The concept of entero‐colonic encephalopathy, autism and opioid receptor ligands

Wakefield, Andrew J.; Puleston, J. M.; Montgomery, Scott; Anthony, A; O’Leary, John; Murch, Simon

doi:10.1046/j.1365-2036.2002.01206.x

Cited by 82 publications

(54 citation statements)

References 101 publications

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“…[19][20][21] Children with autistic spectrum disorders (ASD) frequently have accompanying gastrointestinal (GI) symptoms and pathology, 22,23 which includes inflammation of the GI tract. [24][25][26][27] Many autistic children, particularly those with GI disease, also have a higher propensity for fungal infections. 28,29 We previously reported that a significant number of autistic children with GI disease have ANCA (both anti-PR3 and anti-MPO), and that there is a relationship between individuals with ANCA and severity of intestinal disease.…”

Section: Introductionmentioning

confidence: 99%

Generalized Autoimmunity of ANCA and ASCA Related to Severity of Disease in Autistic Children with GI Disease

Russo

Krigsman

Jepson

et al. 2009

Immunol Immunogenet Insights

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Aim: To assess serum Anti-Neutrophil cytoplasmic Antibody (ANCA-PR3 and MPO) and Anti-Saccharomyces Cerevisiae Antibody (ASCA) levels in autistic children with severe gastrointestinal (GI) disease and to test the hypothesis that there is generalized autoimmunity in a subpopulation of autistic children with severe GI disease and that this autoimmunity is associated with the severity of GI disease. Subjects and Methods:Serum from 40 autistic children with chronic digestive disease (most with ileo-colonic lymphoid nodular hyperplasia (LNH) and inflammation of the colorectum, small bowel and/or stomach), and 24 controls (13 age matched autistic children with no GI disease and 11 age matched children without autism or GI disease) were tested using ELISAs designed to quantitate ANCA (PR3 and MPO) and ASCA levels. ANCA and ASCA concentration of autistic children with GI disease were compared to GI disease severity (including LNH and erythema). Results:We previously reported that 6 of the 40 autistic children with GI disease in this study had anti-PR3 ANCA. All 6 of these also had anti-MPO IgG. In this study, we found that 6 of the 40 autistic children also had ASCA and 4 of these children with ASCA also had both anti-PR3 and anti-MPO ANCA. These 4 with ANCA and ASCA had significantly higher GI disease severity, particularly associated with LNH and erythema.Discussion: These results suggest a general autoimmune response (ANCA and ASCA) in a sub group (high GI disease severity) of autistic children with GI disease. The presence of these autoantibodies may be a useful biomarker for autistic children with severe GI disease.

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Section: Introductionmentioning

confidence: 99%

Generalized Autoimmunity of ANCA and ASCA Related to Severity of Disease in Autistic Children with GI Disease

Russo

Krigsman

Jepson

et al. 2009

Immunol Immunogenet Insights

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“…El incremento del número de vacunaciones y sus respectivos refuerzos, vía las dosis multivalentes, especialmente la vacuna contra el sarampión contenida en la combinación triple viral sarampión-rubéola-paperas ( [40][41][42][43][44][45][46][47][48][49][50][51][52][53] ). 3.…”

Section: Rol De Las Vacunas Sobre La Epidemiaunclassified

El timerosal y las enfermedades del neurodesarrollo infantil

Maya

Luna

2013

An Fac med

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Resumen Se evalúa la relación causal entre el timerosal (etilmercurio), como preservante en las vacunas pediátricas, y el incremento de casos de enfermedades del neurodesarrollo infantil, como consecuencia de la ampliación de los esquemas de inmunización. Se revisó la información científica, relacionando el timerosal y las evidencias que permitan evaluar una posible asociación causal, con estudios epidemiológicos, ecológicos, biomoleculares y toxicológicos, de bioseguridad, toxicológicos fetales y sobre salud reproductiva. Se encontró múltiples asociaciones entre la exposición a timerosal y las enfermedades del neurodesarrollo infantil. Tal neurotoxicidad ocurre en los infantes y fetos de gestantes vacunadas por dosis acumulativa de mercurio. Las diversas evidencias implican al timerosal como el agente causante, agravante o disparador de las enfermedades del neurodesarrollo infantil. La toxicidad del mercurio obligó al retiro progresivo del timerosal de los medicamentos. Lamentablemente, en las vacunas, ha habido una sustancial demora en la demostración de su impacto negativo. Actualmente, existen vacunas sin timerosal, cuyo uso está ocasionando la disminución de la incidencia de las enfermedades del neurodesarrollo infantil. Palabras claveTimerosal; autismo; enfermedades del sistema nervioso; desarrollo infantil; vacunas. Thimerosal and children's neurodevelopmental disorders AbstractThe causal relation of thimerosal (ethylmercury) Dichas estadísticas convertían a los DEA en la mayor epidemia de enfermedades mentales jamás observada en la historia de los EE.UU., significando más casos que enfermedades, tales como el síndrome de Down, la diabetes mellitus tipo 1 y el cáncer pediátrico ( 8 ). Si bien en nuestro medio aún no disponemos de datos estadísticos que estimen la magnitud de este problema, varios países en todo el mundo simultáneamente han notificado incrementos similares. En la China, por ejemplo, donde los DEA eran prácticamente desconocidos, coincidiendo con la introducción de las compañías norteamericanas productoras de vacunas a partir del año 1999, se ha informado sobre 1,8 millones de niños autistas recientemente diagnosticados; asimismo, los DEA también se han incrementado significativamente en la India, Nicaragua, Argentina y en otros países en vías de desarrollo, durante los últimos años ( 19 ). El hecho de observar tan impresionante aumento de casos, como el descrito, descartaba definitivamente la hipó-tesis de que estas enfermedades fueran debidas exclusivamente a un trastorno genético, pues dichas condiciones tardan muchos años en desarrollarse y nunca alcanzan cifras epidémicas, salvo exposiciones ionizantes o catástrofes nucleares.Algunos investigadores adujeron que tal fenómeno podría deberse a cambios y mejoras en los criterios de diagnóstico. Sin embargo, a pesar que desde el año 1994 se comenzó a aplicar en los EE.UU. y en todo el mundo los criterios del DSM IV (Diagnostic and Statistical Manual 4 th Ed.), como fuente obligatoria para el diagnóstico de las enfermedades mentales, ...

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“…As discussed in the introduction, there may be a shared etiology between ASD and hepatic encephalopathy [3,63], which develops following liver failure. Both conditions involve the gut-brain axis.…”

Section: Insights From Hepatic Encephalopathymentioning

confidence: 99%

“…The original hypothesis is that the inflammation, fever, and seizures associated with encephalitis catalyze the synthesis of sulfate from taurine, leading to a partial renewal of sulfated proteoglycans in the brain and in the vasculature. Aligning in part with the hypothesis proposed in [3] that ASD is characterized by a chronic low-grade pathology of biosulfate depletion, loss of barrier integrity, suppressed autophagy, and inflammation, the signaling cascade proposed here does not depend on penetration of opiogenic peptides into the brain.…”

mentioning

confidence: 99%

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Seneff¹,

Lauritzen

Davidson³

et al. 2013

Entropy

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This paper makes two claims: (1) autism can be characterized as a chronic lowgrade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is provoked by a systemic deficiency in sulfate, but associated seizures and fever support sulfate restoration. We argue that impaired synthesis of cholesterol sulfate in the skin and red blood cells, catalyzed by sunlight and nitric oxide synthase enzymes, creates a state of colloidal instability in the blood manifested as a low zeta potential and increased interfacial stress. Encephalitis, while life-threatening, can result in partial renewal of sulfate supply, promoting neuronal survival. Research is cited showing how taurine may not only help protect neurons from hypochlorite exposure, but also provide a source for sulfate renewal. Several environmental factors can synergistically promote the encephalopathy of autism, including the herbicide, glyphosate, aluminum, mercury, lead, nutritional deficiencies in thiamine and zinc, and yeast overgrowth due to excess dietary sugar. Given these facts, dietary and lifestyle changes, including increased sulfur ingestion, organic whole foods, increased sun exposure, and avoidance of toxins such as aluminum, mercury, and lead, may help to alleviate symptoms or, in some instances, to prevent autism altogether. OPEN ACCESSEntropy 2013, 15 373

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The concept of entero‐colonic encephalopathy, autism and opioid receptor ligands

Cited by 82 publications

References 101 publications

Generalized Autoimmunity of ANCA and ASCA Related to Severity of Disease in Autistic Children with GI Disease

Generalized Autoimmunity of ANCA and ASCA Related to Severity of Disease in Autistic Children with GI Disease

El timerosal y las enfermedades del neurodesarrollo infantil

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

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