Two posts on Meryl's fail in one day?

Well, yes. There's that much fail.

Meryl tweeted a few hours ago. Here's what she had to say:

Yes, Meryl. That's totally new research. Completely.

Except that... oh, wait... let's look at the article, shall we?

There's no date at the top. The Daily Fail does that. But look at the comments. The most recent is from....


- Helen, London, 13/6/2006 17:56

Wait, what?

Yep, that's right. Meryl is trying to vindicate the work of the discredited, unethical, censured quack Andrew Wakefield with an article from 2006, nearly four years previous to the GMC decision that has seen Wakefield's public disgrace.

Nice work Meryl.

Oh, and that research? The story was based on preliminary findings. I can't find much mention of it on the web, but Neurodiversity blog mentions it here in the context of US special court findings. Damned if I can find it in PubMed, anyway. Got a copy, Meryl?

posted @ Sunday, April 18, 2010 1:10 AM


Comments on this entry:

# re: Two posts on Meryl's fail in one day?

Left by Sean the Blogonaut at 4/18/2010 10:44 AM
Is their a research and fact checking for dummies?

# re: Two posts on Meryl's fail in one day?

Left by Jason at 4/18/2010 10:51 PM
This info is Courtesy of Jo Benhamu, Australian Skeptics:


I'll be a pain and repost my previous post on Rach's page. This is the "research" in question:

Poorly designed, lacking in declaration of conflicts of interest, sample group came from pool of patients who presented (I believe to Krigsman) for treatment. The paper was also authored by Arthur Krigsman, he of Thoughtful House fame

Walker apparently warned against drawing any conclusions from the research.

It's also mentioned in Michael Fitzpatrick's book "Defeating autism: A Damaging Delusion".

Abstract of presented research
Walker, S.J., Hepner K., Segal, J., & Krigsman A., Department of Physiology & Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27101 USA
Background: Autistic enterocolitis, consisting of a nonspecific ileocolitis coupled with ileocolonic lymphonodular hyperplasia (LNH), was first introduced as a new, potentially virus-induced disease entity eight years ago in a group of ASD children with developmental regression.
Objectives: The primary objective of this study was to examine ileal biopsy tissue in a large cohort of pediatric patients who carry a diagnosis of regressive autism and whose chronic gastrointestinal symptoms warranted diagnostic endoscopic evaluation, for evidence of measles
virus RNA.
Methods: Patients who had been diagnosed with autism and who were referred to a pediatric gastroenterologist for evaluation of chronic GI symptoms were eligible to participate in this IRB approved study. For each patient, medical histories, vaccination records, histopathology reports,
and ileocolonoscopic biopsy tissue were available for evaluation. Terminal ileum (TI) biopsy 6
tissue was assayed by RT-PCR for the presence of measles virus RNA and PCR-positive samples were sequenced.
Results: Medical and clinical data have been collected for >275 patients who fit the study inclusion criteria. PCR analysis on TI biopsy tissue from an initial 82 patients showed that 70 (85%) were positive for the F gene amplicon. Fourteen have been verified by DNA sequence and
an additional 56 amplicons are being sequenced now. Work is ongoing to assay the remaining specimens (~200) and to identify and assay relevant control tissue samples.
Conclusions: Preliminary results from this large cohort of pediatric autistic patients with chronic GI symptoms confirm earlier findings of measles virus RNA in the terminal ileum and support an association between measles virus and ileocolitis /LNH. The key to completing this study is to compare the findings with those in intestinal tissues from
children without autism. We have recently initiated a collaboration with a major children’s hospital
for the provision of these samples.
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