Dr Wakefield articles/papers
Dr. Andy Wakefield
[pdf] 'That Paper' by Andrew Wakefield
From Carmel Wakefield
 Peer Reviewed Papers Support Findings. The following peer-reviewed papers support the findings of the original work by Wakefield and colleagues at the Royal Free Hospital in the UK:
[2009 pdf] Andrew J Wakefield et al. Response to Dr. Ari Brown and the Immunization Action Coalition
[2009 pdf] Hewitson... Wakefield.
Delayed acquisition of neonatal reflexes in newborn primates receiving a
thimerosal-containing Hepatitis B vaccine: Influence of gestational age and
[2010 March] Joan Cranmer’s Fateful Decisions and the Suppression of Autism Science By Mark Blaxill
The Seat of the Soul; The Origins of the Autism Epidemic
by ANDREW WAKEFIELD, MB, BS, FRCS, FRCPath
Andrew J. Wakefielda, FRCS FRCPath; Carol Stottb, PhD; and Kirsten Limbc, BSc
Gastrointestinal comorbidity, autistic regression and Measles-containing vaccines: positive re-challenge and biological gradient
Article-in-press; Medical Veritas: The Journal of Medical Truth; Volume 3, Issue 1, April 2006.
Medical Veritas is the journal of Medical Veritas International (MVI);
[pdf] PAUL ASHWOOD,1,5 ANDREW ANTHONY,2 FRANCO TORRENTE,1,3 and ANDREW J. WAKEFIELD4 Spontaneous Mucosal Lymphocyte Cytokine Profiles in Children with Autism and Gastrointestinal Symptoms: Mucosal Immune Activation and Reduced Counter Regulatory Interleukin-10
[Jan 2001] Measles, Mumps, Rubella Vaccine: Through a Glass, Darkly.
[Oct 2004] Press Release: Thoughtful House scientists make important breakthrough in autism
Measles-containing vaccines and IBD-----Andrew Wakefield, 02 January 2002
Detection of Measles Virus Genomic RNA in Cerebrospinal Fluid of Children with Regressive Autism: a Report of Three Cases J.J. Bradstreet, M.D.; J. El Dahr, M.D.; A. Anthony, M.B., Ph.D.; J.J. Kartzinel, M.D.; A.J. Wakefield, M.B.
F, Ashwood P, Day R, Machado N, Furlano RI, Anthony A, Davies SE, Wakefield AJ, Thomson
MA, Walker-Smith JA, Murch SH.Small intestinal enteropathy with
epithelial IgG and complement deposition in children with regressive autism.Mol Psychiatry. 2002;7(4):375-82.PMID: 11986981 [PubMed - in process]
We have reported lymphocytic colitis in children with regressive autism, with epithelial damage prominent. We now compare duodenal biopsies in 25 children with regressive autism to 11 with coeliac disease, five with cerebral palsy and mental retardation and 18 histologically normal controls. Immunohistochemistry was performed for lymphocyte and epithelial lineage and functional markers. We determined the density of intraepithelial and lamina propria lymphocyte populations, and studied mucosal immunoglobulin and complement C1q localisation. Standard histopathology showed increased enterocyte and Paneth cell numbers in the autistic children. Immunohistochemistry demonstrated increased lymphocyte infiltration in both epithelium and lamina propria with upregulated crypt cell proliferation, compared to normal and cerebral palsy controls. Intraepithelial lymphocytes and lamina propria plasma cells were lower than in coeliac disease, but lamina propria T cell populations were higher and crypt proliferation similar. Most strikingly, IgG deposition was seen on the basolateral epithelial surface in 23/25 autistic children, co-localising with complement C1q. This was not seen in the other conditions. These findings demonstrate a novel form of enteropathy in autistic children, in which increases in mucosal lymphocyte density and crypt cell proliferation occur with epithelial IgG deposition. The features are suggestive of an autoimmune lesion.PMID: 11986981 [PubMed - in process]
Uhlmann V, Martin CM, Sheils O, Pilkington L, Silva I, Killalea A, Murch SB, Walker-Smith J, Thomson M, Wakefield AJ, O'Leary JJ. Potential viral pathogenic mechanism for new variant inflammatory bowel disease.Mol Pathol. 2002 Apr;55(2):84-90.PMID: 11950955 [PubMed - in process]
AIMS: A new form of inflammatory bowel disease (ileocolonic lymphonodular hyperplasia) has been described in a cohort of children with developmental disorder. This study investigates the presence of persistent measles virus in the intestinal tissue of these patients (new variant inflammatory bowel disease) and a series of controls by molecular analysis. METHODS: Formalin fixed, paraffin wax embedded and fresh frozen biopsies from the terminal ileum were examined from affected children and histological normal controls. The measles virus Fusion (F) and Haemagglutinin (H) genes were detected by TaqMan reverse transcription polymerase chain reaction (RT-PCR) and the Nucleocapsid (N) gene by RT in situ PCR. Localisation of the mRNA signal was performed using a specific follicular dendritic cell antibody. RESULTS: Seventy five of 91 patients with a histologically confirmed diagnosis of ileal lymphonodular hyperplasia and enterocolitis were positive for measles virus in their intestinal tissue compared with five of 70 control patients. Measles virus was identified within the follicular dendritic cells and some lymphocytes in foci of reactive follicular hyperplasia. The copy number of measles virus ranged from one to 300,00 copies/ng total RNA. CONCLUSIONS: The data confirm an association between the presence of measles virus and gut pathology in children with developmental disorder.
Wakefield AJ. MMR vaccination and autism. Lancet. 1999 Sep 11;354(9182):949-50. No abstract available.PMID: 10489978; UI: 99418510.
(Adverse Drug Reactions 2000,19(4) 1-19. Authors: Andrew J Wakefield FRCS, Scott M Montgomery PhD.)
A J Wakefield,
S H Murch, A Anthony, J Linnell, D M Casson, M Malik,
M Berelowitz, A P Dhillon, M A Thomson, P Harvey, A
Valentine, S E Davies, J A Walker-SmithVolume 351, Number 9103 28 February 1998
Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and
pervasive developmental disorder in children
American Journal of Gastroenterology, September, 2000
Volume 95, Number 9
A. J. Wakefield, F.R.C.S.,a,b A. Anthony, M.Sc., Ph.D., M.B.B.S.,b S. H.
Murch, Ph.D., F.R.C.P., F.R.C.P.C.H.,b M. Thomson, MB.ChB., M.R.C.P.,
F.R.C.P.C.H.,c S. M. Montgomery, Ph.D.,c S. Davies, M.R.C.Path.,b J. J.
O'Leary, M.D., D.Phil., M.R.C.Path.,b M. Berelowitz, F.R.C.Psych.,e and J.
A. Walker-Smith, M.D., F.R.C.P., F.R.A.C.P., F.R.C.P.C.H.d
OBJECTIVE: Intestinal pathology, i.e., ileocolonic lymphoid nodular
hyperplasia (LNH) and mucosal inflammation, has been described in children
with developmental disorders. This study describes some of the endoscopic
and pathological characteristics in a group of children with developmental
disorders (affected children) that are associated with behavioral regression
and bowel symptoms, and compares them with pediatric controls.
METHODS: Ileocolonoscopy and biopsy were performed on 60 affected children
(median age 6 yr, range 3-16; 53 male). Developmental diagnoses were autism
(50 patients), Asperger's syndrome (five), disintegrative disorder (two),
attention deficit hyperactivity disorder (ADHD) (one), schizophrenia (one),
and dyslexia (one). Severity of ileal LNH was graded (0-3) in both affected
children and 37 developmentally normal controls (median age 11 yr, range
2-13 yr) who were investigated for possible inflammatory bowel disease
(IBD). Tissue sections were reviewed by three pathologists and scored on a
standard proforma. Data were compared with ileocolonic biopsies from 22
histologically normal children (controls) and 20 children with ulcerative
colitis (UC), scored in an identical manner. Gut pathogens were sought
RESULTS: Ileal LNH was present in 54 of 58 (93%) affected children and in
five of 35 (14.3%) controls (p < 0.001). Colonic LNH was present in 18 of 60
(30%) affected children and in two of 37 (5.4%) controls (p < 0.01).
Histologically, reactive follicular hyperplasia was present in 46 of 52
(88.5%) ileal biopsies from affected children and in four of 14 (29%) with
UC, but not in non-IBD controls (p < 0.01). Active ileitis was present in
four of 51 (8%) affected children but not in controls. Chronic colitis was
identified in 53 of 60 (88%) affected children compared with one of 22
(4.5%) controls and in 20 of 20 (100%) with UC. Scores of frequency and
severity of inflammation were significantly greater in both affected
children and those with UC, compared with controls (p < 0.001).
CONCLUSIONS: A new variant of inflammatory bowel disease is present in this
group of children with developmental disorders.
Cite this article as: . Wakefield AJ, Anthony A, Murch SH, Thomson M,
Montgomery SM, Davies S, O'Leary JJ, Phil D, Berelowitz M and Walker-Smith
JA. Enterocolitis in Children With Developmental Disorders. Am J
aUniversity Departments of Medicine, bHistopathology, cPaediatric
Gastroenterology, and dPaediatric Psychiatry, Royal Free and eUniversity
College Medical School, Royal Free Campus, London, United Kingdom, and
University Department of Pathology, Coombe Women's Hospital and Trinity
College, Dublin, Eire