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    Autism: Can a Gluten-free Diet Help?


    Dr. Ron Hoggan, Ed.D.


    • Journal of Gluten Sensitivity Summer 2012 Issue


    Image Caption: Image: CC--National Human Genome Research Institute (NHGRI)

    Celiac.com 11/23/2017 - Many theories have been fielded about autism. Some research careers have been made by investigating autism, while other careers have been seriously damaged when that research threatened some sacred cows of allopathic medicine. Yet despite all of this active research exploring the world of autism, we continue to experience exponential increases in rates at which autism is diagnosed. And debate continues unabated regarding the causes and appropriate treatments. Part of this increasing trend is, doubtless, because we have gotten better at recognizing the various manifestations of this debilitating condition. However, the evidence indicates that there is a dramatic increase in the absolute incidence of autism. Although frightening, this trend may offer some insight into several of the factors that contribute to this condition. That is the crux of my argument here. Since most prior theories have been tested in isolation, as is the norm in medical investigations, measurement of changes induced by individual contributing factors may either be so mild as to escape notice, or may not have been sufficient to induce symptom mitigation. Similarly, if preconceived notions shape resistance to some of these hypotheses, we may miss the most salient characteristics of autism. I have therefore chosen to combine several findings to form a testable hypothesis. I'll let posterity and the reader be the judges of whether this speculation is worthy of further investigation.


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    We begin with Dr. Kalle Reichelt, who sought to understand autism and other psychiatric illnesses through the prism suggested by Dr. Curtis Dohan's work investigating schizophrenic patients. While Dohan et al reported positive results among schizophrenics from a gluten free, dairy free diet, Reichelt and his colleagues identified unique peptides in the urinary excretions from patients on the autistic spectrum and explored their possible connections with gluten and dairy proteins(1). A leaky gut appeared to be a precondition for autism. In 1996, D'Eufemia and others reported increased intestinal permeability in almost half of their autistic patients, using synthetic sugars that can be measured in the urine (2). Gardner has reported disturbed gastrointestinal function in autism.

    Reichelt and Knivsberg have also published reports of improved social interaction and communication among some children with autism following institution of a gluten-free, casein-free diet (4). However, their investigations reveal that the diet must be consistent, strict, and long-lasting to allow the gradual dissipation of the psychoactive peptides from these foods. Others have reported that this dissipation process can take up to 12 months (5).

    It is important to note that, while the work indicating that the symptoms of autism can often be mitigated by the strict, long-term avoidance of gluten and dairy, none of these investigators claimed that this diet can cure autism or even eliminates all of its symptoms. The diet simply helped children improve to the point where they could function better in school and society by mitigating their most severe and limiting symptoms (4). Many of these researchers postulate that improved integrity of the intestinal barrier and reduced ingestion of psychoactive peptides in the diet are a likely root of these improvements.

    Against this backdrop of widespread recognition of gastrointestinal dysfunction, excessive intestinal permeability, and symptom mitigation through dietary restriction in many autistic children, Dr. Andrew Wakefield, along with 12 other researchers, published their discovery of a pattern of intestinal inflammation and compromised barrier function in 11 of 12 subjects with pervasive developmental disorders, including 9 children with autism.

    Based on histories provided by parents, health visitors, and general practitioners, a pattern of behavioral/autistic symptom onset was seen within 14 days of combined vaccination for measles, mumps, and rubella. The average time to symptom onset was about 6 days. In the same report, Wakefield et al state "We did not prove an association between measles, mumps, and rubella vaccine and the syndrome described." Later on the same page, they state "If there is a causal link between measles, mumps, and rubella vaccine and this syndrome, a rising incidence might be anticipated after the introduction of this vaccine in the UK, in 1988." [my emphasis] Wakefield et al identify several reports connecting vaccine-strain measles virus with Crohn's disease and autoimmune hepatitis. They also hearken to earlier work that implicates inflamed or dysfunctional intestines in the behavior changes seen in some children. They point to other factors that suggest a genetic predisposition may also be a precondition of developing autism, along with markers of vitamin B12 deficiency (which many readers will recognize as a common finding in celiac disease and non-celiac gluten sensitivity). Clearly this group was not attacking the MMR vaccine or its importance to public health. Nonetheless, in the same issue of The Lancet, no less than six letters, written by a combined total of 21 authors, attacked Wakefield et al because of the impact that their findings might have on public health.

    Over the ensuing months and years, Wakefield's methods were criticized and denigrated. One of the more emotional attacks alleged academic fraud on Wakefield's part (7). He has been vilified in the public and professional media as a brigand. Yet he and his research group were careful to avoid making any claims beyond having found a form of bowel disease (lymphoid hyperplasia) in 9 of their subjects, and non-specific colitis in 11 of their subjects, along with reporting the close temporal association of onset of behavioral symptoms and MMR vaccines as reported by parents, health visitors, and general practitioners. They would have been remiss had they failed to report this association. Further, there were 12 other researchers who put their names to this research. Surely we cannot suspect that all 13 of these professionals would risk their careers to perpetrate a fraud!
    Meanwhile, as these attacks were ginning up, a research group at the University of Maryland reported that, in genetically susceptible individuals, a protein they dubbed "zonulin" can, when gluten is ingested, induce changes to intestinal permeability (8, 9). Does the gluten free, dairy free diet reduce excessive intestinal permeability? We know it does in people with celiac disease (8), but what impact would or could it have on children with the lymphoid hyperplasia and/or non-specific colitis identified by Wakefield et al? And does reduced zonulin production due to restriction of these foods explain the benefit experienced by many children with autism?

    Perhaps these questions are also relevant to another area of autism research reflected by identification of specific strains of clostridium infection in autism, first postulated by Bolte (10). Dr. S. Finegold and his colleagues demonstrated that 8 of 10 children with late onset autism showed transient reductions of symptoms of autism in response to oral vancomycin which returned when vancomycin was withdrawn (11). This is an antibiotic that is usually used in cases of antibiotic-resistant infections. Because this group identified an unusually large number and variety of strains of clostridium in their autistic subjects, as compared with controls, and because many clostridium variants excrete neurotoxic substances, their use of vancomycin was given to target clostridium.

    However, elements of Finegold's work and Wakefield's work may be taken to suggest some overlap. For instance, could the added clostridium load in autistic children contribute to the intestinal inflammation and permeability seen in Wakefield's report? Or could the MMR vaccinations produce conditions that are more hospitable to antibiotic resistant, neurotoxic strains of clostridia? Or could symptoms induced by MMR lead to administration of antibiotics that provide favorable conditions in the gut for proliferation of clostridium?

    To further complicate this issue, Dr. Stephanie Seneff has identified vitamin D deficiency, and popular use of statin drugs, in combination with reduced dietary consumption of cholesterol and fats as possible factors in autism. She implicates these deficiencies as arising either in utero or in infancy and she specifically cites work demonstrating that cholesterol, fats, and vitamin D are important components of healthy immune function (14).

    Putting it all together

    The hypothesis embodied herein asserts that at some stage the autistic child has: some predisposition to autism; a multi-dimensionally compromised immune system; been exposed to multiple and uncommon strains of clostridium which lead to the colonization of the gut by these antibiotic-resistant bacteria; are suffering from some degree of vitamin D deficiency and are eating a diet that is deficient in fats and cholesterol. Further, as the child develops one or more of the symptoms or sequelae of clostridium colonization or other infection, antibiotics are administered to provide relief from these or other symptoms of infection, sometimes including chronic ear infections. Thus, the competing gut bacteria that might otherwise keep these strains of clostridia in check are wiped out, permitting broader proliferation of multiple strains of clostridia.

    Similarly, the MMR vaccine, which, by design, engages and taxes the immune system. In the immune system's weakened state resulting from vaccination and dietary opioids (13), increased numbers of unusual strains of clostridium, abnormal gut biome, cholesterol deficiency, vitamin D deficiency, and perhaps, other nutrient deficiencies, also reduces systemic surveillance for, and antibody combat with, the clostridia and/or remnants of MMR vaccine. The neurotoxic excreta from clostridia and MMR are released into the intestinal lumen and by zonulin's action to widen the junctions between epithelial cells, these toxins are thus given access to the bloodstream. By the same pathway, opioids, other psychoactive peptides from gluten and dairy, along with other undigested and partly digested proteins, which may be harmful, also reach the bloodstream. From there, they travel to the BBB where zonulin again opens gaps in this barrier and allows the clostridium-derived toxins, opioids, and other impurities access to the brain where they alter blood-flow patterns, damage neurological tissues, and perhaps do other damage that has not yet been recognized. Ultimately, this damage and dynamics lead to impeded social performance, intellectual performance, and sometimes, induce startlingly abnormal behaviors.

    Although this picture appears bleak, and much of it simply reflects the several dietary miscues of the last and our current century, there are corrective steps that can sometimes improve these children's lives. Vitamin D, vitamin B12, and other supplements can be administered to address deficiencies. Because of the associated gut problems, sub-lingual vitamins, and exposure to sunlight without sun screen may both be good starting points. A strict, long-term gluten free, dairy free diet should also be on the menu, even if the whole family has to follow it to ensure that the autistic child does not rebel due to feeling deprived. High levels of cholesterol, saturated and mono-unsaturated fats should also comprise a large part of the diet. One or more courses of vancomycin may also be worth trying. In isolation, the benefits of antibiotics alone will likely be short-lived, as reported by Finegold, but in combination with these other strategies, may extend the benefits of this drug. New developments in antibiotics research may lead to isolation of protective substances from hens' egg shells that may provide more appropriate antibiotic relief and therefore benefit these children even more (15).

    Most of the research, to date, has focused on one of these factors in isolation. However, if an immune system is compromised by any or all of cholesterol deficiency, vitamin D deficiency, vitamin B12 deficiency, dietary shortages of cholesterol and fats, lingering, chronic sequelae of MMR vaccination, opioids from gluten and/or dairy, and an unusual and wide variety of clostridia, then it seems unreasonable to expect to reverse this condition through implementing only one of the interventions suggested by the above. Each and all of these other components should be addressed when attempting to remediate autism. In the context of these dietary and lifestyle changes, appropriate antibiotics may lead to more permanent improvements for the autistic child. This would be the greatest gift that a physician, parent, or caretaker could give to these children. One may hope.

     

    References:

    1. Reichelt KL, Hole K, Hamberger A, Saelid G, Edminson PD, Braestrup CB, Lingjaerde O, Ledaal P, Orbeck H. Biologically active peptide-containing fractions in schizophrenia and childhood autism. Adv Biochem Psychopharmacol. 1981;28:627-43.
    2. D'Eufemia P, Celli M, Finocchiaro R, Pacifico L, Viozzi L, Zaccagnini M, Cardi E, Giardini O. Abnormal intestinal permeability in children with autism. Acta Paediatr. 1996 Sep;85(9):1076-9.
    3. Gardner MLG (1994) in Physiology of the gastrointestinal tract (Johnson LR : edit) Rave Press, NY pp 1795-1820
    4. Knivsberg AM, Reichelt KL, Høien T, Nødland M. A randomised, controlled study of dietary intervention in autistic syndromes. Nutr Neurosci. 2002 Sep;5(4):251-61.
    5. Paul, K., Henker, J., Todt, A., Eysold, R. (1985) Zoeliaki- Kranken Kindern in Abhaengigkeit von der Ernaehrung Seitschrift der Klinische Medizin 40; 707-709. as reported in Reichelt K (1990). The Effect of Gluten-Free Diet on Urinary Peptide Excretion and Clinical State in Schizophrenia. Journal of Orthomolecular Medicine. 5(4): 223-239.
    6. Wakefield AJ, Murch SH, Anthony A, Linnell J, Casson DM, Malik M, Berelowitz M, Dhillon AP, Thomson MA, Harvey P, Valentine A, Davies SE, Walker-Smith JA. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet. 2004 Mar 6;363(9411):750.
    7. Flaherty DK. The vaccine-autism connection: a public health crisis caused by unethical medical practices and fraudulent science. Ann Pharmacother. 2011 Oct;45(10):1302-4. Epub 2011 Sep 13.
    8. Fasano A, Not T, Wang W, Uzzau S, Berti I, Tommasini A, Goldblum SE. Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease. Lancet. 2000 Apr 29;355(9214):1518-9.
    9. Clemente MG, De Virgiliis S, Kang JS, Macatagney R, Musu MP, Di Pierro MR, Drago S, Congia M, Fasano A. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function. Gut. 2003 Feb;52(2):218-23.
    10. Bolte ER. Autism and Clostridium tetani. Med Hypotheses. 1998 Aug;51(2):133-44.
    11. Finegold SM, Molitoris D, Song Y, Liu C, Vaisanen ML, Bolte E, McTeague M, Sandler R, Wexler H, Marlowe EM, Collins MD, Lawson PA, Summanen P, Baysallar M, Tomzynski TJ, Read E, Johnson E, Rolfe R, Nasir P, Shah H, Haake DA, Manning P, Kaul A. Gastrointestinal microflora studies in late-onset autism. Clin Infect Dis. 2002 Sep 1;35(Suppl 1):S6-S16.
    12. http://stephanie-on-health.blogspot.ca/2008/11/sunscreen-and-low-fat-diet-recipe-for.html 
    13. Hoggan R. Considering wheat, rye, and barley proteins as aids to carcinogens. Med Hypotheses. 1997 Sep;49(3):285-8
    14. Seneff S, Davidson R, Mascitelli L. Might cholesterol sulfate deficiency contribute to the development of autistic spectrum disorder? Med Hypotheses. 2012 Feb;78(2):213-7. Epub 2011 Nov 17.
    15. Wellman-Labadie O, Lakshminarayanan R, Hinckeemail MT Antimicrobial properties of avian eggshell-specific C-type lectin-like proteins. FEBS Letters Volume 582, Issue 5 , Pages 699-704, 5 March 2008

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    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