הסיכון שבחיסונים אינו תלוי בגיל ../images/Emo4.gif
כאשר יש מום גנטי או פרה-דיספוזיציה, הנזק יכול לקרות, גם בגיל הרך וגם בגיל הבוגר. כמובן שהסיכון לתת חיסון בגיל שנה , כאשר התינוק בהתפתחות מואצת- הוא סיכון גדול שבעתיים לנזק מוחי. כולנו יודעים שהבסיס של הבעייה בילדים האוטיסטים הוא במוח. כל נושא הוויסות החושי- תחושתי, למידה עצמאית , הפנמה והכללה וכמובן תקשורת ושפה- כולם הם פונקציה של תפקוד חלקי המוח השונים. וכאשר המוח נפגע בגיל שנה- זוהי פגיעה איומה! גם בגיל 6-7 יכולה להיות פגיעה מוחית אם קיים המום או הרגישות הראשונית. וחבל להתחיל לימודים ומייד להרוס לילד את הצ'אנס לתפקד כראוי. מאותה סיבה, נראה לי כי לתת בגיל 13 או 3 זה לא בהכרח יפתור את הבעייה. שוב, בהנחה ויש בעייה דומה לזו שהצגתי- כאשר יש מום ביכולת התגובה הכבדית למתכות כבדות ורעלים. Title The neurotoxic etiology of the autistic spectrum disorders: A replication study. Author Edelson, Stephen B. (1); Cantor, David Organization (1) Edelson Center for Environmental and Preventive Medicine, Inc., 3833 Rowell Road, Suite 110, Atlanta, GA, 30342:
[email protected], www.edelsoncenter.com,
[email protected], www.psycscienceinst.com USA Publication Source Toxicology and Industrial Health, (September, 2000) Vol. 16, No. 6, pp. 239-247. print. Although it has been recognized that autism is a disorder due to dysfunctional central nervous system functioning, a model that can account for the diversity of the symptoms in the syndrome and the concordant anomalies in metabolic functioning, in a sample of 20 autistic individuals, Edelson and Cantor (Edelson S.B., and Cantor D.S. Autism: xenobiotic influences. Toxicol Ind Health 1998: 14 (6) : 799-811.) demonstrated a body burden of neurotoxicants in over 90% of these individuals with 100% of these individuals demonstrating impaired liver detoxication processes. This current study examined an independent sample of 39 autistic individuals and was able to replicate the general findings of Edelson and Cantor. We further evidence the genetic and environmental aspects of this hypothetical process and believe the immune system injury secondary to the immunotoxins causes "activation" of the immune system leading to the production of autoantibodies against haptens (brain proteins attached to chemical molecules), and the subsequent damage as part of the process of neurotoxicity in the autistic spectrum. This process has as its final pathway one of free radical generation and molecular injury. This paper can not go into the complex details of this process at this time. All of the above leads to a spectrum of neurodevelopment dysfunction demonstrated as autism. וכאשר יש מום יווצר נזק גם בגילאים השונים- יפגע ביכולות מוחיות שונות- למידה, ריכוז וקשב, הבנה ויכולות קוגניטיביות שונות. Intra-monocyte pathogens delineate autism subgroups. Author Binstock, T. (1) Organization (1) Researcher in Developmental and Behavioural Neuoanatomy, Estes Park, CO, 80517:
[email protected] USA Publication Source Medical Hypotheses, (April, 2001) Vol. 56, No. 4, pp. 523-531. print. Immune panels of many autism-spectrum children reveal signs of atypical infections and shifted cell counts. In conjunction with trait-related cerebral hypometabolism and hypoperfusion, these findings suggest a hypothesis: Several autism-spectrum subgroups derive from intra-monocyte pathogens such as measles virus, cytomegalovirus, human herpesvirus 6, and Yersinia enterocolitica. Furthermore, with much inter-child variation, their effects manifest as diminished hematopoiesis, impaired peripheral immunity, and altered blood-brain barrier function often accompanied by demyelination. In some such children, one or more of these pathogens persists as a chronic-active, seemingly subclinical infection etiologically significant to the child's autistic traits. Within these subgroups, immune impairments and atypical infections may be treatable. זהו תקציר מהמאמר הדן בבעייתיות של מערכת החיסון וההשתלטות של וירוסים שחלקם הגיע מחיסונים, על מערכת החיסון והמוח. גם הרגישויות השונות במערכת העיכול קשורה לוירוסים אלה , המתנחלים שם ויוצרים דלקת כרונית של המעי ונזק ניכר ספיגת מזון Colonic CD8 and gammadelta T-cell infiltration with epithelial damage in children with autism. Furlano, Raoul I.; Anthony, Andrew; Day, Richard; Brown, Angela; McGarvey, Louise; Thomson, Michael A.; Davies, Susan E.; Berelowitz, Mark; Forbes, Alastair; Wakefield, Andrew J.; Walker-Smith, John A.; Murch, Simon H. (1) Organization (1) University Department of Paediatric Gastroenterology, Royal Free and University College Medical School, Rowland Hill St, Royal Free Campus, London, NW3 2PF UK Publication Source Journal of Pediatrics, (March, 2001) Vol. 138, No. 3, pp. 366-372. print. English Abstract Objectives: We have reported colitis with ileal lymphoid nodular hyperplasia (LNH) in children with regressive autism. The aims of this study were to characterize this lesion and determine whether LNH is specific for autism. Methods: Ileo-colonoscopy was performed in 21 consecutively evaluated children with autistic spectrum disorders and bowel symptoms. Blinded comparison was made with 8 children with histologically normal ileum and colon, 10 developmentally normal children with ileal LNH, 15 with Crohn's disease, and 14 with ulcerative colitis. Immunohistochemistry was performed for cell lineage and functional markers, and histochemistry was performed for glycosaminoglycans and basement membrane thickness. Results: Histology demonstrated lymphocytic colitis in the autistic children, less severe than classical inflammatory bowel disease. However, basement membrane thickness and mucosal gammadelta cell density were significantly increased above those of all other groups including patients with inflammatory bowel disease. CD8+ density and intraepithelial lymphocyte numbers were higher than those in the Crohn's disease, LNH, and normal control groups; and CD3 and plasma cell density and crypt proliferation were higher than those in normal and LNH control groups. Epithelial, but not lamina propria, glycosaminoglycans were disrupted. However, the epithelium was HLA-DR-, suggesting a predominantly TH2 response. Interpretation: Immunohistochemistry confirms a distinct lymphocytic colitis in autistic spectrum disorders in which the epithelium appears particularly affected. This is consistent with increasing evidence for gut epithelial dysfunction in autism.
