoms have disappeared and she seems to be her "old" self. The change was dramatic. I wouldn't have believed it if I hadn't seen this personally. I got tested, and I have the gluten antibodies and genes. A gluten-free trial takes little effort, but could be a literal life-saver.

     

    Thanks for the excellent informational article.

    Hi Sarah,

    Congratulations on your personal discovery. You are very welcome.

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    Guest Ron Hoggan

    Posted

    Hi Paul,

    Very cool. Thank you for sharing your experience.

    I'd suggest that you have neuological symptoms of gluten sensitivity. Ataxia is characterized by a robot-like gait.

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    Dr. Ron Hoggan, Ed.D.
    This article originally appeared in the Winter 2003 edition of Celiac.coms Scott-Free Newsletter.
    Evolution is an interactive process. Those of us who learn quickly and well are more likely to survive, thrive, and reproduce. Learning capacities then, are factors in the survival of our genes. Research is now revealing that cereal grains, along with other allergenic and highly glycemic foods, pose a serious threat to our sustained ability to learn. These foods have been shown to interfere at almost any stage of the learning process, impeding our attempts to focus our attention, observe, ponder, remember, understand, and apply that understanding. Grains can alter learning capacities in four specific ways: as sequelae of untreated celiac disease; through an immune sensitivity to gluten; through dietary displacement of other nutrients and; through the impact of grain on blood sugar/insulin levels.
    There are many reports of learning problems in association with untreated celiac disease. A majority of children with celiac disease display the signs and symptoms of attention deficit disorder (ADD/ADHD)1, 2 a range of learning difficulties3 and developmental delays4-6. Many of the same problems are found more frequently among those with gluten sensitivity7 a condition signaled by immune reactions against this most common element of the modern diet. Grain consumption can also cause specific nutrient deficiencies that are known to play an important role in learning. Grains can also cause problems with blood sugar/insulin levels resulting in reduced capacities for learning. Further, foods derived from grain are an important element in the current epidemic of hypoglycemia, obesity, and Type 2 diabetes8-10. Our growing understanding of the biological impact of cereal grain consumption must move educators to challenge current dietary trends.
    Part of our improved understanding comes from new testing protocols which are revealing that celiac sprue afflicts close to 1% of the general population, making it the most common life-long ailment among humans, with frequencies ranging from 0.5% to more than 5% of some populations11, 12. It is widespread and appears to occur more frequently among populations that have experienced relatively shorter periods of exposure to these grains13. The importance of this newly recognized high frequency of celiac disease becomes obvious when we examine the impact it has on learning and behavior.
    Research has identified ADHD in 66-70% of children with untreated celiac disease, which resolves on a gluten-free diet, and returns with a gluten challenge1, 2. Several investigators have connected particular patterns of reduced blood flow to specific parts of the brain in ADHD13-15. Other reports have connected untreated celiac disease with similarly abnormal blood flow patterns in the brain16. One might be able to dismiss such reports if viewed in isolation, but the increased rates of learning disabilities among celiac patients3, and the increased rates of celiac disease among those with learning disabilities leave little to the imagination17. Further, there is one report of gluten-induced aphasia (a condition characterized by the loss of speech ability) that resolved after diagnosis and institution of a gluten-free diet18. Still other investigations suggest a causal link between the partial digests of gluten (opioid peptides) and a variety of problems with learning, attention, and development.
    Gluten sensitivity, afflicting close to 15% of the general population19, 20 is an immune reaction to one or more proteins in found in grains. When a persons immune system has developed antibodies against any of these proteins, undigested and partly digested food particles have been allowed entry into the bloodstream21. The leakage of food proteins through the intestinal wall signals a failure of the protective, mucosal lining of the gastrointestinal tract, as is consistently found in untreated celiac disease. Many of the same health and learning problems that are found in celiac disease are significantly overrepresented among those with gluten sensitivity for the very good reason that many of the same proteins are being leaked into the blood of those with gluten sensitivity.
    Our cultural obeisance to grains is at odds with the remains of ancient humans. Archaeologists have long recognized that grains are a starvation food—one for which we are not well suited. Grains result in consistent signs of disease and malnourishment in every locale and epoch associated with human adoption of grain cultivation.
    Grains are a poverty food. As we increase our grain consumption, we cause deficiencies in other nutrients by overwhelming the absorptive and transport mechanisms at work in our intestines. For instance, diets dominated by grains have been shown to induce iron deficiency22—a condition that is widely recognized as causing learning disabilities23-29. This should not be surprising since iron is the carrier used to distribute oxygen throughout our bodies, including various regions of our brains. There is little room to dispute the hazards to learning posed by reductions in oxygen supply to the brain. Iron deficiency reduces available oxygen in the brain, revealing yet another dimension of gluten grains as mediators of learning difficulties.
    There is more. The impact of grain consumption on our blood sugar levels is yet another facet of its contribution to learning problems. We evolved as hunter-gatherers, eating meats, and complex carbohydrates in the form of fruits, vegetables, and seeds. Refined sugars were a rare treat wrested from bees with some difficulty. At best, it was a rare treat for our pre-historic ancestors.
    Today, with unprecedented agricultural/industrial production of refined sugars along with cultivation and milling of grain flours, these products have become very cheap and available, particularly over the last fifty years. During that time, we have added enormous quantities of grain-derived starches to the overwhelming quantities of sugar we consume. The result of this escalating dietary trend may be observed in the current epidemic rates of Type 2 diabetes, hypoglycemia, obesity, and cardiovascular disease. In the classroom, we see these trends manifest in students mood swings, behavioral disorders (fluctuating between extreme lethargy and hyperactivity), chronic depression, forgetfulness, and muddled thinking—all of which reflects the inordinate, counter-evolutionary burden placed on many homeostatic systems of the body, particularly those related to blood sugar regulation.
    The pancreas has many functions. One important activity of the pancreas is to stabilize blood sugar levels. When blood sugar is not well regulated, learning is impaired30. The pancreas secretes carefully monitored quantities of glucagon and insulin. The pancreas responds to the presence of proteins, sugar, and starch in the digestive tract by producing insulin. It produces glucagon in response to fats. The balanced presence of both of these hormones in the bloodstream is critical to learning because they regulate the transport of nutrients into cells. Too little or too much insulin can cause blood sugar levels go out of control inducing a wide range of symptoms.
    Today, when the insulin/glucagon balance goes awry, it is frequently due to insulin overproduction due to a diet dominated by sugars and starches. This overproduction is caused by chronic consumption of highly glycemic foods. The resulting elevated levels of insulin cause rapid movement of nutrients into cells, either for storage as fat, or to be burned as energy, causing increased activity levels, "hot spells", sweating, increased heart rate, etc. This energized stage requires a constant supply of sugars and starches to be maintained. Otherwise, it is soon followed by bouts of lethargy, light-headedness, tremors, and weakness, which are all signs of hypoglycemia or very low blood sugar levels.
    Despite having stored much of the blood sugars as fats, there is insufficient glucagon to facilitate its use for energy. As this condition progresses, and as blood sugar levels plummet, periods of irrational anger and/or confusion often result. These moods often result from adrenaline secreted to avoid a loss of consciousness due to low blood sugar levels. The next step in the progression, in the absence of appropriate nutritional intervention, is lapsing into a coma.
    In the short term, the answer to these fluctuations is more frequent consumption of sugars/starches. However, the long term result of such an approach is either a state of insulin resistance, where more and more insulin is required to do the same task, or a state of pancreatic insufficiency, where the pancreas is simply unable to keep pace with the demand for insulin. In either case, once this stage is reached, the individual may be diagnosed with type 2 diabetes. This disease has so increased among North Americans, particularly among children, that an autoimmune form of diabetes, previously called juvenile onset, had to be renamed to "Type 1 diabetes".
    By now, it will not surprise the reader to learn that Type 1 diabetes has also been shown to be significantly associated with gluten. Research reveals that there is considerable overlap between celiac disease and Type 1 diabetes. About 8% of celiacs also have Type 1 diabetes31-33, and 5-11% of Type 1 diabetics have celiac disease34-38. Further, Scott Frazer et al. have repeatedly shown, in animal studies, a causal, dose-dependent relationship between type 1 diabetes and gluten39-42.
    The growing reaction against gluten and other allergenic foods should not be confused with the several dietary fads of the 20th Century. The vegetarian perspective ignores the vitamin deficiencies that result from a strict vegetarian diet. The low-fat craze is another fad that has mesmerized the industrialized world for the last 30-40 years. Fortunately, this perspective has recently come under scrutiny. Despite having served as the driving force behind most physicians dietary recommendations during the last several decades, the low fat dictum is overwhelmingly being discredited by research reported in peer reviewed publications.
    Recognition and avoidance of allergenic and highly glycemic foods is a whole new trend that is based on scientific research and evidence. It reflects an improved understanding of the function of the gastrointestinal tract, the endocrine system, particularly the pancreas, and the immune system. Past dietary fads are consistently deficient in important nutrients that are necessary to our good health and survival. Further, they frequently contain substances that are harmful to us, such as the phytates that are abundantly present in whole grain foods, and interfere with absorption of many minerals.
    It is increasingly clear that grains, especially those that contain gluten, are contraindicated for human learning. The evidence is overwhelming. The mandate of eating to learn is learning to eat as our ancestors did.
    Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered here.
    References:
    Kozlowska, Z: (1991). Results of investigation on children with coeliakia treated many years with glutethen free diet Psychiatria Polska. 25(2),130-134. Paul, K., Todt, J., Eysold, R. (1985) [EEG Research Findings in Children with Celiac Disease According to Dietary Variations]. Zeitschrift der Klinische Medizin. 40, 707-709. Grech, P.L., Richards, J., McLaren, S., Winkelman, J.H. (2000) Psychological sequelae and quality of life in celiac disease. Journal of Pediatric Gastroenterology and Nutrition 31(3): S4 Reichelt, K., Sagedal, E., Landmark, J., Sangvic, B., Eggen, O., Helge, S. (1990a). The Effect of Gluten-Free Diet on Urinary peptide Excretion and Clinical State in Schizophrenia. Journal of Orthomolecular Medicine. 5(4), 169-181. Reichelt, K., Ekrem, J., Scott, H. (1990b). Gluten, Milk Proteins and Autism: DIETARY INTERVENTION EFFECTS ON BEHAVIOR AND PEPTIDE SECRETION. Journal of Applied Nutrition. 42(1), 1-11. Reichelt, K., Knivsberg, A., Lind, G., Nodland, M. (1991). Probable etiology and Possible Treatment of Childhood Autism. Brain Dysfunction. 4, 308-319. Hoggan, R. (1997a). Absolutisms Hidden Message for Medical Scientism. Interchange. 28(2/3), 183-189. Caterson ID, Gill TP. Obesity: epidemiology and possible prevention. Best Pract Res Clin Endocrinol Metab. 2002 Dec;16(4):595-610. Hennessy AR, Walker JD.Silent hypoglycaemia at the diabetic clinic. Diabet Med. 2002 Mar;19(3):261. Kue Young T, Chateau D, Zhang M. Factor analysis of ethnic variation in the multiple metabolic (insulin resistance) syndrome in three Canadian populations.Am J Human Biol. 2002 Sep-Oct;14(5):649-58. Wahab PJ, Meijer JW, Dumitra D, Goerres MS, Mulder CJ. Coeliac disease: more than villous atrophy.Rom J Gastroenterol. 2002 Jun;11(2):121-7. Catassi C, Ratsch IM, Gandolfi L, Pratesi R, Fabiani E, El Asmar R, Frijia M, Bearzi I, Vizzoni L. Why is coeliac disease endemic in the people of the Sahara?Lancet. 1999 Aug 21;354(9179):647-8. Langleben DD, Acton PD, Austin G, Elman I, Krikorian G, Monterosso JR, Portnoy O, Ridlehuber HW, Strauss HW. Effects of Methylphenidate Discontinuation on Cerebral Blood Flow in Prepubescent Boys with Attention Deficit Hyperactivity Disorder.J Nucl Med. 2002 Dec;43(12):1624-1629. 2: Kim BN, Lee JS, Shin MS, Cho SC, Lee DS. Regional cerebral perfusion abnormalities in attention deficit/hyperactivity disorder Statistical parametric mapping analysis. Eur Arch Psychiatry Clin Neurosci. 2002 Oct;252(5):219-25. Lou, H., Henriksen, L., Bruhn, P. (1984). Focal cerebral hypoperfusion in children with dysphasia and/or attention deficit disorder. Archives of Neurology. 825-829. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3. Knivsberg AM. Urine patterns, peptide levels and IgA/IgG antibodies to food proteins in children with dyslexia.Pediatr Rehabil. 1997 Jan-Mar;1(1):25-33. 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. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM. The humoral response in the pathogenesis of gluten ataxia. Neurology. 2002 Apr 23;58(8):1221-6. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness.J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Review. Husby, V., Jensenius, C., Svehag, S.(1985). Passage of Undegraded DietaryAntigen into the Blood of Healthy Adults. Scandinavian Journal of Immunology. 22, 83-92. Ma A, Chen X, Zheng M, Wang Y, Xu R, Li J. Iron status and dietary intake of Chinese pregnant women with anemia in the third trimester. Asia Pac J Clin Nutr. 2002;11(3):171-5. Kapil U, Bhavna A. Adverse effects of poor micronutrient status during childhood and adolescence. Nutr Rev. 2002 May;60(5 Pt 2):S84-90. Review. Youdim MB, Yehuda S. The neurochemical basis of cognitive deficits induced by brain iron deficiency: involvement of dopamine-opiate system. Cell Mol Biol (Noisy-le-grand). 2000 May;46(3):491-500. Otero GA, Aguirre DM, Porcayo R, Fernandez T. Psychological and electroencephalographic study in school children with iron deficiency. Int J Neurosci. 1999 Aug;99(1-4):113-21. Guesry P. The role of nutrition in brain development. Prev Med. 1998 Mar-Apr;27(2):189-94. Review. Bruner AB, Joffe A, Duggan AK, Casella JF, Brandt J. Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls. Lancet. 1996 Oct 12;348(9033):992-6. Soewondo S. The effect of iron deficiency and mental stimulation on Indonesian childrens cognitive performance and development. Kobe J Med Sci. 1995 Apr;41(1-2):1-17. McCarthy AM, Lindgren S, Mengeling MA, Tsalikian E, Engvall JC. Effects of diabetes on learning in children. Pediatrics. 2002 Jan;109(1):E9. Bertini M, Sbarbati A, Valletta E, Pinelli L, Tato L. Incomplete gastric metaplasia in children with insulin-dependent diabetes mellitus and celiac disease. An ultrastructural study.BMC Clin Pathol. 2001;1(1):2. Schuppan D, Hahn EG. Celiac disease and its link to type 1 diabetes mellitus.J Pediatr Endocrinol Metab. 2001;14 Suppl 1:597-605. Holmes GK. Coeliac disease and Type 1 diabetes mellitus - the case for screening.Diabet Med. 2001 Mar;18(3):169-77. x Saukkonen T, Vaisanen S, Akerblom HK, Savilahti E. Coeliac disease in children and adolescents with type 1 diabetes: a study of growth, glycaemic control, and experiences of families.Acta Paediatr. 2002;91(3):297-302. Spiekerkoetter U, Seissler J, Wendel U. General Screening for Celiac Disease is Advisable in Children with Type 1 Diabetes.Horm Metab Res. 2002 Apr;34(4):192-5. Barera G, Bonfanti R, Viscardi M, Bazzigaluppi E, Calori G, Meschi F, Bianchi C, Chiumello G. Occurrence of celiac disease after onset of type 1 diabetes: a 6-year prospective longitudinal study.Pediatrics. 2002 May;109(5):833-8. Hansen D, Bennedbaek FN, Hansen LK, Hoier-Madsen M, Hegedu LS, Jacobsen BB, Husby S. High prevalence of coeliac disease in Danish children with type I diabetes mellitus.Acta Paediatr. 2001 Nov;90(11):1238-43. Aktay AN, Lee PC, Kumar V, Parton E, Wyatt DT, Werlin SL. The prevalence and clinical characteristics of celiac disease in juvenile diabetes in Wisconsin.J Pediatr Gastroenterol Nutr. 2001 Oct;33(4):462-5. MacFarlane AJ, Burghardt KM, Kelly J, Simell T, Simell O, Altosaar I, Scott FW. A type 1 diabetes-related protein from wheat (triticum aestivum): cDNA clone of a wheat storage globulin, Glb1, linked to islet damage.J Biol Chem. 2002 Oct 29. Scott FW, Rowsell P, Wang GS, Burghardt K, Kolb H, Flohe S. Oral exposure to diabetes-promoting food or immunomodulators in neonates alters gut cytokines and diabetes.Diabetes. 2002 Jan;51(1):73-8. Scott FW, Cloutier HE, Kleemann R, Woerz-Pagenstert U, Rowsell P, Modler HW, Kolb H. Potential mechanisms by which certain foods promote or inhibit the development of spontaneous diabetes in BB rats: dose, timing, early effect on islet area, and switch in infiltrate from Th1 to Th2 cells.Diabetes. 1997 Apr;46(4):589-98. Scott FW. Food-induced type 1 diabetes in the BB rat.Diabetes Metab Rev. 1996 Dec;12(4):341-59. Of Relevant interest:
    Gormanous M, Hunt A, Pope J, Gerald B. Lack of knowledge of diabetes among Arkansas public elementary teachers: implications for dietitians. J Am Diet Assoc. 2002 Aug;102(8):1136-8.

    Scott Adams
    BMJ 2004;328:438-439 (21 February) Celiac.com 02/27/2004 – The following report is interesting, but I believe that serological studies done on those with schizophrenia would be a far better way to conduct such a study. Also, the use of such a small control group cannot accurately predict the actual incidence of schizophrenia in those with celiac disease. –Scott Adams
    According to a Danish study published in the British Medical Journal, people with celiac disease may have an increased risk of developing schizophrenia. Previous studies have also suggested an association between these two disorders. The study identified 7,997 people over age 15 who were admitted to a Danish psychiatric unit for the first time between 1981 and 1998 and were diagnosed with schizophrenia. The researchers selected 25 random controls and matched their year of birth and sex, and identified any history of celiac disease, ulcerative colitis or Crohns disease in both groups, and in their parents. A "moderately strong risk relation between coeliac disease and schizophrenia" was discovered in the data, and the researchers stress that these findings only reflect a small proportion of cases, as both disorders are rare. The prevalence of celiac disease among schizophrenics was 1.5 cases per 1,000 compared to 0.5 cases per 1,000 in the larger control group, which means that there is a three times greater risk of schizophrenia in those with celiac disease. Interestingly Crohns disease and ulcerative colitis were not associated with an increased risk of schizophrenia.
    According to Dr. Eaton: More research is needed to understand the link between celiac disease and schizophrenia. The most important question is whether treatment for celiac disease, in the form of a gluten-free diet, would benefit the small proportion of individuals with schizophrenia who are genetically prone to celiac disease but have not been diagnosed with it."

    Scott Adams
    Acta Psychiatr Scand 2005: 1-9. C 2005 Blackwell Munksgaard. Celiac.com 02/09/2006 – After a review of the medical literature, researchers have concluded that many cases of schizophrenia are related to celiac disease or gluten intolerance, and can be successfully treated using a gluten-free diet. Like celiac disease, schizophrenia affects approximately 1% of the population. It is considered one of the top 10 causes of disability worldwide. In many studies the researchers found that in a subset of patients a drastic reduction or total elimination of schizophrenic symptoms occurred after they were treated with a strict gluten-free diet. Based on this the researchers believe that a gluten-free diet may serve as a "safe and economical alternative for the reduction of symptoms in a subset of patients." They conclude: "Large-scale epidemiological studies and clinical trials are needed to confirm the association between gluten and schizophrenia, and address the underlying mechanisms by which this association occurs."


    Jefferson Adams
    Celiac.com 04/29/2009 - A team of researchers based at UK's prospective University of Highlands and Islands (UHI) have found a link between gluten and schizophrenia. According to their latest findings, proteins found in the gluten of wheat, rye and barley might play a role in triggering schizophrenia in people with a genetic risk for the condition, or in worsening symptoms in people who have the disease.
    The research team has been looking into the role played by gluten in schizophrenia and diabetes, as well as hunting for connections between the two disorders. Their research showed that the bodies of certain schizophrenia sufferers could not properly processes gluten, which led to tissue damage.
    As a result of these and other findings, researchers now consider genetic risk factors, together with environmental triggers, to be central to development of both schizophrenia and diabetes. Gluten is one such example.
    According to senior researcher and reader in genetics, Dr. Jun Wei, more than one-third of all people with schizophrenia show "high levels of antibodies against wheat gluten," and may experience some improvement in symptoms with a gluten-free diet.
    Though the studies are still in their early stages, the hypothesis is encouraging, because, as noted by head of UHI department of diabetes and cardiovascular science, Prof Ian Megson, if it is correct, "a simple change in diet might prevent these diseases...in some individuals."
    The research is part of two comprehensive studies at UHI into the connections between schizophrenia and diabetes, and the role played by gluten, and is supported by a £300,000 grant from the Schizophrenia Association of Great Britain (SAGB).
    It would be interesting to see more research done on the connection between celiac disease and schizophrenia, as other studies have indicated that there is a link.

    Source: BBC News


  • Recent Articles

    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

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.