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    High Levels of Maternal Dietary Antibodies Mean Higher Risk for Non-affective Psychosis in Offspring


    Jefferson Adams

    Celiac.com 02/13/2013 - A team of researchers wanted to determine whether levels of immunoglobulin G (IgG) were associated with a later diagnosis of a non-affective psychotic disorder.


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    Photo: CC--flequiThe researchers included H. Karlsson, Å. Blomström, S. Wicks, S. Yang, R.H. Yolken, and C. Dalman. They are affiliated with the Department of Neuroscience at the Karolinska Institute in Stockholm, Sweden.

    To accomplish their goal, the team analyzed archival dried blood spots taken from newborns in Sweden between 1975 and 1985 with verified register-based diagnoses of non-affective psychoses made between 1987 and 2003 and comparison subjects matched on sex, date of birth, birth hospital, and municipality.

    The team reviewed samples from a total of 211 case subjects and 553 comparison subjects who agreed to take part in the study. They pulled data for factors associated with maternal status, pregnancy, and delivery from the Swedish Medical Birth Register.

    They used enzyme-linked immunosorbent assay to analyze the results for levels of IgG directed at gliadin (a component of gluten) and casein (a milk protein) in eluates from dried blood spots. They then calculated odds ratios for levels of IgG directed at gliadin or casein for non-affective psychosis.

    Comparison subjects associated with non-affective psychosis showed levels of anti-gliadin IgG (but not anti-casein IgG) above the 90th percentile of levels observed (odds ratio=1.7, 95% CI=1.1-2.8).

    This connections was not affected by differences in maternal age, immigrant status, or mode of delivery. They also found that gestational age at birth, ponderal index, and birth weight were not associated with maternal levels of anti-gliadin IgG.

    From their study, they concluded that high levels of anti-gliadin IgG in the maternal circulation are associated with an elevated risk for the development of a non-affective psychosis in offspring.

    They point out that more research is needed to identify the mechanisms underlying this association in order to develop preventive strategies.

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  • About Me

    Jefferson Adams is a freelance writer living in San Francisco. He has covered Health News for Examiner.com, and provided health and medical content for Sharecare.com. His work has appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate, among others.

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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
    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."


    Dr. Ron Hoggan, Ed.D.
    This article originally appeared in the Winter 2010 edition of Journal of Gluten Sensitivity.
    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. 


    Jefferson Adams
    Celiac.com 05/29/2014 - Many people with celiac disease report symptoms of depression, which usually subside upon treatment with a gluten-free diet. But a new study out of Australia suggests that gluten can cause depression in people with non-celiac gluten-sensitivity.
    Current evidence shows that many patients with self-reported non-celiac gluten sensitivity (NCGS) continue to have gastrointestinal symptoms on a gluten-free diet, but say that avoiding gluten makes them feel ‘better'. So, why do people with non-celiac gluten sensitivity seem to feel better on a gluten-free diet, even if they still have gastrointestinal symptoms? A team of researchers wanted to know if this might be due to gluten’s effects on the mental state of those with NCGS, and not necessarily because of gastrointestinal symptoms.
    The research team included S. L. Peters, J. R. Biesiekierski, G. W. Yelland, J. G. Muir, and P. R. Gibson. They are affiliated with the Department of Gastroenterology, Central Clinical School of Monash University at The Alfred Hospital in Melbourne, the Department of Gastroenterology at the Eastern Health Clinical School of Monash University in Box Hill, and the School of Health Sciences at RMIT University in Bundoora, Victoria, Australia.
    For their double-blind cross-over study, they looked at 17 women and five men, aged 24–62 years. All participants suffered from irritable bowel syndrome, but not from celiac disease, and their symptoms were controlled on a gluten-free diet. The team gave the participants one of three random dietary challenges over 3 days, followed by a minimum 3-day washout before moving to the next diet. All participants got all three diets over the course of the study.
    For each phase, the team supplemented the challenge gluten-free food with gluten, (16 g/day), whey (16 g/day) or nothing at all (placebo). The team assessed mental state as determined by the Spielberger State Trait Personality Inventory (STPI), cortisol secretion and gastrointestinal symptoms.
    They found that gluten ingestion was associated with higher overall STPI state depression scores compared to placebo [M = 2.03, 95% CI (0.55–3.51), P = 0.010], but not whey [M = 1.48, 95% CI (−0.14 to 3.10), P = 0.07]. They found no differences for other STPI state indices or for any STPI trait measures, and they saw no difference in cortisol secretion between challenges. Gastrointestinal symptoms were similar for each dietary challenge.
    Short-term exposure to gluten specifically induced current feelings of depression with no effect on other indices or on emotional disposition. Moreover, the team saw no gluten-specific trigger of gastrointestinal symptoms. Such findings might explain why patients with non-coeliac gluten sensitivity feel better on a gluten-free diet despite the continuation of gastrointestinal symptoms.
    Source:
    Aliment Pharmacol Ther. 2014;39(10):1104-1112.

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/21/2018 - Would you buy a house advertised as ‘gluten-free’? Yes, there really is such a house for sale. 
    It seems a Phoenix realtor Mike D’Elena is hoping that his trendy claim will catch the eye of a buyer hungry to avoid gluten, or, at least one with a sense of humor. D’Elena said he crafted the ads as a way to “be funny and to draw attention.” The idea, D’Elena said, is to “make it memorable.” 
    Though D’Elena’s marketing seeks to capitalizes on the gluten-free trend, he knows Celiac disease is a serious health issue for some people. “[W]e’re not here to offend anybody….this is just something we're just trying to do to draw attention and do what's best for our clients," he said. 
    Still, the signs seem to be working. D'elena had fielded six offers within a few days of listing the west Phoenix home.
    "Buying can sometimes be the most stressful thing you do in your entire life so why not have some fun with it," he said. 
    What do you think? Clever? Funny?
    Read more at Arizonafamily.com.

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    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
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    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
    The trials are set to begin at Australia’s University of the Sunshine Coast Clinical Trials Centre. The vaccine is designed to allow people with celiac disease to consume gluten with no adverse effects. A successful vaccine could be the beginning of the end for the gluten-free diet as the only currently viable treatment for celiac disease. That could be a massive breakthrough for people with celiac disease.
    USC’s Clinical Trials Centre Director Lucas Litewka said trial participants would receive an injection of the vaccine twice a week for seven weeks. The trials will be conducted alongside gastroenterologist Dr. James Daveson, who called the vaccine “a very exciting potential new therapy that has been undergoing clinical trials for several years now.”
    Dr. Daveson said the investigational vaccine might potentially restore gluten tolerance to people with celiac disease.The trial is open to adults between the ages of 18 and 70 who have clinically diagnosed celiac disease, and have followed a strict gluten-free diet for at least 12 months. Anyone interested in participating can go to www.joinourtrials.com.
    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    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.